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Obstetrics Pre-term labour (Linul) Overview delivery < 36 weeks gestation most common cause of neonatal mortality in developed world 5-10% of all births (unimproved over past 30 years) Risk factors preceded by spontaneous ROM in 1/3rd of cases therapeutically induced in 1/3rd of cases unknown cause in 1/3rd of cases large uterus – multiple gestation or polyhydramnios pelvic infection and bacterial vaginosis cigarette smoking drug abuse, teenage pregnancy, underweight mothers Foetal consequences neonatal death due to severe immaturity respiratory distress syndrome – underdeveloped lungs and deficient surfactant brain and bowel mucosa susceptible to hypoxia hypothermia – low body fat, reduced insulation hypoglycaemia – immature liver with low glycogen stores hyperbilirubinaemia kernicterus The preterm infant may require: o ventilation, exogenous surfactant, intravenous glucose, parenteral feeding, incubation and ultraviolet irradiation Diagnosis medical history o regular uterine contractions every 10 minutes ± spontaneous ROM o progressive cervical dilatation o painless midtrimester foetal loss suggests cervical incompetence avoid digital examination high vaginal swab to exclude infection fibronectin o <40% positive predictive value for delivery within 14 days o ≈97% negative predictive value for delivery within 14 days Management aim to prolong pregnancy or administration of corticosteroids o promotes foetal lung maturation and surfactant production 1 o o single course (two betamethasone injections 24 hours apart) side effects foetal growth restriction impaired myelination insulin resistance hyperglycaemia in diabetic mothers tocolytic agents suppress labour o indicated for threatened delivery < 32 weeks gestation o nifedipine drug of choice Antepartum haemorrhage (Suren) Def: vaginal bleeding after 20 weeks of gestation and before delivery of the baby. Causes @ DDx 1) Placenta Previa a. Def: implantation of the placenta in the lower segment of the uterus. b. Incidence: 1/200 c. RFx: i. PHx of CS (risk varies from 1-4% on subsequent pregnancy, risk is > 10% if more than 4 pregnancies) ii. IVF iii. multiparity iv. age > 35 v. smoking vi. drugs d. Types: i. Type I (marginal) 1. Encroaches on lower segment but doesn’t reach the internal os (2.5cm from the os). ii. Type II (minor) 1. Reaches the internal os but doesn’t cover it. iii. Type III (major) 1. Partially covers the internal os. iv. Type IV (major) 1. Completely covers the internal os. e. Clinical presentation: i. Painless vaginal bleeding that stops spontaneously but may recur. ii. Associated with uterine contraction or irritability. f. Pathophys i. Thinning of the lower part of the uterus ii. Disrupt placental attachment g. Ix: i. U/S – if unstable use transabdominal, if stable can use transabdominal , transvaginal or transperineal. ii. FBE, coags, cross-match 6 units of blood. 2 iii. MUST NOT PERFORMED VE UNTIL PP HAS BEEN EXCLUDED BY U/S h. Mx: i. Depend on the severity: 1. If M & F unstable a. Emergency resuscitation and CS 2. M stable, < 37 weeks a. Conservative medicine, blood transfusion 3. If premature delivery required (< 34 weeks) a. Corticosteroid (?) 4. If bleeding stops a. Observation In hospital at least 48 hrs (60% chance to recur) 2) Placental Abruption a. Def: uterine bleeding following premature separation of the placenta from the uterus, total or partial. b. Incidence: 0.5 – 2.0%, 20% perinatal mortality c. RFx: i. Advanced maternal age ii. Multiparity iii. Multipregnancy iv. Smoking v. Drugs (anti coags) vi. Maternal HT vii. PPROM viii. Chorioamnionitis ix. Abdominal trauma x. Maternal thrombophilia xi. PHx of PA xii. IUGR, polyhydramnios xiii. Low SES d. Clinical presentation i. Sx: 1. Abdominal pain (tender tense uterus) 2. Vaginal bleeding (dark, non-clotting) 3. Uterine contraction 4. Usually close to term 5. Nausea, faintness and restlessness Minor Major Mild VB Sever VB With or w/o contraction Bleeding from venupuncture sites normal Fetal HR Bruising (DIC) 3 ii. Sg: 1. Tachycardia, hypotension, signs of peripheral vasoconstriction 2. ‘woody hard’ uterus on palpation, maybe larger than gestation suggests 3. Difficult to palpate fetus iii. Types: 1. Revealed haemorrhage a. VB, pain not significant 2. Concealed haemorrhage a. Slight bleeding, tense uterus, ?pain (due to retroplacental clot) 3. Mixed haemorrhage a. Some VB, some passage of clots, build up of clots behind placenta 4. Large haemorrhage a. Bruised uterus (blood forced into muscle layers) b. IUF demise iv. Dx: 1. Exam placenta after delivery (?send to laboratory for biopsy) 2. U/S – if negative, it doesn’t exclude PA. v. Mx: Minor Major Emergency CS (stop DIC) Conservative or CS Investigate coags on M (APTT, PT, fibrinogen, D-Dimer) but if results are abnormal consult with haematologist for transfusion Baby is monitored in NICU 3) Vasa Previa a. Def: umbilical vessels run in the membrane close to the internal os instead of the placenta b. Clinical presentataion: i. Small VB at the time of rupture c. Mx: i. CS (because it can cause fetal blood loss) 4) Bleeding from LGT a. Cuases: i. Post coital ii. Cervical condition (ectropion and polyps, carcinoma) iii. Infection (candida, trichomonas) 4 Gynaecology Menopause (PQ) Definitions: Menopause: cessation of menstruation due to the demise of ovarian function, which usually occurs between the ages of 45-57 years (average 51). Premature menopause: menopause occurring under the age of 40 years (2% of women). Climacteric: consists of o Perimenopause: menstrual irregularity and fluctuating menopausal symptoms, for up to 4 years before and 1 year after final period. o Postmenopause: all symptoms and sequelae of ovarian senescence (may be life-long). Symptoms – experienced by up to 80% of women; most commonly experienced around late perimenopause and early postmenopause. Vasomotor: hot flushes, night sweats and palpitations. Psychological: depression, anxiety, unloved feelings, irritability, mood changes, less sexual feelings, sleeplessness, and unusual tiredness. Locomotor: muscle/joint pain and backache. Urogenital: dry vagina, uncomfortable intercourse, and urinary frequency and urgency. Others: light-headed feelings, headaches, new facial hair, dry skin and crawling feelings, and crawling feelings under the skin. Work up: History: medical, drug, menstrual, family, sexual, psychosocial issues, attitudes to menopause and possible therapies, and misconceptions. Examination: breast, pelvic examination including Pap smear. Investigations (when indicated): FBE, serum lipids, triglyceride levels, TFTs, BSLs, bone density scan, and thrombophilia screen. Management: Nonhormonal therapies: o Lifestyle advice: weight control through diet and exercise (30 minutes weightbearing exercise per day), avoid excessive caffeine and alcohol, and stop smoking. 5 o Vasomotor symptoms: venlafaxine, gabapentin, clonidine. o Psychological symptoms: antidepressants, anxiolytics or NSAIDs. o Vaginal symptoms: lubricants. o Urinary symptoms: antispasmodic agents Hormonal therapies: o Regimens: Perimenopausal: continuous oestrogen + cyclical progestogen. Postmenopausal: continuous oestrogen + continuous progestogen. After hysterectomy: continuous oestrogen. Testosterone therapy: lack of evidence, may improve libido and energy levels. Tibolone: stimulates oestrogen, progestogen and testosterone receptors – ‘all-in-one’ postmenopausal therapy. o Routes of administration: o o o Oral. Transdermal. Gel. Intranasal spray. Pessaries or creams (vaginal symptoms). Indications: Relief of menopausal symptoms. Prevention and treatment of osteoporosis. ? Primary cardioprotective role. ? Neuroprotective role (e.g. dementia, depression). Risks: VTEs. ? Cardiovascular disease. ? Breast cancer. Increased gallbladder disease. Early adverse effects: breast tenderness, uterine bleeding, bloating, premenstrual-like symptoms. Length of therapy: as long as women perceive an improved quality of life from the alleviation of menopausal symptoms. Yearly review is appropriate. Osteoporosis: Loss of bone density occurs rapidly initially (15% loss in first 5 years), then continues at a slower rate Diagnosis: bone densitometry at sites such as hip, spine, and wrist. Osteoporosis is defined as bone densities more than 2.5 standard deviation units below young normal mean. 6 Treatment is recommended for young postmenopausal women with scores of 1.5-2.5, older women with scores >2.5 or who have had an osteoporotic fracture. o Bisphosphonate, e.g. alendronate, risedronate: used in women with CV risk factors, recent low-trauma fracture but few menopausal symptoms. o Selective oestrogen receptor modulator, e.g. raloxifene: used in women with an osteoporotic fracture, breast cacner concerns or fear of uterine bleeding. o HT: in younger women. o Others: PTH, strontium ranaleate, calcium, vitamin D, hip protectors and weight bearing exercise. Abnormal bleeding Hx Age of menarche? Typical bleeding pattern of teenage years Typical bleeding pattern on combined OCP Commencement of abnormalities Progression Relation to body weight Ex Clots, flooding, tampons, towels Menstrual calendar Fatigue/dyspnoea from anaemia Irregular, intermenstrual or post coital bleeding Dysparaeunia, pelvic pain, or premenstrual pain Abnormal bleeding at other sites Pallor Pelvi-abdo mass (fibroids) Vulval, vaginal, cervical lesion Menorrhagia Abnormally heavy menstrual bleeding (HMB) >80ml per period Increases with increasing age Commonest cause of iron deficiency anaemia Classified into idiopathic (DUB, where no anatomical causes can be found) or secondary to an organic cause. Organic causes: Fibroids Endometrial or endocervical polyps Endometrial hyperplasia Adenomyosis Hypothyroidism Coagulopathy Presence of IUD 7 Endometrial or endocervical carcinoma Bleeding in pregnancy Dysfunctional Uterine Bleeding Idiopathic menorrhagia, implies a subtle hormone dysfunction Ovulatory DUB presenting as regular HMB o Disordered prostaglandin production o Abnormalities of endometrial vascular development Anovulatory DUB presenting as irregular vaginal bleeding o In adolescents soon after menarche due to low oestrogen concentrations o In PCOS due to unopposed oestrogen stimulation – women tend to have infrequent periods then long periods with heavy bleeding and develop Swiss cheese endometrium – cystic hyperplasia o In the first few years before menopause due to a sharp raise and fall of oestrogen concentrations Intermenstrual bleeding : endometrial pathology Called breakthrough bleeding if woman on combined OCP Post-coital bleeding: cervical carcinoma or be due to cervical ectopy Investigations Exclude pregnancy! Irregular bleeding: Hysteroscopy and endometrial biopsy FBE Coagulopathy, TFT if indicated If women fail to respond to treatment after 3/12 Trans-vaginal pelvic U/S for women at high risk of endometrial pathology: >45yo, wt >90kg, nulliparous, Hx of infertility, F.H. of endometrial or colon Ca Trans-vaginal sonohysterogram distinguishes endometrial polyps from submucous fibroids Endometrial Bx if endometrial thickness is 12mm or greater, or Pipelle sapling +/- Hysteroscopy (gold standard for endometrial pathology) if TVUS is abnormal. Treatment for menorrhagia Medical Iron replacement for anaemia Antifibrinolytic - Tranexamic acid 1 g QID Mean reduction in blood loss (MBL) 50ml, theoretical increased risk of VTE NSAID – Mefenamic acid 500mg TDS MBL 35ml Cyclical oral progestogens e.g. Medroxyprogesterone acetate or norethisterone 8 Long course oral progestogen treatment (3 out of 4 weeks) but has high incidence of side effects COCP Mean reduction in MBL of 50% Synthetic androgen - Danazol MBL 100ml. Many androgenic side effects, incompatible with conception but not licensed as a contraceptive Levo-norgestrel intrauterine system (LNG-IUS) releases progestogen locally. Mean reduction in MBL of 95%. Needs to be replaced every 5 years. 30% women become amenorrhoeic If the woman wants Contraception? – COCP or LNG-IUS To conceive? – Tranexamic acid or NSAID Treat dysmenorrhoea? LNG-IUS or NSAID Surgical Ablation This includes methods under hysteroscopic guidance: Transcervical resection of the endometrium (TCRE), Roller Ablation, Endometrial Laser Ablation (ELA), diathermy and methods without hysteroscopic guidance: Thermal balloon ablation, Microwave endometrial ablation (MEA), Heated saline Ablations successful in 4 out of 5 women, 1 of whom will become amenorrhoeic. Hysterectomy For fibroids, a myomectomy can be done if fertility is to be preserved GnRH analogs can shrink fibroids before hysterectomy, allowing a vaginal rather than abd hysterectomy Post-menopausal bleeding (Lin) Definition Any per vaginal bleeding that occurs in a woman > 12 months after last period **In post-menopausal women not on HRT, any bleeding is abnormal. ** Women on combined HRT may have bleeds in progesterone free period (Bleeds abnormal if they occur at an unscheduled timing or are abnormal in amount) Causes 9 Endometrial carcinoma (TPO. 10% of patients) Atrophic vaginitis (most common) and atrophy of endometrium Cancer of cervix or vulva Endometrial or cervical polyps Endometrial hyperplasia o Can be simple (non-malignant) or atypical hyperplasia (40% progress to adenocarcinoma. Responsive to P therapy or hysterectomy) Submucosal fibroids Oestrogen withdrawal (HRT or ovarian tumour) Foreign bodies e.g. pessaries Disease in adjacent organs Hx taking – Full Hx More specific questions to ask: When did the bleeding start? Were there precipitating factors, such as trauma? What is the nature of the bleeding (temporal pattern, duration, postcoital, quantity)? Are there any associated symptoms such as pain, fever, or changes in bladder or bowel function? What is the medical history and are any medications being taken (eg, hormones, anticoagulants)? Ask risk factors of gynaecological cancer e.g. past or current use of unopposed E, tamoxifen therapy for breast cancer treatment or prevention, PCOS, syndrome X, nulliparity, abnormal pap smear, previous gynae malignancy, FHx of cancer Ex Thorough examination of external and internal genital tract. Determine any bleeding site, note suspicious lesions, lacerations or foreign bodies. Full pelvic and bimanual examination General Ex to look for signs of systemic illness e.g. hepatitis, renal disease, splenomegaly Ix Cervical smear Transvaginal ultrasound Endometrial biopsy +/- hysteroscopy o Required if: Endometrial lining is thicker than 4mm (if on HRT, >5mm) Endometrium shows diffuse or focal echogenicity (heterogeneity) Endometrium is not adequately visualised Woman has persistent bleeding (can be a sign of endometrial Ca even when endometrial thickness is <4-5mm since a thin or indistinct endometrial stripe does not reliably exclude type 2 endometrial cancer) Mx In postmenopausal women, uterine bleeding is usually light and self-limited. If atrophic vaginitis – may be treated with topical oestrogen Exclusion of cancer is the main objective; therefore, treatment is usually unnecessary once cancer (or premalignant histology) has been excluded. 10 Pre-menstrual syndrome Definition & Incidence PMS is characterized by the presence of both physical and behavioral symptoms that occur repetitively in the second half of the menstrual cycle & are relieved immediately when menstrual flow begins. The sx’s must be severe enough to impact on lifestyle, relationships or work, and not part of another psychiatric disorder. Affects up to 95% percent of women of reproductive age. 5% of women are severely incapacitated by these symptoms. Typical age of presentation is 30-40 years Pathophysiology: Hormonal theory: o Rapidly declining levels of progesterone late in the luteal phase (day 26-27) Other contributing factors o Increased renin-angiotensin-aldosterone activity o Changing prostaglandin levels o Vitamin deficiency o Excess prolactin secretion o Endogenous endorphin depletion Psychosocial factors: o Negative anticipation of menstruation o Underlying predisposing personality o Stereotypic expectation of PMS o General stress Sx More than 150 symptoms have been ascribed to PMS Most common physical manifestations of PMS are o Breast tenderness o Fluid retention and weight gain o Headaches o Aching joints Most common psychological symptom of PMS is o Affective labile mood – tearfulness, irritability, anger (occurring in >80%) o Anxiety or tension o Depression o Loss of interest, difficulty concentrating, loss of energy, sleep disturbance, appetite disturbance Other common Sx: acne, oversensitivity to environmental stimuli, anger, easy crying, and gastrointestinal upset. Hot flashes, heart palpitations, and dizziness occur in 15 to 20 percent of patients Dx Specific symptoms should be characteristic of PMS The timing with this these symptoms occur.i.e. Should occur in the luteal phase The severity of the symptoms i.e. should impair some facet of the woman’s life Absence of hormone or drug ingestion and the exclusion of other diagnoses o Physical Ex to exclude gynaecological, endocrine or other systemic disease; breast Ex, vaginal Ex & pap smear 11 o Ix: TFT, U&E, serum P and oestradiol in mid-luteal phase, PRL (if galactorrhoea or oligomenorrhoea present) DDx Menopause syndrome, Mastalgia, other causes of fluid retention (renal or adrenal, hyper or hypo thyroid), PCOS (PMS may be a feature of E excess), Psychiatric disorders (depression, mania) Rx Mild to moderate Sx o Pyridoxine (Vitamin B6) 100 mg daily; if ineffective after 3 cycles, try o Evening primrose oil capsules (gamma lineoleic acid) 1000 mg bd with food (day 12 to first day of next cycle) o A progestogen may be tried after or with evening primrose oil 4 e.g. Dydrogesterone 5 mg bd days 12-25; after 2 months increase to 10 mg bd Severe Sx o SSRI: Fluoxetine 20 mg daily for 10-14 days before menstruation, or 10-20 mg daily continuously 11 OR o Non-SSRI: Clomipramine 25 mg (o) nocte for 2 cycles, increasing if necessary Specific treatments o Spironolactone for fluid retention o Bromocriptine or evening primrose oil for breast tenderness o Mefanamic acid for dysmenorrhoea EBM (ie. RCT evidence) SSRI’s (PMS) Spironolactone (fluid retention) Bromocriptine OR Evening primrose oil ○ ○ ○ ○ Mixed evidence COCP & POP Pyridoxine (Vit B6) NSAIDs Ca2+ or Mg2+ Worth Trying Exercise Homeopathy & herbal remedies Relaxation therapy eg. massage (breast tenderness) Prolapse (Kat) Definition Utero-vaginal prolapse – abnormal descent of the uterus and/or vagina o First degree – cervix stays in vagina o Second degree – protrudes from introitus (especially when stand or strain) o Third degree (procidentia) – uterus protrudes beyond introitus Cystocoele – prolapse of the anterior vaginal wall Urethrocoele – prolapse of lower anterior wall Rectocoele – prolapse of the posterior vaginal wall Enterocele – prolapse of the vaginal vault Epidemiology Common condition which increases in prevalence with age 12 Risk Factors / Causes Parity Increased birth weight Age Post-menopause Increased abdominal pressure Inherited connective tissue disorders Pelvic surgery History Vaginal o Dragging or bearing down sensation in vagina o Appearance of lump or bulge at vaginal entrance o Difficulty inserting tampons o Ulceration of prolapsed epithelium may discharge, bleeding Bowel/Bladder o Difficulties with bladder or bowel emptying or urinary or faecal incontinence o Hydronephrosis (ureteric kinking) – severe cases o Urinary retention – descent of bladder base below urethra o Rectal prolapse and haemorrhoids sometimes associated Other o Low back pain (often reported – may or may not be related) o Decreased libido Examination Abdominal exam o Exclude organomegaly or mass (causing raised pressure) Pelvic exam o Look for prolapse, ulceration, atrophy o Assess anterior and posterior vaginal walls and cervical descent with patient straining using Sims’ speculum in L lateral position o Combined VE and PR exam can help differentiate enterocele from rectocele Investigations Prolapse is essentially diagnosed on history/examination May wish to investigate urinary or bowel symptoms further Management Options are tailored to the individual Multi-disciplinary team often required if complex Reassure patient that the condition is not life threatening or particularly dangerous 13 Type Options General measures Address reversible risk factors Manage obesity, constipation, chronic cough (smoking, asthma, CF), oestrogen deficiency Pelvic floor exercises Shown to improve Sxs of prolapse and incontinence Unlikely to reduce prolapse that has extended beyond introitus Poor long term compliance Consider physiotherapy or nurse adviser Intra-vaginal oestrogen supplementation May enhance effect of pelvic floor exercises if post-menopausal With ↑ use of oestrogen consider DVT prophylaxis if other risk factors e.g. immobility Vaginal packing To manage chafing/ulceration of externalised epithelium – should respond in 2-3wks (can then undertake definitive Rx) Pack cotton gauze smeared with oestrogen cream into vagina to reduce prolapse (replace daily) Rubber rings that are fitted into vagina to reduce prolapse Lower part sits in posterior fornix, upper part near symphysis Also come as ‘shelf’ pessaries (rarely used unless rings not retained) Remove, wash and re-insert regularly (every 3-6 months) May increase physiological discharge and rates of anaerobic infection Should not affect enjoyment of intercourse Aim to correct anatomical defect, maintain sexual function and treat associated urinary or bowel dysfunction Medical Vaginal pessaries Surgical Corrective surgery (see below) Details Prolapse Surgery Traditionally involves vaginal hysterectomy, midline suturing of vaginal fascia and excision of redundant vaginal epithelium with o Newer operations exist but are not well evaluated o Synthetic mesh or slings sometimes used if woman’s own tissue is inadequate o Non-absorbable synthetic materials are potentially more durable but ↑risk of chronic infection or rejection o Some procedures to obliterate vaginal cavity (e.g. Le Fort) can be performed relatively quickly under LA in selected cases Re-operation common (up to 30%) o Decreasing time intervals between each successive repair o Multiple surgeries associated with progressive scarring, loss of vaginal length and calibre and deterioration in sexual, bladder and bowel function o Surgery may exacerbate pelvic neuropathy by direct trauma to nerves Surgical repair will not necessarily improve sexual enjoyment 14 o Also consider low libido, relationship problems, inflammatory conditions of vaginal or vulva, psychological influences Pelvic floor surgery may be adversely affected by subsequent pregnancy Prolapse Surgery Anterior colporrhaphy most commonly performed Vaginal wall incision made and defect allowing herniation closed Redundant vaginal epithelium excised and incision closed Avoid anterior repair if concurrent stress incontinence Posterior colporrhaphy (as for anterior, but on opposite side) Surgery on posterior vaginal wall may cause dyspareunia Enterocele Similar to ant/post repair, but peritoneal sac containing small bowel should be excised and pouch of Douglas closed Uterovaginal Vaginal hysterectomy with adequate support of vault to utero-sacral ligaments If uterine conservation required can do Manchester operation or sacrohysteropexy (abdominal approach) Sacrocolpoplexy – vault attached to sacrum using mesh, POD closed Sacrospinous ligament fixation – vaginal procedure where vault sutured to ligament(s) Cystocoele Rectocoele Vault Urogynaecology Incontinence – Review the structure and function of the lower urinary tract. Bladder: - - Average capacity is 400mL Lined with transitional epithelium Detrusor muscle = 3 layers (longitudinal-circular-longitudinal) of whorls of smooth muscle. Triangular area between ureteric orifice and internal meatus is known as the trigone Base of the bladder is related to the cervix, with only a thin layer of connective tissue intervening. It is separated from anterior wall of the vagina by the pubocervical fascia. Transitional epithelium – water tight and stretchy Urethra: - Female urethra is usually about 3.5cm long Transitional epithelium Two layers of smooth muscle: inner = circular and outer = longitudinal 15 - As it passes through two layers of urogenital diaphragm (triangular ligament), it is embraced but the striated fibres of the deep transverse perineal muscle Posteriorly it is related to the anterior vaginal wall, to which it is firmly attached in it lower two-thirds. Medial fibres of the pubococcygeus of the levator ani muscles are inserted into the urethrea and vaginal wall. When they contract, they pell the anterior vaginal wall and the upper part of the urethra forwads, forming an angle between the eposterior wall of the urethra and the bladder. In voluntary voiding, the angle disappears so base of bladder and posterior urethra form a straight line. Potential cause of stress incontinence is absence of this angle. List the types of urinary incontinence and the specific symptoms which accompany each. Urinary incontinence: Defn: involuntary loss of urine that is objectively demonstrable and is a social or hygiene problem Prevalence increases with age: 5% of women aged 15-44, 10% of 45 – 64 and 20% of 65 and older Urinary incontinence is mainly defined by pathophysiology but common symptoms are: 16 - Stress incontinence (sx not dx): loss of urine on physical effort (cough, sneeze, laugh, lifting objects/babies) Urge incontinence: is loss of urine accompanied with sudden desire to void Overflow incontinence: loss of urine when bladder is over-distended but no detrusor activity Frequency: passing urine seven or more times a day or waking up to void more than once a night Types: 1. Urethral causes a. Urodynamic stress incontinence Causes i. Abnormal descent of bladder neck and proximal urethra unequal transmission of IA pressure reversal of normal pressure gradient negative urethral closure pressure ii. Laxity of suburethral support from pelvic floor and vaginal wall etc. Damage to nerve supple of PF and urethral sphincter from childbirth Menopause and associated tissue atrophy damaged pelvic floor Congential laxity (connective tissue issues( Chronic causes – obesity, COPD increase IAP, constipation Sx i. Stress incontinence is the main symptom ii. Urgency iii. Frequency iv. Urge incontinence v. Also possible awareness of prolapse Exam i. Patient coughs and incontinence observed ii. VE – asses for prolapse and woman’s ability to elevate bladder neck iii. Cystourethrocele may be present vi. Also possible awareness of prolapse Treatment i. Prevention Shorten second stage of labour and reduce trauma during delivery Pelvic Floor exercise – before/during pregnancy ii. Conservative management Physiotherapy (pelvic floor exercise) – need proper instruction and regular use, can use perineometry and weight cones to improve chance of success iii. Surgery 17 Aims: restoration of proximal urethra and bladder neck to appropriate area of IAP transmission and/or increase urethral resistance Colposuspension Artificial sphincter Peri-urethral injections (contigen collagen, subcutaneous fat and microparticulate silicon) b. Detrusor over-activity: when detrusor muscle contracts apparently spontaneously during the filling phase Causes i. Neuropathy seems to be the most substantiated factor ii. Poor toilet training and psychological factors have been implicated iii. Generally idiopathic Sx i. Urgency ii. Urge incontinence iii. Frequency iv. Nocturia v. Stress incontinence vi. Enuresis vii. Occasionally voiding difficulties Exam i. Must examine for prolapse ii. Must excluded possibility of mass compressing the bladder as a cause Treatment i. Bladder retraining, biofeedback or hypnosis ii. Anticholinergics iii. End stage = bladder augmentation c. Retention with overflow: failure of bladder emptying and voiding difficulties chronic retention and overflow 18 Causes i. LMN/UMN lesions ii. Urethral obstruction iii. Drugs: antihistamines, anticholinergics, tricyclic antidepressants Sx i. Poor stream ii. Incomplete bladder emptying iii. Straining to void Ix i. Cystometry required to make diagnosis ii. Bladder U/S or IV urogram to exclude reflux d. Congenital i. Epispadias stress incontinence ii. Plain XR shows symphysial separation e. Misc i. UTI/faecal impaction in elderly 2. Extra-urethral causes a. Congenital i. Bladder exstrophy: absence of anterior abdominal and bladder wall ii. Ectopic ureter b. Fistula: abnormal opening between the urinary tract and ‘outside’ Causes i. Obstructive labour compression of bladder ii. Pelvic surgery/malignancy/radiotherapy Outline their investigations and management. 1. MSU 2. Urinary diary +/ – pad test 3. Uroflowmetry – measurement of urine flow rate a. Past history of urinary retention 4. Cystometry – measurement of pressure-volume relationship in bladder a. Urge incontinence b. Stress incontinence c. Frequency 5. Videocystourethrography 6. IV Urography 7. US – can estimate post-micturition residual urine 8. MRI 9. Cystourethroscopy 10. Urethral pressure profilometry 19 Gynaecology Oncology Case 05- Ovarian oncology and cysts (Alan) Physiological cysts Follicular cyst o Most common benign ovarian tumour o Diameter up to 10cm, smaller cysts do not need intervention o Can be caused by ovulation induction and gestational trophoblastic disease due to gonadotropin overstimulation o Pelvic ultrasound should be repeated in 4-6 weeks time o If symptomatic or not resolved in 8-16 weeks, treat with wait until half way through pregnancy before removing the cyst laparoscopically (lower chance of miscarriage) Symptoms are menstrual disturbances, endometrial hyperplasia Luteal cyst o More common on the right side, <3cm = corpora lutea o Can rupture causing intraperitoneal bleeding on days 20-26 of menstrual cycle o Sometimes, it fills with fluid or blood, creating a cyst that can grow to 6cm across. o can rupture causing hemoperitoneum, hypotension, and peritonitis haemorrhagic corpus luteal cysts are usually seen in the first trimester, with most resolving by 12 weeks' gestation o Treatment is laparoscopy if ruptured or torsion Germ cell tumours Happens more commonly in <30 years old All three germ layers are present Benign Dermoid cyst (25% of all ovarian tumours) o Bilateral in 11%, 60% are asymptomatic 3.5-10% can have torsion 1-4% can rupture, risk is higher in pregnancy and labour o Unilocular cyst <15 cm in diameter, has predominantly ectodermal structures Skin, teeth, hair, nervous tissue, thyroid, bronchus, intestine Mesodermal structures can be present too: bone, cartilage, muscle 20 Mature solid teratoma o Rare, less cystic than dermoid cyst Malignant Dysgerminoma (2-5% of ovarian malignancy) o <30 yo, 10% bilateral o Mean diameter 15cm, spread via lymphatics o Can coexist with choriocarcinoma, endodermal tumour or teratoma (10%) Do beta hCG o Pure dysgerminoma is mostly Stage 1=good prognosis Choriocarcinoma o Secretes beta hCG, usually diagnosis is done when haematological spread has occurred Yolk sac (endodermal) o Usually in <40 yo o Can rupture causing pain, aggressive and fast growing Diagnosed late, with extensive metastases o Areas of necrosis, haemorrhage o Often makes AFP, can be measured to monitor treatment Teratoma o about 20% of all malignant tumors, mainly in <20 yo o gliomatosis peritonei, caused by rupture. Seeding of neural tissue in the peritoneum if the metastases are immature, it indicates a poorer prognosis Epithelial tumours (60 to 80% of ovarian tumors) Most ovarian neoplasia are of this category, they are mesothelial in nature Benign (more in <40 yo) Serous cystadenoma o Bilateral in 10%, inner surface is cuboidal or columnar and maybe ciliated o Usually smaller than mucinous cystadenoma o Sometimes psamoma bodies (round collections of calcium) are present Mucinous cystadenoma (10-15% of all ovarian tumours) o Large unilateral, multilocular cysts Has columnar mucin secreting cells, produces thick glutinous o pseudomyxoma peritonei is a rare complication, this follows preoperative rupture and spreading of tumour cells mucin in the peritoneum can cause bowel obstruction 50% 5 year survival, 18% 10 year survival Treatment is surgically debulking the metastases and abdominal chemotherapy Endometrioid cystadenoma (5%) 21 o Most are malignant, edges are badly defined o Looks like and can co-exist with endometriosis Brenner tumours o Wolffian metaplasia, usually benign and <2cm in diameter o between 2 to 3 cm, solid, well circumscribed and may be calcified o 75% occur in >40 yo Clear cell (mesonephroid tumour) o Rarely benign, almost all are malignant Malignant Serous carcinoma o Commonest malignant ovarian tumor (33% of ovarian tumours) o Presents with ascites due to metastases o Often bilateral o Psamoma bodies often are seen Mucinous carcinoma o Multilocular, large like its benign counterpart but contains solid areas 25cm cyst is not uncommon o Pseudomyxoma peritonei Endometrioid carcinoma o Most are malignant, edges are badly defined o Looks like and can co-exist with endometriosis o 15% can have endometrial carcinoma, where both are separate primary tumours (not metastasis) Clear cell carcinoma o Cannot be distinguished from the other surface epithelial tumors by their gross appearances. They are partially cystic but may be entirely solid. Necrosis and haemorrhage may be seen in the solid areas. o May be a variant of endometrioid tumour, as they frequently co-exist o Strong association with endometriosis Borderline epithelial tumour o Most are confined in the ovary, usually serous or mucinuous o Good prognosis even if metastases are found, they often regress when primary lesion is removed Sex cord stromal tumours (3% of all ovarian tumor) Benign Theca cell tumour o Almost all are benign, incidence is high in 60yo 5-10 cm o Has systemic effects Precocious puberty, postmenopausal bleed, endometrial hyperplasia and cancer 22 Fibroma o ~50yo o commonest ovarian stromal tumor o Meig’s syndrome is rare (1%): ascites and pleural effusion 40% of fibroma> 6cm Sertoli-leydig cell tumour o ~30yo o Rare, <0.2% of all ovarian tumours o 75% make androgen, many non-functional, some make oestrogen Malignant Granulosa cell tumour o Usually solid, but can develop cysts o 75% of pure granulosa cell tumors are functional and makes estrogen Fibrosarcoma o Very rare Sertoli-leydig cell tumour (rare) o 50% makes male hormones Gynandroblastoma o producing both ovarian (granulosa and/or theca) and testicular (Sertoli and/or Leydig) cells or tissue Natural history of Ovarian Cancers 2/3 present with cancer spread beyond the pelvis because of insidious and nonspecific symptoms or fast growing tumour Metastases commonly happen via o Direct (peritoneum, omentum, peritoneal surface of bowels) o Lymphatic (pelvic and para-aortic nodes) o Haematological (brain, lungs) Risk factors o Nulligravida o Obesity (>30 BMI) o Tubal ligation (protective) o Clomiphene citrate for infertility treatment o HRT o Family history (BRCA 1 and 2) o History of breast cancer HOPC o Abdominal pain or discomfort o Abdominal distension or lump (77%) o Bowel changes (70%), urinary frequency (34%), weight loss, menstrual changes Examination findings o Pelvic mass +/- enlarged lymph nodes (groin, neck) 23 o Hormonal changes Investigations o FBE, EUC o ultrasound pelvis + CA 125 can combine to give an estimate on the risk of malignancy o definitive diagnosis is made using laparotomy Treatment o Laparotomy with vertical incision Objective is to remove all macroscopically visible neoplastic tissues Usually involves total hysterectomy, bilateral salpingooophorectomy and infracolic omentectomy if the cancer has spread extensively If the tumour is unilateral and low stage (no spread): unilateral salpingo-oophrectomy will suffice Do sampling of peritoneal fluids or saline washing o Interval bulking For unresectable disease, it is possible to laparotomy after an initial chemotherapy. Chemotherapy is then resumed as soon as possible after surgery o Any ovarian cancers with Stage >1c should have adjuvant therapy Chemotherapy 5-6 cycles at 3-4 weekly intervals Platinum based chemo drugs are best o Caboplatin, paclitaxel (Taxol, usually in combination with carboplatin as first line regime and is not platinum based) Radiotherapy Experimental, not usually used in practice occasionally used for women with ovarian cancer, especially if it is confined to the pelvic cavity Prognosis Characteristics Benign Germ cell tumours <30 years old 2-3% malignant, but 33% for <20 yo Dermoid cyst Mature teratoma Epithelial tumours Most ovarian cancers are in this category Serous cystadenoma Mucinous cystadenoma Endometrioid cystadenoma Brenner tumours Clear cell Malignant Dysgerminoma Choriocarcinoma Yolk sac (endodermal) Teratoma Serous carcinoma Mucinous carcinoma Endometrioid carcinoma Clear cell carcinoma Borderline epithelial tumour 24 Sex cord stromal tumours o Most common ones are granulosa and theca tumours, produces steroid hormones (usually oestrogen) In general, have better prognosis compared to other ovarian tumours Granulosa cell tumour Theca cell tumour Fibroma Sertoli-leydig cell tumour Granulosa cell tumour Theca cell tumour Fibrosarcoma Sertoli-leydig cell tumour Gynandroblastoma The 5-year survival rates are as follows: Stage I - 73%, Stage II - 45%, Stage III - 21%, Stage IV - Less than 5% References http://atlasgeneticsoncology.org/Tumors/OvarSexCordStromID5223.html 25 http://www.babycenter.com.au/pregnancy/complications/ovariancystexpert/ http://www.med-ed.virginia.edu/courses/path/gyn/ovary3.cfm#germ http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-risk-factors ENDOMETRIAL CANCER (Dan) EPIDEMIOLOGY Most common gynaecological malignancy in Australia (1400 new cases and >250 deaths each year) 1 in 80 lifetime risk of an Australian woman developing endometrial cancer Median age of diagnosis is 60-65 years; 10-20% of cases are found in premenopausal women; rare below the age of 40 Risk factors: age, anovulation, obesity, hypertension, diabetes and insulin resistance, past or family history of endometrial, breast (especially if treated with tamoxifen) or ovarian cancer, HNPCC syndrome, and inappropriate endogenous or exogenous oestrogen unopposed by progestogens (e.g. PCOS, anovulation, oestrogen-only HRT) Protective factors: oral contraceptive pill, parity, combined oestrogen/progestogen HRT Hx: Abnormal vaginal bleeding – postmenopausal bleeding, menorrhagia or intermenstrual loss Endometrial cancer cells incidentally found on cervical (Pap) smear Incidental finding on ultrasound examination (abnormally thick endometrium >4mm in postmenopausal woman) Ix: All women >40yrs and all women with risk factors who have abnormal vaginal bleeding must have endometrial cancer excluded as the cause of bleeding Gold standard: Hysteroscopically directed curettage → histology o Alternative: Pipelle endometrial sampling Staging: surgical + CXR (disseminated disease) STAGING Stage Extent of cancer I Confined to the uterine body A. No myometrial invasion B. Invasion of <50% myometrium C. Invasion of >50% myometrium II Extending to cervix A. No cervical stromal invasion B. Cervical stromal invasion III Outside the uterus A. Extension through uterine serosa or positive peritoneal cytology B. Involvement of adnexal structures C. Involvement of pelvic or para-aortic lymph glands IV At distant site 26 A. Invasion of bladder or bowel mucosa B. Distant metastases or involvement of inguinal nodes Rx: SURGICAL Total hysterectomy and bilateral salpingo-oophorectomy (radical hysterectomy) ± pelvic/para-aortic lymphadenectomy Adjuvant radiotherapy: for disease that has spread beyond the uterus MEDICAL High-dose progestogen therapy: produces a clinical response in 30% of women, few side effects Chemotherapy: for symptomatic disseminated or recurrent disease o Most effective agents: carboplatin, Taxol, Adriamycin PROGNOSIS 80% of women with endometrial cancer present with localised disease o 5-year survival in women with localised disease >90% Prognosis is poorer in the presence of metastatic nodal disease Cervical Cancer Second most common cancer in women worldwide (most in developing countries) Aus: 6.9 per 100 000. Two main types: o Squamous cell carcinoma – usually preceded by a pre-malignant phase of about 10y. Screening has reduced incidence, more for SCC than Adenocarcinoma. o Adenocarcinoma (~15%) – less known about these lesions. Presentation Abnormal vaginal bleeding – usually post-coital, may be irregular or postmenopausal. More advanced disease – discharge, weight-loss, mets Patho-physiology Main Risk Factors HPV (types 16, 18, -in 70% case) Smoking (doubles risk) Immune suppression Multiple sexual partners Early age of coitarche Multiparity Normal metaplasia in the transformation zone disrupted – dysplasia - HPV implicated (but not sufficient) Dysplasitic epithelium: o Lack normal maturation – nuclei larger, variable in shape and size, more actively dividing o CIN1 – affects deepest third CIN2 – affects deepest 2/3rd CIN3 – full thickness o Bethesda system: Low grade (CIN1) vs High grade (CIN2, CIN3) Studies have indicated that at the ages of greatest sexual activity, the prevalence of HPV can be as high as 40% in the female population (6). Around 90% of these infections will 27 spontaneously resolve (6) and many women may not even know that they were infected. It is in the smaller subgroup of women who have the persistent infection that there is a chance that Cervical Intraepithelial Neoplasia (CIN)-also known as ‘lesions’-will develop. In the clinical setting, LSIL is followed up quite conservatively as it may disappear in time. Spontaneous regression from it has been reported to be around 50% (3), to as high as 70 – 90% (8). LSIL, however, can convert to HSIL, which poses the greater risk of leading to invasive carcinoma, and is sometimes known as the ‘precursor to cervical cancer’. It should be understood that dysplasia does not always begin as LSIL and progress to HSIL and that HPV infection, in some cases, can directly result in HSIL Screening – Pap Smear Recommended Australian Cervical Screening Start at age 18-20 or 1-2 years after first intercourse Repeat every 2 years until 70 if had two normal smears in past 5 years Sensitivity 66% (hence may get false negative – regular smears important) Specificity 92% Results of Pap Smear – 10% of smears abnormal – vast majority will not have cancer Negative smear Repeat in 2 years LSIL Repeat in 6 months, if abnormality persists, refer for colposcopy HSIL Refer for colposcopy Inconclusive for HSIL Has some features of high grade epithelial abnormality Unsatisfactory Repeat 6-12 weeks later (don’t take in the presence of blood/infection) Colposcopy Allows visual examination of the cervix to check for CIN Inspect – apply Lugol’s iodine – low and high grade lesions will show glycogen depletion Paint with dilute acetic acid – abnormal cells turn white (have high density of optically dense chromatin) Green filter – used to visualize neovascularisation – shows up as thin lines or tiny red spots Biopsies can then be taken. Management of CIN – Surgical: Remove abnormal tissue by destroying or cutting out tissue Radiotherapy: Used more for later stages Excisional: large loop excisin, cold knife, etc. Large-loop excision of transformation zone – Most popular, area of suspected CIN of depth 10mm removed Cheap, quick, easy to perform and gives tissue for examination. Cx: haemorrhage, 1% incidence of cervical stenosis, and cervical incompetence Ablative: laser ablation, cryotherapy, cold coagulatin 28 Prognosis 29