Obs & Gynae Flashcards
At what gestation does PV bleeding turn from being referred to as a threatened miscarriage to an antepartum haemorrhage?
- Threatened miscarriage → <24 weeks gestation
- Antepartum haemorrhage → 24 weeks - onset of labour
What are the most common causes of antepartum haemorrhage?
- Placenta praevia (painless PV bleed)
- Placental abruption (sudden onset, severe, continuous pain, woody on palpation)
- Vasa praevia (painless, dark red)
- Local → cervical polyps, vaginitis, cervicitis. Often post-coital.
- Unexplained → in the absence of maternal or foetal compromise, it is managed expectantly.
What are the risk factors of placenta praevia?
- Previous C-Section → key risk factor to remember
- Previous TOP
- Multiparity
- Mother >40 years old
- Smoking
- Previous placenta praevia
How does placenta praevia present?
- 20 week anomaly scan → used to assess the position of the placenta & diagnose placenta praevia.
- Painless vaginal bleeding (antepartum haemorrhage)
- Usually occurs later in pregnancy, >36 weeks
- Examination:
- Non-tender uterus
- Lie & presentation may be abnormal → transverse
- Do not do a digital vaginal examination/speculum as this may provoke a severe haemorrhage
How is placenta praevia managed?
If diagnosed at 20 week scan:
- Repeat transvaginal USS at 32 weeks & then 36 weeks.
- If still present at 36 weeks then:
- Planned delivery between 36-37 weeks → reduce risk of spontaneous labour & bleeding
- Corticosteroids given between 34 & 35+6 weeks
If premature labour or APH:
- Emergency c-section
How does placental abruption present?
History:
- Sudden onset, severe, continuous abdominal pain → most common, posterior abruptions may present with back pain.
- Vaginal bleeding
- Uterine contractions
- Dizziness and/or loss of consciousness
Examination:
- Hypotension & tachycardia → if patient is in shock
- Characteristic ‘woody’ abdomen on palpation → tense all the time, suggests a large haemorrhage
- Abnormalities on CTG
- Foetal heart → absent or distressed
How is a placental abruption managed?
Initial steps:
- Stabilise mother if major/massive haemorrhage
- CTG monitoring of foetus
- USS → useful in excluding placenta praevia, but not great at diagnosing an abruption
- Antenatal steroids offered if between 24 & 34+6 weeks
- Anti-D prophylaxis → if rhesus negative
No signs of foetal distress:
- <36 weeks → observe closely
- > 36 weeks → induce & deliver vaginally
Signs of foetal distress/maternal compromise:
- Immediate c-section, regardless of gestation
If the foetus is dead:
- Induce vaginal delivery, unless the mother is haemodynamically compromised & ongoing massive haemorrhage → C-section indicated in this instance.
How does vasa praevia present?
- Diagnosed during ultrasound in some cases
- APH → painless vaginal bleeding, foetal bradycardia
- In Labour:
- Foetal distress
- Dark-red bleeding following ROM
- Examination → pulsating foetal vessels may be seen through the dilated cervix
How is vasa praevia managed?
For asymptomatic women:
- Corticosteroids from 32 weeks to mature foetal lungs
- Elective C-section for 34-36 weeks
If APH occurs → emergency c-section
What are the definitions of primary & secondary PPH?
- Primary PPH → 3rd stage labour (baby out, pre placenta) to 24hrs of birth
- Secondary PPH → from 24hrs-12 weeks after birth
To be classified as postpartum haemorrhage, there needs to be a loss of:
- > 500ml after vaginal delivery
- > 1000ml after a c-section
What are the causes of PPH?
The 4 T’s
- Tone
- Most common cause of primary PPH (90%)
- Normally contraction of the uterus in 3rd stage causes of compression of intramyometrial blood vessels & bleeding from the placental site stops promptly.
- If there is uterine atony/poor contractility, this compression does not occur
- Trauma
- Bleeding from an episiotomy, vaginal tear, cervical laceration, or rupture of the uterine wall.
- Genital tract lacerations are more common after an instrumental birth
- Tissue
- Retained products of conception (RPOC) is when placental tissue has not delivered within 30mins active management, or 60mins physiological management.
- This presence of tissue prevents effective uterine contraction & partial placental separation results in bleeding from the placental bed.
- Thrombin
- Coagulopathies can cause PPH, DIC is important to be aware of.
- DIC can occur in association with a number of different causes → maternal sepsis, placental abruption, PPH (blood loss causes DIC, DIC exacerbates blood loss).
How is a primary PPH managed initially?
Key questions to answer:
- Has the placenta been delivered & is it complete?
- Is the uterus firmly contracted?
- If so, is the bleeding due to trauma?
Management to stabilise the patient:
- A-E approach
- Insert two large-bore cannulas
- Bloods → FBC, U&E, clotting screen, group & save
- Fluids as required
- O- blood if rapid blood loss
- Oxygen
What management is considered during a primary PPH?
-
Mechanical
- Rubbing the uterus → if atonic, stimulates uterine contraction. Bimanual compression may also be performed.
- Catheterisation → bladder distension prevents uterus contractions
- Placental delivery → if still present, a gentle attempt at umbilical cord traction should be tried. If still retained, regional block/GA will be required for manual removal of placenta. A hand is passed into the uterus through the cervix to strip off the placenta.
-
Medical
- Oxytocin → IV bolus of 5 IU, followed by an infusion of 50 IU in 500ml crystalloids.
- Tranexamic acid → IV, antifibrinolytic that reduces bleeding.
- Other oxytocics to stimulate uterine contraction→ IV/IM ergometrine, IM carboprost, sublingual misoprostol.
-
Surgical
- Intrauterine balloon tamponade → insert an inflatable balloon into the uterus to press against bleeding
- B-Lynch suture → suturing the uterus to compress it
- Uterine artery ligation → ligation of one or more of the arteris supplying the uterus to reduce blood flow
- Hysterectomy → last resort, but could save a woman’s life
What are the two most common causes of a secondary PPH?
RPOC or infection (endometritis)
What are the risk factors of endometrial cancer?
- Develops due to the presence of unopposed oestrogen (oestrogen without progesterone) → stimulates the endometrial cells & increases the risk of endometrial hyperplasia & cancer.
- Endogenous Risk factors:
- Obesity → due to aromatisation in body fat of peripheral androgens to oestrogens. 1/3 of cases are linked to obesity.
- Nulliparity
- Early onset menses, late menopause
- PCOS → lack of ovulation
- Anovulatory menstrual cycles
- Exogenous Risk Factors
- Tamoxifen → oestrogenic effect on endometrium
- HRT, without progesterone therapy
- Non-oestrogen risk factors → Type 2 diabetes (increased insulin production, which stimulates endometrial cells), Lynch syndrome
How does endometrial cancer present?
- Abnormal uterine bleeding → post-menopausal, heavy, intermenstrual, post-coital, or unscheduled bleeding whilst on HRT
- Increased vaginal discharge → blood-stained, watery or purulent (pyometrium)
- Advanced disease → pelvic pain, oedema, rectal bleeding, weight loss, fatigue
What are the 3 key investigations for suspected endometrial cancer?
- Transvaginal ultrasound for endometrial thickness → normal <4mm post-menopause
- <5mm normal if HRT is being taken
- Pipelle biopsy → sample of endometrial tissue to examine for hyperplasia or cancer.
- Hysteroscopy with endometrial biopsy
