Efnisyfirlit

• Front Matter
• Preface
• Acknowledgements
• Foreword
• List of editors and contributors
• List of reviewers
• Chapter 1 The newborn
• Key points
• Definitions of prematurity and growth
• Changes to the cardiorespiratory system
• Figure 1.1 The normal newborn baby.
• Neonatal resuscitation
• Figure 1.2 Changes in fetal circulation at birth (IVC, inferior vena cava; SVC, superior vena cava; degree of oxygenation shown in circles).
• Figure 1.3 Algorithm for neonatal resuscitation.
• Temperature control
• Table 1.1 Apgar scores for neonates2
• Vitamin K and hepatitis B vaccination
• Feeding
• Postnatal care
• Examination of the neonate
• Figure 1.4 Examination of the hips of a newborn infant.
• Newborn screening
• Table 1.2 Australian Standard Vaccine schedule (July 2013)
• Premature infants
• Jaundice
• Long-term developmental outcomes
• Taking the baby home
• References
• MCQ
• Chapter 2 Sexual development and puberty
• Key points
• Introduction
• Normal embryological development of the internal and external genitalia
• Figure 2.1 Male and female urogenital differentiation.
• Human sex development
• Abnormal embryological development — disorders of sex development
• Definition and classification
• Sex chromosome DSD
• 46XX DSD
• Box 2.1 Possible presentations of Müllerian anomalies
• Müllerian anomalies
• Aetiology
• Presentation
• Investigation
• Congenital adrenal hyperplasia
• Other causes of XX fetal virilisation
• 46XY DSD
• Androgen receptor defects — androgen insensitivity syndrome
• Figure 2.2 A: Normal Müllerian development. B: Bicornuate uterus. C: Complete septate uterus.
• Figure 2.3 A: A hysteroscopic view of a uterine septum showing that the uterine cavity is divided by a central fibrous band of tissue. This can be removed surgically. B: The appearance of a bicornuate uterus at laparoscopy. Note the peritoneal band between the two horns.
• Gonadal dysgenesis
• Figure 2.4 The sequence of pubertal events in the female.
• Androgen biosynthetic defects
• Puberty: timing and its problems
• Normal puberty
• Central control of puberty: pulsatile GnRH
• Stages of puberty
• The growth spurt
• Thelarche
• Adrenache
• Menarche
• Urogenital changes
• Figure 2.5 The Tanner stages of breast and pubic hair development.
• Delayed puberty
• History and examination
• Precocious puberty
• Box 2.2 Common causes of delayed puberty
• Hypergonadotrophic hypogonadism
• Hypogonadotrophic hypogonadism
• Reversible
• Irreversible
• Eugonadism
• Investigating pubertal abnormalities
• Treatment of delayed puberty
• Specific conditions associated with eugonadism
• Treatment of precocious puberty
• Further reading
• Embryology
• Reproductive endocrinology
• DSD consensus statement
• Other
• MCQS
• OSCE
• Chapter 3 Fundamentals of gynaecology: the menstrual cycle and clinical interaction
• Key points
• Introduction
• The menstrual cycle
• Neuroendocrinology
• Hypothalamus
• Pituitary
• Phases of the menstrual cycle
• Follicular phase
• Luteal phase
• Ovarian follicular development
• The LH surge and ovulation
• The endometrium
• Menstruation
• Figure 3.1 Hormonal changes during the menstrual cycle. The menstrual cycle is a cycle of the hypothalamic–pituitary–ovarian axis, as well as a cycle of the targets of the ovarian hormones — the endometrium of the uterus. Therefore, the menstrual cycle includes both an ovarian cycle, which includes the follicular phase, ovulation, and the luteal phase, and an endometrial cycle, which includes the menstrual, the proliferative, and the secretory phases.
• Gynaecology history taking and examination
• Figure 3.2 The endometrial cycle. The ovarian cycle includes the follicular phase, in which the follicle develops, and the luteal phase, in which the remaining follicular cells develop into the corpus luteum. The endometrial cycle has three phases: the menstrual, the proliferative, and the secretory.
• Figure 3.3 Taking a history.
• The presenting issue
• Past gynaecological history
• Other history
• Examination
• Conclusion
• Further reading
• MCQS
• OSCE
• Chapter 4 Sexual activity and contraception
• Key points
• Introduction
• Figure 4.1 Various methods of contraception: A — monophasic OCP; B — triphasic OCP; C — POP (minipill); D — postcoital contraception; E — male condom; F — female condom; G — diaphragm; H — IUDs; I — Implanon rod and insertion trocar.
• Hormonal contraceptive methods
• Combined oral contraceptive pill (COCP) — ‘The Pill’
• Box 4.1 Risks and benefits of the combined oral contraceptive pill
• Risks
• Benefits
• Types of Pill
• Box 4.2 Hormones in oral contraceptive pills
• Oestrogens
• Synthetic
• Bio-identical**
• Progestogens
• Missed tablets
• The vaginal ring
• Other combined delivery systems
• Progestogen-only pill (POP) or minipill
• Injectable progestogen-only contraception
• Progestogen implants
• Non-hormonal contraception
• Intrauterine devices (IUDs)
• Inert IUDs
• Copper IUDs
• Progestogen-releasing IUDs
• Frameless IUDs
• Insertion
• Pregnancy
• Contraindications to IUD use
• Barrier methods of contraception
• Condoms — male and female
• Diaphragms and spermicides
• Natural family planning
• Emergency contraception (EC)
• Combined emergency contraception
• Progestogen-only EC
• Other hormonal methods of emergency contraception
• Non-hormonal emergency contraception
• Permanent contraception
• Vasectomy
• Tubal occlusion
• Termination of pregnancy
• Surgical termination of pregnancy
• Vacuum aspiration or curettage
• Manual vacuum evacuation
• Complications
• Medical termination
• Further reading
• MCQS
• OSCE
• Chapter 5 Sexually transmitted infections
• Key points
• Introduction
• Passengers and parasites
• Pubic lice
• Treatment
• Trichomonas
• Treatment
• Bacterial sexually transmitted infections
• Chlamydia
• Box 5.1 Notifiable sexually transmissible diseases in Australia
• Symptoms and transmission
• Investigations
• Treatment
• Gonorrhoea
• Symptoms and transmission
• Investigations
• Treatment
• Syphilis
• Transmission
• Symptoms
• Diagnosis
• Treatment
• Viral sexually transmitted infections
• Human papilloma virus (HPV)
• Clinical HPV
• Subclinical HPV
• Genital herpes simplex virus — HSV
• Symptoms and transmission
• Diagnosis
• Treatment
• Molluscum contagiosum
• Hepatitis
• Hepatitis A (HAV)
• Hepatitis B (HBV)
• Hepatitis C (HCV)
• Human immunodeficiency virus
• Box 5.2 Serological markers for hepatitis B
• HB surface antibody
• HB core antibody
• HB surface antigen
• HBe antigen
• Transmission
• Symptoms
• Investigations and treatment
• Antenatal screening for HIV
• Further reading
• MCQS
• OSCE
• Chapter 6 Fertility
• Key points
• Natural fertility, the fertile phase of the cycle and sexual function
• Lifestyle factors
• Ovulation
• Figure 6.1 The hypothalamic–pituitary–ovarian axis in the regulation of follicular maturation and steroidogenesis. A = androgens, E2 = oestradiol, FSH = follicle-stimulating hormone, GnRH = gonadotrophin-releasing hormone, LH = luteinising hormone.
• Figure 6.2 The menstrual cycle showing hormonal, ovarian and endometrial changes.
• Sperm production
• Figure 6.3 The hypothalamic–pituitary–testicular axis. Gonadotrophin-releasing hormone (GnRH) is released from the hypothalamus, stimulating release of luteinising hormone (LH) and follicle-stimulating hormone (FSH). FSH stimulates germ cell epithelium and LH induces testosterone production by the Leydig cells. Both testosterone (T) and inhibin (IN) downregulate gonadotrophin release.
• Figure 6.4 Three seminiferous tubules undergoing active spermatogenesis. Elongate spermatids are present along the luminal border of each tubule.
• Table 6.1 WHO lower reference limits for normal semen analysis2
• Fertilisation
• Implantation
• Figure 6.5 The endometrium in the follicular phase of the cycle. A: Ultrasound appearance of proliferative phase; B: Dominant 20 mm follicle in the ovary; C: Histology of proliferative phase endometrium.
• Figure 6.6 The endometrium in the secretory phase of the cycle. A: Ultrasound appearance of mid-secretory phase; B: Corpus luteum in the ovary with peripheral vascular ‘ring of fire’; C: Histology of mid-secretory phase endometrium low power and D: High power.
• Figure 6.7 Three-dimensional representation of early intrauterine pregnancy at 5 weeks 3 days. A: Coronal view of 6 mm gestation sac in the right fundal region of the endometrial cavity; B: Magnified image of the gestation sac shows 3 mm yolk sac. No embryo is yet visible. The strong endometrial decidual reaction around the gestation sac indicates successful implantation.
• References
• MCQS
• OSCE
• Chapter 7 Problems of fertility
• Key points
• Epidemiology
• Pathophysiology
• History and examination
• Investigations
• Male
• Female
• Ovulation
• Figure 7.1 Diagnostic testicular biopsies. A: Normal testis; B: Maturation arrest of spermatogenesis; C: Sertoli cell only; D: Hypospermatogenesis.
• Figure 7.2 Transvaginal ultrasound image of polycystic ovary. This ovary contained in excess of 60 antral follicles of 2–9 mm.
• Tubal patency
• Cervical factors
• Treatment
• Male
• Figure 7.3 Ultrasound tubal patency test. A: Transvaginal transverse view of the uterus showing balloon of catheter in the upper endometrial cavity prior to injection of contrast material; B: Filling of both fallopian tubes with contrast material. Subsequent identification of free contrast in the pelvis confirmed tubal patency.
• Female
• Anovulation
• Tubal factor infertility
• Endometriosis
• Unexplained infertility
• IVF/ICSI
• Figure 7.4 Intracytoplasmic sperm injection. The egg is held by a suction pipette (left) and the sperm injected into the cytoplasm.
• Medicolegal and ethical issues
• Further reading
• MCQS
• OSCE
• Chapter 8 Chronic pelvic pain
• Key points
• Introduction
• Definition and epidemiology
• Assessment of pelvic pain
• Clinical history
• Box 8.1 Clinical history for acute pelvic pain
• Box 8.2 Examination for the woman with CPP
• Physical examination
• Investigations
• Figure 8.1 Hydrosalpinx in three patients. Transvaginal images show tubular fluid-filled structures of varying size. A: Incomplete septation related to the folding of the tube. B: Low-level echoes within the tube. C: Surface nodularity.
• Figure 8.2 Laparoscopic view of a pelvis with severe endometriosis. Note the right ovarian endometrioma with the chocolate material that is typical for severe ovarian disease. The normal left ovary is seen to the left of the image; the uterus is anterior and the sigmoid is to the left and inferior.
• Pathophysiology
• Figure 8.3 Adenomyosis on MRI. The junctional zone (arrow) in this patient measures 16 mm, indicating diffuse adenomyosis. Also note the cystic lesion anterior to the uterus and superior to the bladder, which is a pathologically proven serous cystadenoma.
• Figure 8.4 Laparoscopic view of a normal pelvis. Note the left-sided corpus luteal cyst with the surface vascular markings. The Pouch of Douglas can be seen easily and the uterus is a normal size and shape. There is no evidence of peritoneal disease or other abnormality.
• Primary dysmenorrhoea
• Box 8.3 Common causes of CCP
• Mittelschmerz pain
• Pathological gynaecological causes
• Endometriosis
• Uterine leiomyomas
• Adenomyosis
• Figure 8.5 A hysteroscopic image of a submucous myoma. Note the exophytic growth into the uterine cavity. There are gas bubbles on the left, since fluid is used as a distention medium for the uterine cavity. There is an electrosurgical loop to the left and inferiorly. The first pass of a resection procedure has been performed, with the white myoma fibres exposed in the centre of the image.
• Pelvic venous congestion syndrome
• Ovarian remnant and residual ovary syndrome
• Other gynaecological causes
• Figure 8.6 Liver adhesions typical of Fitz-Hugh–Curtis syndrome.
• Non-gynaecological causes of chronic pelvic pain
• Gastrointestinal tract
• Box 8.4 Differential diagnosis for acute pelvic pain
• Urinary tract
• Figure 8.7 Glomerulations with cystoscopic hydrodistension in a patient with interstitial cystitis. A: Mucosal haemorrhages during emptying phase after hydrodistension. B: Glomerulations after refilling the bladder.
• Musculoskeletal system
• Neurological
• Psychosocial
• Figure 8.8 Potential management options for premenopausal women with CPP.
• Managing chronic pelvic pain
• Further reading
• MCQS
• OSCE
• Chapter 9 The physiological changes of pregnancy
• Key points
• Cardiovascular changes
• Figure 9.1 Physiological changes of pregnancy. Schematic representaton of some of the physiological changes occurring during pregnancy and the postpartum period.
• Intrapartum and postpartum haemodynamic changes
• Figure 9.2 Cardiac output during pregnancy, labour, and the puerperium. Values during pregnancy are measured at the end of the first, second, and third trimesters. Values during labour are measured between contractions. For each measurement, the relative contributions of heart rate (HR) and stroke volume (SV) to the change in cardiac output are illustrated.
• Normal findings on examination of the cardiovascular system in pregnancy
• Figure 9.3 The findings on auscultation of the heart in pregnancy. MC, mitral closure; TC, tricuspid closure; A2 and P2, Aortic and pulmonary elements of the second sound.
• Figure 9.4 Plasma and erythrocyte increase during pregnancy.
• Haematological changes
• Renal changes
• Clotting system
• Respiratory changes
• Glucose metabolism
• Thyroid function
• Figure 9.5 Pulmonary physiology in pregnancy. Anatomical and functional effects of pregnancy that influence pulmonary physiology. ERV: expiratory reserve volume; FRC: functional residual capacity; RV: residual volume; TLC: total lung capacity.
• Calcium metabolism
• Pituitary changes
• Anterior pituitary
• Intermediate lobe
• Posterior pituitary
• Adrenal gland
• Gastrointestinal system
• Skin, hair and nails
• Musculoskeletal system
• Figure 9.6 Effects of pregnancy on the lumbar spine. A: Non-pregnant. B: Pregnant. There is a marked increase in lumbar lordosis and a narrowing of the interspinous spaces during pregnancy.
• Figure 9.7 Changes in posture during pregnancy. The first figure and the subsequent dotted-line figures represent a woman’s posture before growth of the uterus and its contents have affected the centre of gravity. The second and third solid figures show that as the uterus enlarges and the abdomen protrudes, the lumbar lordosis is enhanced and the shoulders slump and move posteriorly.
• Reproductive system
• Figure 9.8 Physiological hypertrophy of the uterus during pregnancy. A: gross appearance of a normal uterus (right) and a gravid uterus (left) that was removed for postpartum bleeding; B: small spindle-shaped uterine smooth muscle cells from a normal uterus. Compare this with C: large, plump hypertrophied smooth muscle cells from a gravid uterus (B and C, same magnification).
• Figure 9.9 Breast during pregnancy. A: Haematoxylin and eosin (H & E) stain ×20; B: H & E ×100. At low magnification in micrograph A, the breast lobules (Lo) are seen to have enlarged greatly at the expense of the intralobular tissue and interlobar adipose tissue, although septa S of interlobular tissue still remain. At higher magnification in B, the acini (A) are dilated. The lining epithelial cells (E) vary from cuboidal to low columnar and contain cytoplasmic vacuoles. The intralobular stroma is much less prominent and contains an infiltrate of lymphocytes, eosinophils and plasma cells. As pregnancy progresses, the acini begin to secrete a protein-rich fluid called colostrum, the accumulation of which dilates the acinar and duct lumina as seen in micrograph B.
• Figure 9.10 Maternal–fetal oxygen transfer. The circled numbers represent approximate values of the partial pressure of oxygen (mmHg).
• Fetal physiology
• References
• MCQS
• Chapter 10 Problems in early pregnancy
• Key points
• Miscarriage
• Definition and epidemiology
• Figure 10.1 Risk of spontaneous miscarriage.
• Aetiology and pathophysiology
• Diagnosis
• Figure 10.2 A: Transvaginal image of small-for-dates embryo at 8 weeks gestation. Colour Doppler illustrates vascularity only in the myometrium, confirming no embryonic cardiac activity. B: Live 7 week embryo for comparison. C: Large empty gestation sac of >25 mm diameter indicative of missed miscarriage.
• Management
• Ectopic pregnancy
• Epidemiology
• Sites
• Pathophysiology of tubal damage
• Figure 10.3 Sites and rate of occurrence at each site of ectopic implantation.
• Diagnosis
• Figure 10.4 A: Coronal section of the uterus and the uterine tube illustrating an ectopic pregnancy in the ampulla of the tube. B: Ectopic tubal pregnancy (6 weeks). The sonogram of the uterine tube (left) shows a small gestational sac (arrow).
• Emergency treatment
• Management and implications
• Figure 10.5 Ectopic pregnancy in the right fallopian tube, seen at laparoscopy.
• Fertility outcomes
• Figure 10.6 Management of suspected ectopic pregnancy.
• References
• MCQS
• OSCE
• Chapter 11 Antenatal care
• Key points
• WHO provides care for pregnant women?
• Figure 11.1 Pre-implantation genetic diagnosis.
• Pre-conception counselling: health education for optimal pregnancy
• Booking visit: the first antenatal consultation
• Box 11.1 Taking a medical and obstetric history
• Dating the pregnancy
• Box 11.2 Examination at booking visit
• Minor symptoms and complications
• Diet and weight during pregnancy
• Teratogenesis, alcohol, smoking and recreational drugs
• Dental care
• Routine blood and other investigations
• First trimester ultrasound
• Figure 11.2 Critical periods in human prenatal development.
• Figure 11.3 3D monochorionic twin pregnancy at 12 weeks’ gestation.
• Figure 11.4 Image of nuchal translucency measurement in first trimester.
• Diagnostic tests for karyotype
• Second trimester
• Figure 11.5 Surface-rendered three-dimensional ultrasound image of a 24-week fetus with isolated unilateral left cleft lip.
• Figure 11.6 Different types of twinning.
• Box 11.3 Routine antenatal examination
• Inspection
• Palpation
• Box 11.4 Common complications of the second trimester of pregnancy
• Figure 11.7 A: Progressive increase of fundal height. B: The lie of the baby. This refers to the relationship of the long axis of the fetus to the uterus: longitudinal is normal.
• Third trimester
• Figure 11.8 Abdominal palpation.
• Figure 11.9 Fetal lie at term.
• Box 11.5 Minor complications of pregnancy in the third trimester
• Investigations
• Physiology
• Multiple pregnancy
• Twin pregnancies should be classified by chorionicity
• Preparation for birth
• Social considerations during the antenatal period
• Seatbelts
• Air travel
• Exercise
• Occupational work
• Sexual activity
• References
• MCQS
• OSCE
• Chapter 12 Fetal growth and development
• Key points
• The placenta and its embryology
• Evaluation of fetal growth and wellbeing
• Figure 12.1 Evaluation of fetal growth and wellbeing.
• Methods for establishing gestational age and their accuracy
• The toolkit for assessment of fetal wellbeing
• Fetal movement
• Assessment of maternal symphysio-fundal height
• Ultrasound
• Amniotic fluid volume
• Blood flows
• Umbilical arteries
• Middle cerebral artery
• Ductus venosus
• Uterine Arteries
• Karyotype, infection and results of screening tests
• Figure 12.2 Blood flow waveforms.
• The small fetus
• Normal small
• Incorrectly diagnosed small
• Abnormal small
• Starved small
• Figure 12.3 Profound IUGR presenting at 24½ weeks’ gestation. Chromosomally and structurally normal fetus. Serial growth scans are shown. Eventual decision for delivery at 34 weeks’ gestation with an estimated fetal weight of 1000 g. Delivery of a live healthy male infant who has had no significant compromise in early childhood life.
• Management
• Large-for-dates fetus
• Figure 12.4 Ultrasound of the clinically large-for-dates fetus with diabetes showing an appropriate sized head circumference (HC) but a disproportionately enlarged abdominal circumference (AC) that contributes to an overall increased estimated fetal weight (EFW).
• Figure 12.5 The Pederson hypothesis.
• Fetal wellbeing in late pregnancy and labour
• Monitoring fetal wellbeing
• Fetal heart monitoring and fetal scalp sampling
• Table 12.1 Normal ranges for scalp and cord blood sampling
• Hypoxic–ischaemic encephalopathy
• Box 12.1 CTG descriptive features and normal ranges
• Baseline
• Baseline variability
• Accelerations
• Decelerations
• Early
• Variable
• Complicated variable
• Prolonged
• Late
• Box 12.2 Grading of hypoxic-ischaemic encephalopathy
• Mild
• Moderate
• Severe
• Cerebral palsy
• Perinatal mortality
• Rhesus isoimmunisation
• Figure 12.6 Mechanism of Rhesus isoimmunisation secondary to fetal red cells entering into maternal circulation.
• Pathophysiology
• Investigations
• Prevention of Rhesus isoimmunisation
• References and further reading
• MCQS
• OSCE
• Chapter 13 Infections in pregnancy
• Key points
• Serious maternal infection with fetal consequences
• Influenza
• Epidemiology and pathophysiology
• Clinical presentation
• Diagnosis
• Table 13.1 Fetal susceptibility to damage during development
• Management and outcomes
• Urinary tract infection
• Epidemiology and pathophysiology
• Clinical presentation
• Diagnosis
• Management and outcomes
• Maternal infection with direct fetal consequences (malformation and/or neonatal illness)
• Figure 13.1 Pathways for transmission of perinatal infection.
• Rubella
• Epidemiology and pathophysiology
• Figure 13.2 Congenital rubella syndrome.
• Clinical presentation
• Management and outcomes
• Cytomegalovirus
• Epidemiology and pathophysiology
• Figure 13.3 Rubella serology after maternal exposure.
• Figure 13.4 CMV-affected neonate.
• Figure 13.5 CMV avidity index.
• Clinical presentation
• Diagnosis
• Management and outcomes
• Varicella zoster virus
• Epidemiology and pathophysiology
• Figure 13.6 CMV natural history.
• Clinical presentation
• Diagnosis
• Figure 13.7 Varicella.
• Management and outcomes
• Parvovirus B19
• Epidemiology and pathophysiology
• Clinical presentation
• Diagnosis
• Figure 13.8 Parvovirus rash.
• Management and outcomes
• Toxoplasmosis
• Epidemiology and pathophysiology
• Figure 13.9 Toxoplasmosis life cycle.
• Pathophysiology
• Clinical presentation
• Diagnosis
• Management and outcomes
• Syphilis
• Listeria monocytogenes
• Maternal infection with consequences to the neonate
• Group B streptococcus
• Epidemiology and pathophysiology
• Clinical features
• Diagnosis
• Management and outcomes
• Figure 13.10 Genital herpes.
• Herpes simplex virus
• Epidemiology and pathophysiology
• Diagnosis and management
• Chorioamnionitis
• Epidemiology and pathophysiology
• Clinical features and diagnosis
• Table 13.2 Pathogens responsible for chorioamnionitis
• Management and outcomes
• Hepatitis B virus
• Epidemiology and pathophysiology
• Diagnosis
• Figure 13.11 Hepatitis B serology time course.
• Impact and outcomes
• Management
• Hepatitis C virus
• Epidemiology and pathophysiology
• Diagnosis and management
• Human immunodeficiency virus
• References
• MCQS
• OSCE
• Chapter 14 Medical disorders in pregnancy
• Key points
• Nausea and vomiting of pregnancy
• Hyperemesis gravidarum
• Etiology
• Clinical picture
• Diagnosis
• Investigations
• Treatment
• Hypertension
• Definitions
• Preeclampsia
• Box 14.1 Classification system for hypertension in pregnancy
• Preeclampsia
• Gestational hypertension
• Chronic hypertension
• Figure 14.1 The causes of maternal death globally.
• Figure 14.2 Longitudinal changes in blood pressure with normal pregnancy.
• Pathophysiology
• Clinical assessment
• Eclampsia
• Prevention
• Treatment
• Figure 14.3 MRI of the brain in eclampsia: patient with hypertensive encephalopathy secondary to eclampsia with HELLP (haemolysis, elevated liver enzymes, and low platelets) syndrome. A: T2-weighted magnetic resonance imaging (MRI) showing the extensive cerebral oedema in the posterior white matter regions with less involvement of the grey matter. B: A higher level of the same scan sequence as in A, showing some frontal lobe involvement. C and D: Diffusion-weighted images (DWI) with only one small area of involvement. The lack of DWI changes is consistent with this being a vasogenic type of oedema, and the patient had a good recovery without residual deficit.
• Postpartum management
• Gestational hypertension
• Chronic hypertension
• Diabetes
• Epidemiology
• Pathophysiology
• Figure 14.4 Newborn with caudal regression syndrome — the most specific but rare congenital anomaly in pregnancies complicated by diabetes.
• Figure 14.5 Insulin sensitivity index.
• Maternal signs and symptoms
• Screening for GDM
• Therapy
• Fetal monitoring
• Prognosis
• Thromboembolism
• Figure 14.6 Distribution of VTE in pregnancy and puerperium: number of VTEs per week.
• Incidence
• Clinical assessment
• Investigations and the use of diagnostic radiation in pregnancy
• Treatment
• Next pregnancy and contraception
• Prophylaxis for VTE
• Anaemia
• Clinical features of anaemia
• Investigation of anaemia
• Iron deficiency in pregnancy
• Iron supplementation
• References
• MCQS
• OSCE
• Chapter 15 Labour and delivery
• Key points
• Introduction
• The physiology of normal labour
• Figure 15.1 Descent of the fetus through the pelvis during the course of labour. A: The fetus presents in a longitudinal lie, presenting cephalically by the vertex. The head is engaged transversely and is flexed. B: As the head descends through the birth canal there is internal rotation so that the occiput is anterior. C: The head extends for delivery. D: The head then returns to the transverse position, through external rotation. E, F: This is followed by delivery of the anterior and posterior shoulders.
• The three Ps
• Passenger
• Passage
• Figure 15.2 The pelvic planes.
• Power
• Stages of labour
• First stage
• Second stage
• Third stage
• Progress of the presenting part
• Maternal physiological changes during labour
• Fetal physiological changes during labour
• Management of normal labour and delivery
• The partogram and progress in labour
• Pain management in labour
• The second stage of labour: delivery
• Figure 15.3 The partogram provides a graphical representation of progress in labour. This multiparous woman is defined as being in labour (4 cm dilated) at 8 a.m. Progress is recorded with further vaginal examinations (x) and progress is slow, falling behind the action line (_ _ _ _). An amniotomy (ARM) and oxytocin are used to improve the rate of progress. Delivery occurs soon after full dilatation is reached. Details of fetal and maternal wellbeing are also recorded.
• The third stage of labour: delivery of the placenta
• Management of abnormal labour and delivery
• Failure to progress in labour
• Fetal distress in labour
• Assisted vaginal delivery
• Figure 15.4 Examples of obstetric forceps. Simpson forceps are an example of a classic pair of forceps used for delivery of a fetus presenting in an occiput-anterior position. Kielland forceps are less frequently used, principally for rotational delivery (rotating from occiput-posterior to occiput-anterior before advancing through the birth canal). The Kielland forceps have less pelvic curve, allowing them to be used as a rotational instrument.
• Perineal trauma
• Figure 15.5 Effecting delivery with a ventouse (Silc cup). A: The cup is applied to the vertex, taking care not to traumatise the vaginal wall. Vacuum is applied and time allowed for the chignon to develop, providing a better seal. B, C, D: Traction is applied while the mother is pushing, in coordination with uterine contraction. As the head advances through the birth canal the accoucheur mimics the normal mechanics of labour. An episiotomy may be needed as the head crowns for delivery — the cup can be removed at this point.
• Unusual presentations
• Persistent occipito-posterior or occipito-transverse position
• Box 15.1 Potential maternal and fetal complications from instrumental delivery
• Forceps
• Maternal
• Fetal*
• Ventouse
• Maternal
• Fetal*
• Figure 15.6 An example of a fourth-degree tear. The rectal mucosa has already been repaired (midline) and the external anal sphincter is now been repaired with a series of interrupted sutures. Bilateral tears in the vaginal wall can be seen and will be repaired next.
• Figure 15.7 Using the Mauriceau–Smellie–Veit manoeuvre to deliver the after-coming head of a fetus presenting as breech.
• Face and brow presentations
• Breech presentation
• Transverse or oblique lie
• Caesarean delivery
• Induction of labour
• Table 15.1 Bishop score for cervical assessment prior to induction of labour
• Delivery of multiple pregnancies
• Summary
• References
• MCQS
• OSCE
• Chapter 16 Obstetric emergencies
• Key points
• Introduction
• Maternal and perinatal mortality
• Table 16.1 Maternal mortality rates across the world3
• Table 16.2 Causes of direct maternal deaths, Australia 2003–20052
• Table 16.3 Causes of indirect maternal deaths, Australia 2003–20052
• Table 16.4 Perinatal mortality definitions4
• General obstetric complications
• Maternal collapse
• Figure 16.1 Basic life support.
• Figure 16.2 Adult cardiorespiratory arrest.
• Figure 16.3 Degrees of placental abruption. A: Concealed abruption; B: Revealed abruption; C: Complete placental separation.
• Perimortem caesarean delivery
• Antenatal obstetric complications
• Antepartum haemorrhage
• Placental abruption
• Placenta praevia
• Figure 16.4 Grades of placenta praevia. Grade I: low lying placenta: extends into the lower uterine segment but does not reach the internal os; Grade II: marginal placenta praevia: reaches the internal os but does not cover it; Grade III: partial placenta praevia: the placenta partially covers the internal os; Grade IV: complete or total placenta praevia: the placenta completely covers the internal os.
• Placenta accreta
• Vasa praevia
• Figure 16.5 Transvaginal ultrasound demonstrating the fetal head on the left, and the large umbilical vein (coloured in red) coursing over the internal os of the cervix (to the right).
• Figure 16.6 At caesarean delivery for the vasa praevia in figure 16.5, placenta showing fetal blood vessels within the amniotic membrane consistent with the diagnosis of a velamentous cord insertion, which is necessary for vasa praevia to occur.
• Peripartum emergencies
• Cord prolapse
• Shoulder dystocia
• Risk factors and complications
• Figure 16.7 Shoulder dystocia where the fetal shoulders are impacted on the maternal bony pelvis.
• Management
• Amniotic fluid embolism
• Figure 16.8 McRoberts position.
• Postpartum haemorrhage
• Prevention
• Management
• Figure 16.9 Bimanual compression of the uterus.
• Surgical management
• Table 16.5 Risk factors for postpartum haemorrhage
• Advanced surgical techniques
• Preterm birth
• Definition
• Incidence
• Risk factors
• Prevention
• Progesterone
• Smoking cessation
• Bed rest
• Antibiotics
• Diagnosis
• Management
• Steroids
• Tocolysis
• Antibiotics
• Transfer to a tertiary unit
• Prognosis
• References
• MCQS
• OSCE
• Part 1
• Part 2
• Chapter 17 Routine care of postpartum women
• Key points
• The puerperium
• Physiological changes in the puerperium
• Involution
• Figure 17.1 Normal involution: fundal height by days after birth.
• Ovarian function
• Perineal trauma
• Urinary and bowel function
• Cardiovascular system
• Social and emotional changes in the puerperium
• Supporting the transition into motherhood
• Supporting mother–baby attachment
• Addressing perinatal mental health issues
• Lactation
• Why is breastfeeding important?
• Figure 17.2 The development of mammary glands. A: Ventral view of an embryo of approximately 28 days showing the mammary crests; B: Similar view at 6 weeks showing the remains of these crests; C: Transverse section of a mammary crest at the site of a developing mammary gland; D–F: Similar sections showing successive stages of breast development between the 12th week and birth.
• Breast developmental stages
• Figure 17.3 Mammary milk line indicating where accessory nipples or glands may form.
• Figure 17.4 Normal female breast development from prepubertal to adult.
• The breast in pregnancy
• The lactating breast
• The composition of breastmilk
• Figure 17.5 The lactating breast.
• How breastfeeding works
• Transmission of drugs in breastmilk
• Complications of lactation
• Mastitis
• Breast abscess
• Six-week postpartum visit
• Complications of the puerperium
• Infections and sepsis
• Box 17.1 Risk factors for puerperal sepsis
• Venous thromboembolism
• Secondary postpartum haemorrhage
• Conclusion
• References
• MCQS
• OSCE
• Chapter 18 Abnormal uterine bleeding
• Key points
• Introduction
• Background and epidemiology
• Box 18.1 Differential diagnosis of AUB
• Pregnancy
• Structural
• Palm
• Systemic and iatrogenic
• Coien
• Others
• Detailed aetiology
• Polyps
• Figure 18.1 Pedunculated polyp attached to the right lower uterine wall. Note the vascularity on the polyp surface. The curved endometrial cavity can be seen at the top of the screen.
• Adenomyosis
• Leiomyoma (myoma, fibroid)
• Malignancy
• Localised causes
• Cervix
• Figure 18.2 Typical location of myomas within the uterus.
• Vagina
• Other
• Coagulopathy
• Ovulatory disorders
• Endocrine
• Thyroid deficiency
• PCOS
• Hepatic failure
• Iatrogenic
• Endometrium
• History
• Investigations
• Treatments
• Conservative
• Medical
• Hormonal
• Progestogens
• Combined oral hormones
• Gonadotrophin releasing hormone analogue (GnRHa)
• Other
• Non-hormonal
• Non-steroidal anti-inflammatories
• Tranexamic acid
• Surgical
• Localised removal
• Endometrial ablation
• Figure 18.3 A: Enlarged uterus with a 5 cm myoma that extends intramurally to submucosally; B: The uterus opened and the myoma being removed. C: The myoma completely removed and the uterine defect seen on the left in the background. D: The myoma just prior to removal from the abdomen and the repaired uterus with sutures in the background. This full-thickness myomectomy will require caesarean delivery for any future pregnancy.
• Hysterectomy
• Figure 18.4 A: Normal endometrium in a women with heavy menstrual bleeding prior to endometrial ablation. The left ostium can be seen as the dark circle at the top right-hand side of the image. B: The endometrium in a woman treated by endometrial ablation. Note the absence of endometrium and the coagulated white surface of the superficial myometrium. The ostia can be seen on either side of the image.
• Radiological
• Uterine artery embolisation
• Magnetic resonance guided focused ultrasound (MRgFUS)
• Figure 18.5 A: Thermachoice device; B: Thermablate device; C: NovaSure device; D: Cavaterm device.
• Conclusions
• Further reading
• MCQS
• OSCE
• Chapter 19 The menopause and beyond
• Key points
• Introduction
• Potential symptoms around the menopause
• Box 19.1 Oestrogen deficiency symptoms
• Premature menopause
• Osteoporosis
• Table 19.1 Menopause symptom score
• Box 19.2 Clinical risk factors for osteoporosis
• Cardiovascular disease
• Figure 19.1 Bone density (DEXA) scan of the femur of a 50-year-old woman showing early osteoporosis. The shaded zone in the graph represents the normal bone density range, which decreases from menopause. The white square represents this patient’s bone density.
• Non-hormonal management of the menopause
• Figure 19.2 Psychological, social and sexual influences around menopause.
• Vasomotor symptoms
• Non-hormonal prescriptive therapies
• Non-prescriptive therapies
• Therapies for other symptoms
• Hormonal therapies
• Routes of administration
• Indications for hormone therapy
• Cardiovascular disease
• Risk of stroke
• Venous thromboembolism risk
• Figure 19.3 WHI disease rates for women on combination hormone therapy or placebo.
• Breast cancer risk
• Figure 19.4 Summary of the likely significant risks and benefits after 5 years of combined HRT in a woman without cardiovascular risk factors commencing hormone therapy from early menopause.
• Cognition and dementia
• Figure 19.5 Summary of main risks and benefits of oestrogen-only HRT (CVD = cardiovascular disease).
• Other effects
• Care of the individual
• Assessment and counselling
• Examination and routine investigations
• Hormone therapy regimens
• Figure 19.6 Hormone therapy regimens.
• Oestrogen-only therapy
• Testosterone therapy
• Length of therapy
• Tailoring therapy
• Options for the management of osteoporosis
• Long-term goals for healthy ageing
• Postmenopausal bleeding
• Clinical evaluation
• Benign causes of PMB
• Endometrial cancer
• Figure 19.7 Ultrasound images in women with postmenopausal bleeding. A: Thin regular endometrium 2.2 mm; B: Thickened cystic endometrium suggestive of endometrial hyperplasia; C: Thickened endometrium suggestive of polyp with associated feeder vessel; D: Saline hysterography outlines the polyp in the fluid filled cavity; E: Markedly thickened highly vascular endometrium, histology confirmed carcinoma (sagittal section of uterus); F: Pulsed Doppler pattern of high velocity low resistance flow in an aggressive endometrial carcinoma, which occupies most of the body of the uterus (transverse section of uterus). Ultrasound is not diagnostic for endometrial hyperplasia or carcinoma.
• Figure 19.8 Age-adjusted rate of cancers of the endometrium and cervix in Australian women. Blue line diagram represents endometrial (uterine cancer) (range 0–68 cases per 100 000). Green bar chart represents cervical cancer (range 0–13 cases per 100 000).
• Cervical cancer
• Non-gynaecological causes
• References
• Further reading and useful websites
• Algorithms
• MCQS
• OSCE
• Chapter 20 Incontinence
• Key points
• Introduction
• Urinary incontinence
• Applied anatomy and physiology
• Causes
• Types of urinary incontinence
• Effect of urinary incontinence
• Table 20.1 Common or important types of incontinence and related bladder dysfunction
• Can urinary incontinence be prevented?
• Investigation and management
• History
• Examination and investigation
• Management
• Figure 20.1 Screen snapshot of intraoperative video image showing a substantial stream of clear fluid expressed per urethra by Crede’s manoeuvre (suprapubic pressure) with 300 mL normal saline in the bladder in a woman undergoing a tension-free vaginal tape procedure for severe stress incontinence (uninserted tape seen in lower section of picture). Elimination of incontinence following insertion of the tape can be demonstrated by repeating the Crede’s manoeuvre (not shown).
• Figure 20.2 A 2-day bladder diary recorded by a 64-year-old woman presenting with symptoms of overactive bladder. There appears to be some restriction in fluid intake, which is a common and usually ineffective management strategy. Eight episodes of urinary incontinence are recorded (the woman has estimated the volume of urine lost) and the apparent bladder capacity of 170 mL is well below normal for her age. This could be explained either by a true reduction in bladder capacity or incomplete bladder emptying. In this case the incontinence is urge incontinence, however very similar charts can be seen in women with severe stress incontinence. The woman is voiding up to nine times during the day (abnormal) and up to twice at night (age-dependent, normal for this patient).
• Figure 20.3 A: Section of cystometric recording and B: ultrasound imaging of bladder, in a woman with mixed urinary incontinence that had failed to respond to pelvic floor exercises and anticholinergic medication. Figure 20.3A shows that retrograde filling of the bladder has stopped at 150 mL (the woman was reporting marked urgency). Soon after cessation of filling most of the content of the bladder has been lost as result of a spontaneous detrusor contraction. This is recorded as the first incontinence leak — diagnosis severe idiopathic detrusor overactivity. There is an offset between the recorded leakage and the detrusor contraction due to latency in transmission of pressure in the very long fluid-filled lines and the pressure transducers. The patient was then asked to cough and a small volume of fluid was lost and in the absence of a detrusor contraction — diagnosis urodynamic stress incontinence. This is recorded as the second incontinence leak. The transvaginal image of the bladder was taken using a specialised probe and shows an almost empty bladder with a measured detrusor thickness of 10.1 mm, which is significantly increased and suggestive of a chronic problem with hypercontractility of the detrusor.
• Faecal incontinence
• Structure and function of the anal canal
• Causes of faecal incontinence
• Investigation and management
• Conclusion
• References
• MCQS
• OSCE
• Chapter 21 Genital prolapse
• Key points
• Introduction
• Prevalence and incidence
• Applied anatomy and physiology
• Figure 21.1 The relationships of the muscles of the pelvic floor and sidewalls and their attachments from an abdominal view. The arcus tendineus fasciae pelvis has been removed on the left, showing the origins of the levator ani muscles. On the right, the arcus tendineus fasciae pelvis remains intact showing the attachment of the lateral vagina via the endopelvic fascia (cut away).
• Risk factors
• Prevention of prolapse
• Clinical evaluation
• Figure 21.2 Complete genital eversion. The anterior lip of the cervix (POPQ point C) is clearly visible. Points Aa and Ba are also visible but more difficult to identify because the external urethral meatus is hidden and because it is not clear to novices where the cervix ends and anterior vagina begins. In practice, once identified, the distance between the points and the hymenal ring are measured with a tape. With that caveat, a reasonable estimate from this two dimensional image is that point C is between +8 cm and +10 cm, Ba is about +8 cm (note where the concentric lines that identify the vagina end) and Aa is about +2 cm.
• Figure 21.3 Anterior and apical compartment prolapse (previous hysterectomy). The posterior compartment is retracted by the Sims speculum.
• Table 21.1 Definitions of POPQ points used in the description of genital prolapse*7
• Staging of prolapse
• Figure 21.4 Schematic line drawing identifying POPQ points Aa, Ba, C, D, Ap and Bp. TVL = total vaginal length, gh = width of genital hiatus, pb = width of perineal body.
• Table 21.2 POPQ staging of pelvic organ prolapse7
• Older terminology
• Quality of life
• Management
• Pelvic floor exercises
• Vaginal packing
• Vaginal pessaries
• Surgery
• Figure 21.5 Pelvic Floor Impact Questionnaire short form 7.
• Figure 21.6 Types of vaginal pessary. A: Smith’s, B: Hodge’s, C: Hodge’s with web support, D: Risser, E: Gehrung, F: ring with web support, G: ring, H: cube, I: Gelhorn, rigid, J: Gelhorn, flexible, K: Inflatoball, L: doughnut. In Australia, the most commonly used are the ring and Gelhorn pessaries.
• Summary
• References
• MCQS
• OSCE
• Chapter 22 Germ cell tumours of the ovary
• Key points
• Introduction
• Epidemiology
• Classification of germ cell tumours
• Primitive germ cell tumours
• Figure 22.1 Macroscopic image of a dysgerminoma. The tumour has a cerebriform architecture. The fallopian tube is attenuated along the surface.
• Figure 22.2 Photomicrograph of a dysgerminoma. This tumour has linear arrays of neoplastic cells in a fibrous stroma.
• Biphasic or triphasic teratomas
• Monodermal teratomas and somatic-type tumours associated with dermoid cysts
• Figure 22.3 Large mature teratoma removed at laparotomy.
• Figure 22.4 Photomicrograph of a mature teratoma (dermoid) of the ovary with the multiple types of cells demonstrated.
• Staging
• Presentation
• Investigations
• Table 22.1 Tumour marker profile for malignant germ cell tumours
• Management
• Figure 22.5 Ultrasound images of ovarian dermoids.
• Further reading
• MCQS
• OSCE
• Chapter 23 Gestational trophoblastic disease
• Key points
• Introduction
• Benign trophoblastic tumour: hydatidiform mole
• Figure 23.1 Complete molar pregnancy.
• Figure 23.2 Photomicrograph of molar pregnancy.
• Figure 23.3 Ultrasound image of hydatidiform mole, showing vesicle-like echolucent areas.
• Table 23.1 Comparison of partial and complete mole
• Malignant trophoblastic disease: gestational trophoblastic neoplasia
• Figure 23.4 Partial molar pregnancy. A: Sonographic image of a 13-week gestation with triploidy demonstrating the placenta (arrows) to be markedly thickened, containing scattered small cystic areas consistent with villous swelling. The fetus (fetus, arrowhead) is seen within the amniotic cavity. B: Immature placenta with focal villous enlargement. C: Early partial mole with scattered swollen villi (upper centre) seen in the dissecting microscope.
• Figure 23.5 Choriocarcinoma.
• Table 23.2 FIGO adapted modified WHO prognostic scoring system for gestational trophoblastic neoplasia
• Recurrence
• Further reading
• MCQS
• OSCE
• Chapter 24 Cervical cancer screening
• Key points
• Introduction
• Anatomy and histology of the cervix
• What causes cervical cancer?
• Natural history
• Figure 24.1 Natural history of HPV infection and CIN.
• Table 24.1 Transition time of cervical intraepithelial neoplasia
• What is HPV?
• Figure 24.2 Structure of the HPV virus. Most HPV exists in episomal (circular) DNA. The important genomic sites are called open reading frames (ORFs). In the episomal state, E2 regulates both the long control region (LCR), which is responsible for regulation of viral transcription, and E6 and E7, the two sites most often responsible for malignant transformation.
• Immune response
• HPV vaccines
• Table 24.2 Features of commercially available HPV vaccines1
• Screening
• Pap test
• Figure 24.3 Tools used to perform a Pap test.
• Figure 24.4 Preparation of the conventional Pap smear slide.
• Improving the system
• Liquid-based cytology
• Human papilloma virus testing
• Table 24.3 Risk of CIN III on follow-up
• Cervical screening terminology
• Box 24.1 Epithelial cell abnormalities used to describe cervical cytology specimens
• Squamous abnormalities
• Glandular abnormalities
• LGSIL
• Table 24.4 Outcome
• HGSIL
• Figure 24.5 Management algorithm for possible LGSIL or LGSIL.
• Special circumstances
• Pregnancy
• Immune-suppressed
• Post-hysterectomy
• Figure 24.6 Management algorithm for possible HGSIL.
• Figure 24.7 Management algorithm for HGSIL.
• Figure 24.8 Colposcopic equipment used for examination of cervix.
• Adolescents
• Colposcopy
• Figure 24.9 Colpo-photograph of a high grade lesion with punctation (A) and mosaicism (B).
• Table 24.5 Modified Reid colposcopy
• Treatment modalities
• Conservative treatments
• Electro-coagulation diathermy (ECD)
• Cryosurgery
• Laser surgery
• LEEP
• Figure 24.10 Loop electrode excision procedure (LEEP).
• Figure 24.11 A–C Photomicrographs of histological changes denoting CIN I, II, III.
• Cold knife cone biopsy
• Definitive treatments — hysterectomy
• Post-treatment surveillance
• Prognosis after treatment
• Figure 24.12 Treatment and follow-up algorithm.
• Obstetric outcomes
• Table 24.6 Conservative treatment for cervical intraepithelial neoplasia
• Reference
• Further reading
• MCQS
• OSCE
• Chapter 25 Cervical cancer
• Key points
• Introduction
• Histological types
• Growth pattern
• Presentation
• Figure 25.1 Cervical cancer incidence and mortality 1968–2007.
• Pattern of spread
• Staging of cervical cancer
• Box 25.1 Histological subtypes
• Squamous cell carcinoma
• Other epithelial
• Adenocarcinoma
• Miscellaneous
• Prognostic factors for lymph node metastases
• Management
• Confirmation of diagnosis
• Figure 25.2 FIGO staging.
• Table 25.1 FIGO staging
• Table 25.2 Stage and rate of lymph node metastases
• Assigning a FIGO stage
• Determining spread
• Assigning treatment
• Table 25.3 Types of radical hysterectomy and indications
• Treatment
• Stage IA
• Early stage disease (stage IB–IIA)
• Primary surgery
• Primary radiation therapy
• Locally advanced disease (Stage IIB–IVA)
• Recurrent disease
• Table 25.4 Incidence of recurrence
• Prognostic factors for survival
• Special circumstances
• Conservative management in the young patient
• Table 25.5 Survival by FIGO stage
• Occult disease found on loop excision
• Box 25.2 Indications for radical trachelectomy
• Pregnancy
• Diagnosis after hysterectomy
• Further reading
• MCQS
• OSCE
• Chapter 26 Uterine cancer
• Key points
• Introduction
• Epidemiology
• Figure 26.1 Uterine cancer incidence and mortality rates.
• Clinical presentation
• Table 26.1 Risk factors for endometrial cancer
• Diagnosis
• Figure 26.2 Transvaginal ultrasound showing an endometrial polyp without tissue diagnosis.
• Figure 26.3 Hysteroscopic view of vascular polyp with irregular surface highly suspicious of endometrial cancer.
• Figure 26.4 FIGO staging of endometrial carcinoma.
• Histologic types
• Table 26.2 Histological subtypes of endometrial cancer
• Table 26.3 Key features of type 1 and type 2 endometrial cancers
• Figure 26.5 Opened hysterectomy specimen of endometrial cancer showing an enlarged uterus with extensive tumour replacing the native endometrium and infiltrating into the myometrium (deep myoinvasion).
• Management
• Figure 26.6 Histopathology of uterine carcinosarcoma (HE stain) showing malignant epithelial (left) and stromal elements (right).
• Follow-up
• Further reading
• MCQS
• OSCE
• Chapter 27 Cancer of the ovary
• Key points
• Introduction
• Aetiology of ovarian cancer and risk factors
• Figure 27.1 A: The p53 signature, B: haematoxylin and eosin (H&E), C: p53, and, D: H2AX.
• Figure 27.2 Photograph of gross stage IB ovarian cancer. The normal uterus sits between the clamps with both ovaries having multilocular and irregular cystic masses.
• Epithelial ovarian cancers
• Clinical presentation
• Table 27.1 Most frequent presenting symptoms of ovarian cancer
• Management
• Table 27.2 FIGO staging of ovarian cancer
• Preoperative investigations
• Figure 27.3 A to E: Spectrum of findings in different patients with ovarian cancer and peritoneal dissemination. Owing to ascites, diaphragmatic implants are well visualised; these may be focal along the diaphragm (A) or appear as diffuse plaque-like thickening of the parietal peritoneum (B). Broad tumour formations (arrow in B), representing omental caking adjacent to the transverse colon, are also seen. Peritoneal implants from papillary serous cancer may present as subtle calcifications (arrows in C) on the liver and splenic surfaces. Peritoneal implants encompassing the cul-de-sac can be differentiated from the small primary ovarian cancer (asterisk in D). Multiple nodular implants are demonstrated (E), including in the right posterior diaphragm, in the right liver lobe adjacent to the right adrenal gland, and along the intersegmental fissure. In addition, there are multiple small nodules along the gastrosplenic ligament and lymph nodes adjacent to the hepatic artery.
• Figure 27.4 A: Sister Joseph’s nodule. B: Computed tomography shows an umbilical subcutaneous nodule (arrow), which is Sister Joseph’s nodule.
• Surgical management
• Figure 27.5 High-grade ovarian serous carcinoma involving the omentum. High-grade serous carcinoma has a strong tendency to involve the omentum, forming a ‘caking’ appearance. The omentum was bread-loafed to reveal the solid tumour mass.
• Table 27.3 Risk of malignancy index (RMI)
• Postoperative treatment
• New approaches
• Figure 27.6 A view through the thoracoscope in a patient with multiple pulmonary metastases due to ovarian cancer (lower part of photo).
• Table 27.4 Classification of ovarian cancer
• Borderline epithelial tumours
• Further reading
• MCQS
• OSCE
• MCQ Answers
• Chapter 1
• Chapter 2
• Chapter 3
• Chapter 4
• Chapter 5
• Chapter 6
• Chapter 7
• Chapter 8
• Chapter 9
• Chapter 10
• Chapter 11
• Chapter 12
• Chapter 13
• Chapter 14
• Chapter 15
• Chapter 16
• Chapter 17
• Chapter 18
• Chapter 19
• Chapter 20
• Chapter 21
• Chapter 22
• Chapter 23
• Chapter 24
• Chapter 25
• Chapter 26
• Chapter 27
• OSCE Answers
• Chapter 2: Sexual development and puberty
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 3: Fundamentals of gynaecology: the menstrual cycle and clinical interaction
• History
• Examination
• The best students
• Chapter 4: Sexual activity and contraception
• History
• Examination
• Options and information
• The best students
• Chapter 5: Sexually transmitted infections
• History
• Examination
• Investigations
• The best students
• Chapter 6: Fertility
• History
• Examination
• Management
• The best students
• Chapter 7: Problems of fertility
• History
• Examination
• Investigations
• The best students
• Chapter 8: Chronic pelvic pain
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 10: Problems in early pregnancy
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 11: Antenatal care
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 12: Fetal growth and development
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 13: Infections in pregnancy
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 14: Medical disorders in pregnancy
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 15: Labour and delivery
• History
• Examination
• Investigations
• Diagnosis
• Management
• The best students
• Chapter 16: Obstetric emergencies
• Part 1
• Assessment
• Management
• Part 2
• Management
• The best students
• Chapter 17: Routine care of postpartum women
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 18: Abnormal uterine bleeding
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 19: The menopause and beyond
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 20: Incontinence
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 21: Genital prolapse
• History
• Examination
• Investigations
• Management options
• The best students
• Chapter 22: Germ cell tumours of the ovary
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 23: Gestational trophoblastic disease
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 24: Cervical cancer screening
• History
• Discussion
• Management
• The best students
• Chapter 25: Cervical cancer
• History
• Examination
• Investigations
• The best students
• Chapter 26: Uterine cancer
• History
• Examination
• Investigations
• Management
• The best students
• Chapter 27: Cancer of the ovary
• History
• Examination
• Investigations
• Management
• The best students
• Index
• A
• B
• C
• D
• E
• F
• G
• H
• I
• J
• K
• L
• M
• N
• O
• P
• Q
• R
• S
• T
• U
• V
• W
• X
• Y