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Obstetrics + gynaecology > Pregnancy complications > Flashcards

Pregnancy complications Flashcards

1
Q

What is ectopic pregnancy and what are the RF?

A

Any pregnancy outside the uterus, usually the ampulla/isthmus of the uterine tube

RF: prev EP, PID/endometritis (cos of adhesions), failed sterilisation, failed contraception (uterine tube ciliary dysmotility), pelvic surgery, embryo transfer

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2
Q

Presentation of ectopic pregnancy?

A
  • Acute (25%): amenorrhoea for 6-8w, followed by lower abdo pain (one side then spreads), uterine bleeding (late), referred shoulder tip pain (blood irritate diaphragm), brown discharge, syncope, rupture –> haemodynamic instability, peritonism
  • Subacute: short period of amenorrhoea, recurrent bleeding + pain
  • Complications: rupture - hypovolaemic shock - organ failure; comps of surgery (pain, VTE, infection, damage to other structures)
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3
Q

Differentials for pain + bleeding in early pregnancy

A
  • Pregnancy: incomplete/threatened miscarriage
  • Gynae: acute salpingitis, pelvic peritonitis, ovarian cyst problem, acute PID
  • Other: appendicitis, diverticulitis, UTI
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4
Q

How is ectopic pregnancy diagnosed?

A
  • TV USS: empty uterus, fluid in pouch of Douglas, may see an extra-uterine heartbeat
  • Urine/serum beta-hCG: if the hCG is >1500 and no intrauterine preg on US is EP until proven otherwise (by laparoscopy), if hCG<1500 and pt is stable then test again in 48h (if unstable just do lap)
  • In pregnancy hCG should double every 48h, in MC should halve every 48h, and if anything outside this range then assume is EP
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5
Q

How is ectopic pregnancy managed?

A
  • Stabilise, may need blood products
  • If stable + hCG <1500 (ie not ruptured): IM methotrexate removes pregnancy, avoids surgery, but s/e of drug + can’t conceive for 3-6m after cos teratogenic + may fail
  • Conservative: if rupture unlikely may do watchful waiting with hCG monitoring every 48h, complications in 25%
  • Definitive management: remove EP via laparoscopic salpingectomy (if other tube already damaged can do salpingotomy to try to preserve fertility)
  • if an unusual type like abdominal or cervical remove from there
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6
Q

What are the RF for gestational trophoblastic disease?

A

Age <20 or >35, previous GTD (even with different partner), previous miscarriage

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7
Q

Types of gestational trophoblastic disease?

A

*Pre-malignant (molar pregnancy). Abnormal chromosome number at fertilisation forms oedematous avascular placental tissue, usually there’s no fetus (tho is possible), placenta becomes a mass of grape like vessels (hydatidiform mole)

  • Malignant (rarer).
  • Invasive mole when molar pregnancy disseminates
  • Choriocarcinoma: cancer of trophoblastic cells
  • Placental trophoblastic site tumours
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8
Q

How does gestational trophoblastic disease present?

A
  • Abdo pain + bleeding in early pregnancy
  • Soft + boggy uterus
  • Hyperemesis, hyperthyroidism (hCG can mimic TSH), anaemia, large for dates uterus, spontaneous miscarriage (pass a grape-like villous ~20w)

Blood shows very high b-hCG levels

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9
Q

Management of gestational trophoblastic disease?

A
  • Molar pregnancy: suction curettage, check hCG, replace blood loss
  • Malignant: stage, chemo +/- surgery
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10
Q

What is the difference between hyperemesis gravidarum and vomiting of pregnancy?

A

N+V of pregnancy: common, starts around 4-10w and gone by 20w
HG: persistent severe vomiting causing >5% weight loss, dehydration + electrolyte imbalance. Prob because hCG stimulates the CTZ - basically the severe form. Most common 8-12w, may persist up to 20w

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11
Q

RF for hyperemesis gravidarum

A

Primigravida, h/o HG, raised BMI, multiple pregnancy, hydatidiform mole

Smoking reduces the risk

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12
Q

Differentials for vomiting in pregnancy

A

There are more likely if starts from 11w

Gastroenteritis, cholecystitis, hepatitis, pancreatitis, H pylori/ulcer, UTI, metabolic abnormalities, neurological, drug-induced

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13
Q

What are the complications of hyperemesis gravidarum and how do you avoid these?

A
  • Wernicke’s encephalopathy (lack of thiamine B1), Mallory-Weiss tears, central pontine myelinolysis, acute tubular necrosis, SFGA/pre-term baby
  • For mild cases adv small meals, avoiding fatty food, try ginger root (little evidence); antihistamines first line choice for the vomiting (eg prochlorperazine) or cyclizine
  • Ondansetron or metoclopramide second line
  • May need admission for hydration IV
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14
Q

What is miscarriage and how may it present?

A

Pregnancy loss <24w of gestation, most occur in T1, are the result of around 20% of pregnancies

CF include an incidental finding, PV bleeding (mild-severe), suprapubic cramps, haemodynamic instability, tender/distended abdomen

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15
Q

Risk factors for miscarriage

A

> 35 (chromosomal defects), prev MC, obesity, chromosomal abnormalities in the mother or father, previous uterine surgery, APS/other coagulopathies, smoking/alcohol/drugs in pregnancy, uncontrolled HTN/DM/thyroid issues, meds like ibuprofen/methotrexate/retinoids, cervical incompetence, infections, food poisoning

Things NOT associated: heavy lifting, bumping abdomen, sex, air travel, stress

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16
Q

What investigations are done in the early pregnancy unit for suspected miscarriage?

A
  • TV USS - FHB should be seen from 5-6w, estimate gestational age from CRL, look for gestational sac + yolk sac with fetal pole
  • Serial hCG for EP
  • FBC, G+S, RhD status, triple swabs, CRP if pyrexial
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17
Q

What are the causes of miscarriage?

A

Usually no cause is found but possible causes include:

  • Genetic - development halts, abnormal fetus expelled
  • Endocrine - early failure of the corpus luteum, may be due to poorly-controlled thyroid or diabetes
  • Maternal illness -severe fever, specific infections like syphilis or toxoplasmosis, heart/renal/hepatic disease
  • Lifestyle - smoking, antidepressants, NSAIDs, alcohol, >3 cups caffeine per day
  • Cervical incompetence - from physical damage
  • Autoimmune - antiphospholipid antibodies
  • Thombophilic - defects in natural coagulation inhibitors
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18
Q

Describe the types of miscarriage

A
  • Threatened - mild early bleeding typically at 6-9w, uterus enlarged but Os closed, most continue as normal pregnancy
  • Incomplete - pain, bleeding, open Os, some PoC passed but some retained, can cause shock
  • Inevitable - heavy bleeding, pain, internal Os open, fetus may be viable or not
  • Missed - asymptomatic/h/o threatened miscarriage, ongoing discharge, SFD uterus, empty gestation sac, no evidence of yolk sac/embryonic pole
  • Complete - pain + bleeding then they stop, uterus involution, no PoC remain. Most are after 16w
  • Septic - similar to complete but uterine/adnexal tenderness, pyrexia, other septic signs - need IV ABx + fluids as well as the med/surgical MC management
  • Spontaneous T2 loss at 12-24w, SROM/cervical dilatation
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19
Q

How would you manage a lady who has had a miscarriage?

A
  • Treat complications
  • If RhD neg and >12w/having surgical management at any gestation need anti-D immunoglobulin
  • Conservative: unpredictable (up to weeks), may cause heavy bleeding + pain, may retain POC; CI in infection or when higher haemorrhage risk
  • Surgical: manual vacuum aspiration <12w or evacuation of retained POC. Comps: uterus perforation, trauma, adhesions (Asherman syndrome), but good as planned + good for infections + pt unaware
  • Medical: prostaglandin analogue to stimulate cervical ripening + myometrial contraction (e.g. misoprostol), +/- mifepristone (anti-progesterone), takes 48-72h, may bleed for up to 3w
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20
Q

What is recurrent miscarriage and what are the RF?

A

3 or more successive miscarriages (this is the point when you investigate)

RF: higher age (fewer + reduced quality oocytes), high no prev MC, lifestyle

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21
Q

What are the causes of recurrent miscarriage and how would you diagnose these?

A

Mostly weak-associations, things to exclude include APS, parental chromosome translocations and anatomical defects

Ix: bloods for APS (lupus anticoagulants, anticardiolipin antibodies), thrombophilia screen, cytogenic abnormalities, pelvic USS, parental blood karyotyping

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22
Q

How do you manage recurrent miscarriage?

A
  • Psychological impact
  • Recurrent MC clinic
  • Genetic counselling, clinical geneticist if indicated
  • Manage thrombophilias
  • Anatomical suggested by recurrent T2 losses + cervical length shortening
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23
Q

Pathophysiology of red cell isoimmunisation

A
  • RhD negative woman carrying a RhD positive fetus - sensitising event - fetal + maternal cells mix - maternal IgG antibodies formed against RhD antigens - primary event
  • Usually this fetus is fine (as the sensitising event is usually the delivery, so antibodies aren’t made until this point), but in next pregnancy the antibodies can cross the placenta and bind to the fetal RBCs with the RhD antigens - fetus then destroys it’s own RBCs - leads to haemolytic disease of the newborn
  • Sensitising events include APH, invasive testing (CVS, amnio, FBS), ectopic pregnancy, ECV, trauma, IUD, miscarriage, TOP, delivery
24
Q

How is red cell isoimmunisation prevented?

A
  • G+S done at booking and 28w - if found to be RhD negative then anti-D immunoglobulin is given at 28w and 34w as prophylaxis
  • Give anti-D asap, but deffo within 72h, after a sensitising event (to minimise risk of antibodies being made)
  • If it happens in T2/3 larger anti-D dose + do Kleihauer test to quantify how much mixing has happened
25
Q

What are the different types of twinning?

A
  • Monozygotic: 1 embryo makes more than 1 pregnancy, identical twins. Higher risk from IVF. Monochorionic, diamniotic most common (share a placenta), but can be monoamniotic as well (share a sac, more dangerous), or conjoint
  • Dizygotic: 2 eggs + 2 sperm so 2 embryos, separate fertilisations, non-identical. Half mixed gender and half single gender. Most are DCDA, some share a placenta (higher risk of TTTS). RF are maternal FH of twins, higher parity, ovulation induction + fertility drugs
26
Q

What are the complications of twin pregnancies?

A
  • Physiological responses are exagerrated
  • Unrelated to zygosity: anaemia, N+V, miscarriage (one fetus may be resorbed, or both MC), APH, PET, IUGR (usually of one), pre-term labour (x6 risk, as uterus over-distended)
  • Monozygotic: TTTS, conjoined twinning, higher risk of structural abnormalities
  • Labour: obstruction, locked twins (v rare, 1st twin breech and 2nd cephalic so chins lock), 2nd twin higher risk of asphyxia from placental separation/cord prolapse
27
Q

How are twin pregnancies managed?

A
  • Growth scans every 2-4w
  • Delivery: lower threshold for ELCS, if more than twins deffo CS, if vaginal birth allow a maximum of 30 mins between the 1st and 2nd delivery
28
Q

Define antepartum haemorrhage

A

PV bleeding after 24w (before this is threatened miscarriage)

29
Q

How would you assess a pregnant woman who is bleeding?

A
  • History: quantity, fresh/brown/mucus, have membranes ruptured, was it provoked e.g. post coital, pain, fetal movements, RF for abruption
  • Examination: signs of shock, abdo/uterus pain or tense, presentation, CTG, avoid speculum until PP excluded, triple swabs
30
Q

What are the causes of antepartum bleeding?

A
  • Haemorrhage from placenta/uterus: placenta praevia, placental abruption, uterine rupture, marginal placental bleed (non-compromising)
  • Lower genital tract lesions: heavy show/onset of labour, cervical ectropion or cancer, cervicitis, polyps, vulval varices, trauma, infection
  • Bleeding from fetal vessels eg. vasa praevia
31
Q

Define placenta praevia

A

When all or part of the placenta implants in the lower uterine segment, beside/anterior to the presenting part

It develops between 26 and 28w; if placenta is within 2cm of the cervix before 26w this is low lying placenta (most don’t become PP)

32
Q

What causes placenta praevia and what are the risk factors?

A

Caused by delayed implantation of the blastocyst

RF: previous CS, high parity, age>40, multiple pregnancy, prev PP, h/o endometritis

33
Q

Why does placenta praevia cause APH?

A
  • Bleeding as placenta separates whilst the lower uterine segment forms + cervix effaces - venous sinuses bleed
  • This may be spontaneous, from minor trauma or the fetus moving
  • Higher risk of a big bleed because the lower segment contracts less-efficiently
34
Q

How is placenta praevia classified?

A
  • Anatomical: grades I to IV (grade I/II milder and if placenta is anterior they can have SVD)
  • Minor (placenta low but not covering internal Os) or major (placenta covers internal Os)
35
Q

How does placenta praevia present?

A
  • Painless PV bleeding (spotting-major), tends to recur
  • Pain only happens if there is also some abruption or they’re in labour
  • Other signs: malpresentation, normal uterus palpation, may have haemodynamic instability
  • MUST NOT DO A DVE; can do a careful speculum to see where bleed from (like prob just O+G doctors)
36
Q

What investigations would you request in an antepartum haemorrhage?

A

Bloods: FBC, clotting, G+S, XM, Kleihauer if RhD neg (to quantify), U+E, LFT (exclude HELLP)

  • CTG if >26w
  • US TA + TV (TVUS safe and more sensitive)
37
Q

How is placenta praevia managed?

A
  • Anti-D Ig if RhD-
  • Treat blood loss with oral iron or transfusion
  • ELCS at 38w
  • Asymptomatic low placenta at 20w scan - repeat scan later
  • If symptoms: if preterm try to keep until fetus more mature, in hospital, then CS
38
Q

What is placenta praevia accrete?

A

V lethal condition, attachment of placenta to myometrium – placenta doesn’t separate during labour - risk of PPH

RF: previous CS (higher risk where there is scar tissue), placenta praevia

39
Q

Define placental abruption

A

Placenta separates prematurely from the uterus, the detached part can’t function so fetus is compromised

40
Q

What are the RF for abruption?

A

Previous abruption, PET/HTN, abnormal fetal lie, polyhydramnios, abdo trauma, smoking (worst fetal prognosis), thrombophilia, multiple pregnancy

41
Q

How does placental abruption present?

A
  • Painful bleeding - concealed type you may not see
  • Woody tender uterus
  • Retained clot may cause abnormal clotting factor consumption leading to DIC
  • Couvelaire uterus: bleeding through uterus wall so it appears bruised
  • Woman is often in labour so ask about pain in between contractions
  • Shock out of keeping with visible loss
42
Q

How is placental abruption managed?

A
  • Fluids until XM available, blood products as needed, or activate major haemorrhage protocol if have had to transfuse 4 units, after delivering fetus give plt + FFP
  • EMCS if any sign of maternal/fetal compromise (unless SVD is already imminent)
  • IOL if at term and no compromise
  • Conservative if partial or marginal
  • Anti-D if RhD neg within 72h
43
Q

What are the complications of placental abruption?

A

Stillbirth, afibrinogenaemia (release of thromboplastin - DIC - low/no fibrinogen), renal failure due to hypovolaemia/DIC

44
Q

What is vasa praevia?

A

V rare - fetal umbilical vessel is across the Os and in the membranes - ROM can tear it - rapid exsanguination of the fetus

CF: ROM then immediate vaginal bleeding + fetal bradycardia

45
Q

How should you manage a neonate born to a RhD negative mother?

A
  • Take cord blood for FBC, blood grouping + DAT to demonstrate antibodies
  • Kleihauer test: add acid to maternal blood, fetal cells are resistant
  • If they have HDN: transfusions, UV phototherapy
Affected fetus
oedematous (hydrops fetalis, as liver devoted to RBC production albumin falls)
jaundice, anaemia, hepatosplenomegaly
heart failure
kernicterus
treatment: transfusions, UV phototherapy
46
Q

What are the complications of RhD isoimmunisation in the fetus?

A

Oedema: hydrops fetalis because liver has to make RBCs so stops making albumin
Jaundice, anaemia, hepatosplenomegaly
Heart failure
Kernicterus - high bili from haemolytic deposited in basal ganglia

47
Q

What is TTTS?

A

One twin becomes oliguric + IUGR, the other has polyhydramnios/cardiomegaly/hydrops

80% mortality if don’t ablate the communicating vessels + remove the excess fluid

48
Q

What are risk a/w monoamniotic monozygotic twins?

A

Spontaneous miscarriage, malformations, IUGR, TTTS

49
Q

What increases the chance of having dizygotic twins?

A

Previous twins, FH, increasing maternal age, multigravida, induced ovulation + IVF

50
Q

What are the possible complications of dizygotic twins?

A
  • Antenatal: polyhydramnios, pregnancy-induced HTN, anaemia, APH, hyperemesis
  • Fetal: perinatal mortality, prematurity (twins 37w, triplets 33w), low birth weight, malformations
  • Labour complications: PPH, malpresentation, cord prolapse, entanglement
51
Q

What advice would you give to a woman with a low-lying placenta at the 16-20w scan?

A
  • Rescan at 34w
  • No need to limit activity or intercourse unless they bleed
  • If it is still there at 34w they’ll rescan every 2w
  • If high presenting part/abnormal lie at 37w would do CS
52
Q

What is false labour?

A

Occurs in the last 4w with contractions in lower abdomen that are irregular every 30min, no cervical changes

53
Q

What are the hormonal effects of molar pregnancy?

A
  • Significantly raised beta hCG
  • bHCG similar structure to LH, FSH + TSH –> can stimulate thyroid to produce T3 + T4 - can cause sx of thyrotoxicosis
  • High T3 + T4 negative feedback so TSH becomes low
54
Q

How are ectopic pregnancies managed?

A
  • Expectant: monitoring bhCG over 48h, intervene if rising. For small, unruptured asymptomatic EP with no fetal heart beat, beta HCG <200. Can be done if there’s another intrauterine pregnancy
  • Medical: methotrexate. If small, unruptured, no pain, no fetal heart beat, hCG <1500. can’t be done if there’s an intrauterine pregnancy
  • Surgical: if big, ruptured, severe pain, visible fetal heart beat, hCG >1500; can do if another intrauterine pregnancy present
55
Q

What may cause bleeding during pregnancy in each trimester?

A

T1: spontaneous abortion, ectopic pregnancy, hydatidiform mole

T2: spontaneous abortion, hydatidiform mole, placental abruption

T3: bloody show, placental abruption, placenta praevia, vasa praevia

Any time: STIs, cervical polyps

Obstetrics + gynaecology (13 decks)

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