Complications & Pathologies of Pregnancy Flashcards

1
Q

What is miscarriage defined as?

A

Spontaneous loss of pregnancy before 24 wks gestation (defined as the spontaneous loss of pregnancy before the fetus reaches viability. The term therefore includes all pregnancy losses from the time of conception until 24 weeks of gestation)

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2
Q

What is an abortion?

A

A voluntary termination of pregnancy

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3
Q

What is the incidence of spontaneous miscarriage?

A

15%

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4
Q

What is a threatened miscarriage?

A

Bleeding from gravid uterus before 24 wks gestation +/- pain & there is a viable foetus & no evidence of cervical dilation

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5
Q

What is inevitable miscarriage?

A

Cervix begun to dilate-open cervix with bleeding that could be heavy (+/-clots)

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6
Q

What is an incomplete miscarriage?

A

Only partial expulsion of the products of conception

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7
Q

What is a complete miscarriage?

A

When there is a complete expulsion of products

  • Passed all products of conception (POC)
  • Cervix closed & bleeding has stopped (should ideally have confirmed the POC or should have had a scan previously that confirmed an intrauterine pregnancy)
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8
Q

Define a septic miscarriage?

A

Ascending infection into uterus-can spread throughout pelvis

  • Especially in cases of an incomplete miscarriage
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9
Q

What type of miscarriage is it when a foetus has died but the uterus has made no attempts to expel the products of conception?

A

Missed miscarriage

  • No symptoms, or could have bleeding/brown loss vaginally
  • Gestational sac seen on scan
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10
Q

What is a viable pregnancy?

A

“viable pregnancy” after 22-24 weeks is a pregnancy when there is a chance that if delivered the baby can survive

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11
Q
A
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12
Q

What is the role of the ovary?

A

Egg store & hormone release

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13
Q

What is the muscle of the uterus called?

A

Myometrium

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14
Q

What is the role of the cervix?

A

To keep canal narrow during pregnancy & dilates during labour to allow baby out- Also allows spermatozoa up but not bacteriato prevent infection

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15
Q

When progesterone keeps rising in the hormone cycle what does this indicate?

A

Egg is fertilised

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16
Q

What does progesterone (or progestogen) do to the endometrium?

A

Thickens the lining, changes cells
- Turns endometrium into decidua-increases vascularity (monthly shedding occurs here and is akin to falling of leaves from a decidual tree)
- Between glands & vessels the stromal cells enlarge & become procoagulant-stops bleeding

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17
Q

What is fertilised by sperm?

A

Egg (‘chorion’)
Outer edge of chorion=trophoblast cells on outside of the fertilised egg

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18
Q

Trophoblast cells produce which hormone?

A

B-hCG (Beta-human Chorionic Gonadotrophin)

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19
Q

What is the target for B-hCG?

A

Target is corpus luteum in the ovary

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20
Q

What is the function of B-hCG & what is it used for clinically?

A

Its function is to stimulate the corpus luteum to produce progestogen, which stops decidua from shedding

It forms the basis of pregnancy tests - Stimulates ovary to produce progesterone throughout pregnancy & stops decidua from shedding

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21
Q

Where does the fertilised egg burrow into?

A

Into the decidua

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22
Q

What are trophoblasts & what do the do?

A

Are placental cells that only exist in pregnancy. It is a fetal cell.

Invade mother’s blood vessels & eventually link these vessels up with those of the foetus

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23
Q

Where are decidual stromal cells located & what is their purpose?

A

Between vessels (of mother) - they are procoagulant & stop trophoblast cells causing too much bleeding when they invade mothers blood vessels

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24
Q

Fill in the blanks: Projections of chorion (chorionic ..(1)…) covered in ..(2).. cells start to move into the decidua. Eventually the chorionic …(1)… are bathed in the mother’s blood forming the forerunner of the …(3)….

A

1) Villi
2) Trophoblast
3) Placenta

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25
Why does B-hCG return to normal (ie zero)?
No trophoblasts left in mother
26
Why do miscarriages happen (causes)?
- Unknown (it is very common for no cause to be obvious) Causes include: 1. Fetal problem eg chromosomal abnormality, 2. Placenta/membranes/cord problem eg infection, 3. Uterus/cervix problem (eg cervical incompetence) 4. Maternal health issues (eg drug taking)
27
What is an ectopic pregnancy & where is the most common site of it?
Pregnancy in the wrong anatomical site Most common site is in the fallopian tube (lack of proper decidual layer & small size of tube predispose to haemorrhage & rupture) If presents early woman may not even know she is pregnant
28
What is a molar pregnancy?
Form of PRE cancer of trophoblast cells- enlarged abnormal chorionic villi with abundant trophoblast
29
What can occur if a molar pregnancy persists?
Can rarely give rise to a malignant tumour called CHORIOCARCINOMA
30
What are the causes of molar pregnancy?
- Normal ovary-certain genes are switched off in ova by methylating them - Normal testis-different genes are switched off in sperm by methylating them - Mums changes promote early baby growth & dad's changes promote early placenta growth via trophoblast proliferation-overall effect is balanced growth of baby & placenta Molar pregnancy has various causes but can be caused by 2 sperm fertilising one egg with NO chromosomes - Result is imbalance in methylated genes - trophoblast cells proliferate A problem because in the testis dad has inactivated several genes by adding methyl groups to stretches of DNA --massive overgrowth of trophoblast cells and therefore overgrowth of placenta -- no or all but non-existent fetal growth
31
How is molar pregnancy treated post surgical removal?
If BhCG returns to normal – no further treatment. If BhCG stays high (persistent disease) - cure by methotrexate
32
Why can babies be so big in those with DM (uncontrolled)?
Effects of too much Glc in mother
32
Why can babies be so big in those with DM (uncontrolled)?
Effects of too much Glc in mother (there is decreased maternal insulin)
33
Does Glc cross the placenta?
YES, so insulin goes up in baby - baby CANNOT reduce Glc so mum keeps sending more across the placenta
34
In a baby what does longterm high insulin & high Glc cause?
Massive growth-susceptibility to IUD
35
What are the problems encountered with diabetes in pregnancy?
1st trimester: Malformations 3rd trimester: Intrauterine death (probable sudden metabolic and hypoxic problems) Labour: Huge babies that obstruct labour Neonatal period: hypoglycaemia
36
Why is good Glc control in diabetes needed BEFORE conception?
To prevent malformations - and then is needed all the way through to prevent metabolic complications
37
What is acute chorioamnionitis?
Neutrophils present in membranes (chorioamnionitis), cord & fetal plate of placenta--acute inflammation Ascending infection-bacteria are typically perineal or perianal flora (e.g. E.coli) which ascend vagina & get into the amniotic sac Presentation: Mother has fever & raised neutrophils BUT mother can be well! Baby=IUD, Ill in 1st days of life (neonatal unit) or cerebral palsy later on in life
38
How does ascending infection affect the babys brain?
Neutrophils produce cytokine ‘storm’. This activates some brain cells, which then get damaged by normal hypoxia of labour.
39
Do opiates cross the placenta?
YES
40
IVDU that become pregnant are prebooked to deliver beside neonatal unit. WHY?
So baby can be admitted to neonatal unit & treated for heroin withdrawal for example Pregnancy often proceeds well if mother eating properly Immediate withdrawal from heroin when baby is born-later withdrawal from methadone
41
What is an overtwisted cord a common cause of ?
IUD & neonatal illness Problem is caused by a normal, active baby moving & twisting round its own cord
42
What is APGAR?
Appearance, Pulse, Grimace, Activity and Respiration
43
What is placental abruption?
Separation of placenta from uterine wall-results in hypoxia in baby Can get both a haematoma & bleeding per vagina Often causes APH in mother
44
What are the causes of placenta abruption?
- HT - Trauma - Other - e.g. Cocaine
45
What is the most common cause of heavy painless vaginal bleeding?
PLACENTA PRAEVIA - Most common in multiparous women, multiple pregnancies & those with previous CS
46
What symptoms is abruption likely to come with?
Pain or at least a tender, firm abdomen
47
Apart from placenta praevia & placental abruption what are some other causes of APH?
Placenta accreta, vasa praevia, local lesions of genital tract etc. Once these are ruled out may consider a cancer (ask about last smear test)
48
How is placenta praevia diagnosed?
USS Transvaginal may be required to provide accurate measurement of how placenta is related to the cervix This is safe to do, but vaginal exam is not safe as may exacerbate haemorrhage
49
How does major (grades III & IV) differ from minor (grades I & II) placenta praevia?
Grade IV => centre of placenta over cervical os Grade I => placenta in lower uterine segment, but not close to os
50
How is placenta praevia managed?
ABCDE approach IV access, cross match and transfusion if shocked Foetal monitoring CTG US if diagnosis in doubt and patient stable Maternal monitoring HR, BP, temp. Steroids if preterm delivery likely - IV betamethasone Magnesium sulphate if preterm delivery imminent Anti-D if rhesus negative
51
What are some complications of placenta praevia?
- Premature delivery - PPH - Hysterectomy - Blood loss
52
Onset of labour before how many weeks is defines as 'preterm'?
37 completed weeks gestation 32-36 weeks mildly preterm 28-32 weeks very preterm 24-28 weeks extremely preterm
53
What is labour defined as?
Onset of contractions with progressive cervical change
54
Ruptured membranes but no contractions yet. What is this condition called?
PPROM (Prelabour premature rupture of membranes)
55
What are some complications of PPROM?
- Preterm delivery (resulting in neonatal morbidity (e.g. low birth weight, resp hypoplasia, sepsis)) - Chorioamnionitis (inflam of foetal membranes due to bacterial infection) leading to sepsis in baby &/or mother - Abruption
56
What does a negative fFN (foetal fibronectin) show?
Labour unlikely in the next 2 weeks (If positive, likely in next 2 weeks--therefore steroids, tocolysis, analgesia & hospital observation may be indicated)
57
What is management for PPROM after speculum exam- cervic closed & negative fFN test (also got high vaginal swab for infection)?
Prophylactic Abx to reduce risk of chorioamnionitis & corticosteroids (IM dexamethasone or betamethasone) Corticosteroids administered to induce foetal lung maturation-effect is maximal 24hrs after second dose
58
What are tocolytics used for?
To stop contractions to allow time for steroids to work before birth or allow transfer to an appropriate facility for birth
59
What are some signs of Respiratory Distress Syndrome?
STERNAL and SUBCOSTAL RECESSION Increased RESP RATE Expiratory Grunting Diminished Breath Sounds Cyanosis Nasal Flaring
60
How is respiratory distress syndrome managed?
OXYGEN Early treatment with SURFACTANT (used to promote lung maturity) Continuous positive airway pressure (CPAP)
61
What is shoulder dystocia?
When the anterior fetal shoulder becomes impacted behind the maternal pubic symphysis after delivery of the fetal head
62
How is shoulder dystocia managed?
A series of manoeuvres are used to dislodge the shoulder As fetal oxygen levels can drop steeply during the management of shoulder dystocia, effective teamwork and a well-rehearsed approach to management is essential. A helicopter view of the situation is important in order to anticipate what will be needed. Eg. a senior obstetrician, a paediatrician to attend to baby immediately after the birth, a scribe to keep a note of timings which can help decide on what manoeuvre to try next
63
Between what stages of the normal process of birth of foetal head would shoulder dystocia occur?
Between complete extension & restitution (external rotation)
64
What are the dangers of shoulder dystocia?
- Umbilical cord entrapment - Inability of child's chest to expand properly - Severe brain damage or death due to hypoxia or acidosis if delay in delivery - Brachial plexus damage
65
What is the acronym for management of shoulder dystocia?
H – Call for Help E – Evaluate for Episiotomy L – Legs (McRoberts Position) P – Suprapubic Pressure E – Enter Manouvers (Internal Rotation) R – Remove the Posterior Arm R – Roll the Patient (Onto all Fours)
66
What does McRoberts position involve?
Flexing the hips by around 60 degrees to open up the pelvis
67
What is the purpose of an episiotomy in shoulder dystocia?
To create space to allow the internal manoeuvres (internal rotation & removal of posterior arm) to be attempted
68
What is primary PPH?
In first 24 hours after delivery >500ml blood (common 1/20 women) Severe Haemorrhage >2000ml
69
What is secondary PPH & what is it often caused by?
>24hrs to up to 6 weeks post delivery Often caused by RPOC
70
What is the immediate management of PPH?
Call for help! ABCDE... Empty Bladder Rub up uterine fundus by massaging above the umbilicus
71
What medications can be used in PPH?
Oxytocin 5iu slow iv injection Ergometrine 0.5mg slow iv injection (not if high BP) Oxytocin infusion Tranexamic acid 1g IV Carboprost 0.25mg im (max 8 doses) Misoprostol (800 micrograms)
72
What are the surgical management options of PPH?
Intrauterine Balloon tamponade Interventional Radiology B-Lynch Suture Hysterectomy
73
Manage PPH based on ..?.. not just EBL
Clinical signs - May also need fluid replacement +/- Blood products
74
What is a cord prolapse?
The descent of the umbilical cord through the cervix alongside (occult) or past (overt) the presenting part in the presence of ruptured membrane. Higher incidence in the case of breech presentation When the umbilical cord prolapses below the presenting part of the fetus it is highly likely to become compressed and thus reduce oxygen supply to the fetus
75
How is cord prolapse managed?
- Call for Help! - Replace cord into vagina (not uterus) - Perform digital elevation of the presenting part - Catheterise and fill bladder to elevate presenting part. - Encourage mother to adopt Knee-Chest or left lateral position with raised hips - Consider tocolysis - Arrange for a Category 1 C-Section.
76
Why in cord prolapse do we: 1) replace the cord into the vagina 2) catheterise the bladder 3) Knee chest position
1) Reduces the chance of it becoming compressed or of the vessels going into spasm because of the lower temperature outside the body. It is still at risk of compression due to the fetal presenting part being above it. 2) Takes time so if there is immediate access to CS then this step may be omitted. It can be a very helpful step if an ambulance transfer is required to reach a hospital. 3) Uses gravity to shift fetus out of the pelvis- often combined with the Trendelenburg (head down) position
77
What is primary cervical weakness?
Cervix that is not able to hold pregnancy-cause not known in most cases
78
What is secondary cervical weakness?
Operation prior or removal of cervix-leads to weakness
79
Where can fluid build up in ectopic pregnancy?
Pouch of Douglas
80
Do twins make a women at risk for a preterm labour in their next pregnancy?
NO
81
What is an incomplete miscarriage & what is needed for it?
Cervix is partially opened-uterus cant fully expel contents (need medical evacuation either on ward, theatre or medication) - vaginal bleeding (may be heavy)
82
What is a transvaginal probe definitely beneficial for in terms of placenta praevia?
Posterior placenta praevia - to find posterior edge (can be used in anterior too)
83
Can preeclampsia cause HELLP?
YES it can
84
When does gestational diabetes resolve?
Almost immediately after delivery
85
What is the first line for a septic miscarriage?
Amoxiclav-duration course for 7 days (may need IV)
86
What can be used to end an early pregnancy?
Mifepristone & Misoprostol
87
What is used after surgical removal of a molar pregnancy if worry of further issues or if hasn't worked?
METHOTREXATE (acts against rapidly multiplying cells)
88
If methotrexate is needed as management for ectopic pregnancy how long is it before can get pregnant?
Cant get preg for at least 3 months after (often 6 months if for molar preg)
89
How long should wait to see if miscarriage happens itself before intervening?
Typically 7-10 days
90
What is the aetiology of spontaneous miscarriage?
- Abnormal conception (chromosomal, genetic, structural) - Uterine abnormality (congenital, fibroids) - Cervical weakness (primary, secondary) - Maternal (increasing age, diabetes) - Unknown In practice it is often difficult to identify the underlying factor because of changes in the fetal tissue after death interfere with chromosomal analysis or adequate structural examination. It is estimated from studies that up to 50% of spontaneous miscarriages may be due to abnormal chromosomes.
91
What is the management for miscarriages?
Threatened=conservative, most stop bleeding and are ok Inevitable=If bleeding heavy may need evacuation Missed - Conservative - Medical-prostaglandins (misoprostol) - Surgical - SMM (surgical management of miscarriage) Septic= Abx & evacuate uterus
92
How does an ectopic pregnancy present?
Period of amenorrhoea (with +ve urine pregnancy test) +/- vaginal bleeding, pain in abdomen, GI or urinary symptoms
93
How is an ectopic pregnancy investigated & managed?
Scan- no intrauterine gestational sac, may see adnexal mass, fluid in pouch of douglas Serum BHcg levels-may need to serially track levels over 48 hr intervals Management is methotrexate or surgery (mostly laparoscopic-salpingectomy etc) or conservative (mostly reserved for patients whose serum beta HCG levels are low & they are haemodynamically stable)
94
In a miscarriage HCG levels are known to reduce by what?
50% over the course of 48 hrs
95
What is the difference between salpingectomy and salpingotomy?
Salopingectomy = remove the tube Salpingotomy = leave a damaged tube, remove the embryo
96
What is an antepartum haemorrhage (APH) and what can cause it?
Haemorrhage from the genital tract after the 24th week of pregnancy but before delivery of the baby Causes: - Placenta praevia (placenta attached to the lower segment of the uterus) - Placental abruption (placenta has started to separate from the uterine wall before the birth & is associated with a retroplacental clot) - APH of unknown origin - Local lesions of the genital tract - Vasa praevia (very rare)-rupture of foetal vessels in the foetal membrane
97
What is placenta praevia and what is the RXOG classifications of it?
All or part of the placenta implants in the lower uterine segment RXOG Classification: - Low lying=placenta is <20mm from internal os - Placenta previa=Covering the os
98
How does placenta praevia present?
- Painless PV bleeding - Soft, non tender uterus - Malpresentation of foetus - Incidental (e.g. following a US)
99
In wat situations may a conservative approach be used for placenta praevia?
Conservative approach may be used to prolong pregnancy & gain foetal maturity & then deliver via CS (between 36-37 wks gestation). CS as cervix dilatation will cause bleeding
100
How is PPH managed?
Medical- Oxytocin, ergometrine, carboprost, tranexamic acid Balloon tamponade Surgical=B lynch suture, ligation of uterine arteries, iliac vessels, hysterectomy
101
What is a placental abruption?
Haemorrhage resulting from premature separation of the placenta before the birth of the baby (incidence 0.6% of all pregnancies) – associated with a retroplacental clot
102
What are the 3 clinical types of placental abruption?
* Revealed (see blood) * Concealed (bleeding inside between uterine wall & the placenta-uterine contents increase in volume & the fundal height is larger than that would be consistent for that gestation- In some situations the blood penetrates the uterine wall and the uterus appears bruised and this is know as a Couvelaire uterus) * Mixed (concealed & revealed)
103
How does placental abruption present?
- PAIN (severe, abdominal) - Vaginal bleeding (may be minimal) - Increased uterine activity
104
How is APH generally managed?
Varies from expectant treatment to attempting a vaginal delivery to immediate CS depending on: - Amount of bleeding - General condition of mother and baby - Gestation
105
What are the complications of placental abruption?
- Maternal shock, collapse - Fetal distress then death - Maternal DIC, renal failure - PPH - Couvelaire uterus
106
What are the categories of preterm labour (onset of labour before 37 weeks completed gestation)?
32-36 wks=Mildly preterm 28-32=Very preterm 24-28=Extremely preterm Spontaneous or induced (iatrogenic) Babies should be resuscitated if born after 22 completed weeks of gestation
107
What are reasons for preterm?
Pre eclampsia, infection, PPH & placenta praevia
108
How is preterm diagnosis done?
Contractions with evidence of cervical change on VE Test=Fetal fibronectin
109
At what weeks is preterm generally regarded as very poor prognosis?
<24-26 weeks Decisions made in discussion with parents and neonatologists
110
What steps are carried out in preterm cases considered viable?
- Consider tocolysis to allow steroids/transfer - Steroids unless contraindicated - Transfer to unit with NICU facilities - Aim for vaginal delivery
111
What is tocolysis?
Drugs preventing uterine contractions, labour suppressants
112
What are some examples of neonatal morbidity that can result from prematurity?
- RDS - Intraventricular haemorrhage - CP - Visual impairment - Hearing loss
113
When is chronic HT in relation to pregnancy?
Hypertension either pre-pregnancy or at booking (≤ 20 weeks gestation)
114
What are the grades of HT?
Mild HT– Diastolic BP 90-99, Systolic BP 140-49 Moderate HT- Diastolic BP 100-109, Systolic BP 150-159 Severe HT- Diastolic BP ≥110, Systolic BP ≥ 160
115
What is gestational HT (PIH-pregnancy induced HT)?
BP as above but new hypertension (develops after 20 weeks)
116
What is pre-eclampsia defined as?
New hypertension > 20 weeks in association with significant proteinuria
117
What is significant proteinuria and how is it tested for?
Automated reagent strip urine protein estimation > 1+ Spot Urinary Protein: Creatinine Ratio > 30 mg/mmol 24 hours urine protein collection > 300mg/ day
118
In what demographic of mothers is essential/chronic HT more common?
Commoner in older mothers
119
What pre-pregnancy care for essential/chronic HT be provided and what monitoring should be done?
Change anti-hypertensive drugs if indicated eg. - ACE inhibitors (eg. Ramipril / Enalopril cause birth defects impaired growth) - Angiotensin receptor blockers (eg losartan, Candesartan) - Anti diuretics - Lower dietary sodium Aim to keep BP < 150/100 (labetolol (B blocker), nifedipine (CCB), methyldopa) Monitor for superimposed pre-eclampsia Monitor fetal growth May have a higher incidence of placental abruption
120
What is pre-eclampsia defined as?
Mild HT on two occasions more than 4 hours apart Moderate to severe HT + proteinuria of more than 300 mgms/ 24 hours (protein urine > + protein:creatinine ratio > 30mgms/mmol)
121
What is the pathophysiology of pre-eclampsia?
Immunological Genetic predisposition - secondary invasion of maternal spiral arterioles by trophoblasts impaired - reduced placental perfusion - imbalance between vasodilators / vasoconstrictors in pregnancy (prostocyclin / thromboxane)
122
What are some risk factors for developing PET?
First pregnancy Extremes of maternal age Pre-eclampsia in a previous pregnancy (esp. severe PET, delivery <34 weeks, IUGR baby, IUD, abruption) Pregnancy interval >10 years BMI > 35 Family history of PET Multiple pregnancy Underlying medical disorders - chronic hypertension - pre-existing renal disease - pre-existing diabetes - autoimmune disorders like – eg. antiphospholipid antibodies, SLE
123
Can preeclampsia be a multisystem organ disorder?
Yes-renal, liver, vascular, cerebral, pulmonary
124
What are the maternal complications of PET?
- eclampsia - seizures - severe hypertension – cerebral haemorrhage, stroke - HELLP (hemolysis, elevated liver enzymes, low platelets) - DIC (disseminated intravascular coagulation) - renal failure - pulmonary odema, cardiac failure
125
What are the fetal complications of PET?
Impaired placental perfusion → IUGR, fetal distress, prematurity, increased PN mortality
126
What are the symptoms/signs of severe PET?
– headache, blurring of vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands face legs - Severe Hypertension; > 3+ of urine proteinuria - clonus / brisk reflexes ; papillodema, epigastric tenderness - reducing urine output - convulsions (Eclampsia)
127
What are the biochemical and haematological abnormalities seen in severe PET?
Biochemical abnormalities - raised liver enzymes, bilirubin if HELLP present - raised urea and creatinine, raised urate Haematological abnormalities - low platelets - low haemoglobin, signs of haemolysis - features of DIC
128
How is PET managed?
- Frequent BP checks, Urine protein - Check symptomatology – headaches, epigastric pain, visual disturbances - Check for hyper-reflexia (clonus), tenderness over the liver - Blood investigations – Full Blood Count (for hemolysis, platelets), Liver Function Tests, Renal Function Tests – serum urea, creatinine, urate Coagulation tests if indicated Fetal investigations - scan for growth cardiotocography (CTG)
129
The only cure for PET is delivery of the baby and placenta but what is involved in the conservative management that aims for foetal maturity?
- close observation of clinical signs & investigations - anti-hypertensives (labetolol, methyldopa, nifedipine) - steroids for fetal lung maturity if gestation < 36wks Consider induction of labour / CS if maternal or fetal condition deteriorates, irrespective of gestation Risks of PET may persist into the puerperium therefore monitoring must be continued post delivery
130
How are seizures/impending seizures (PET/eclampsia related) treated?
Magnesium sulphate bolus + IV infusion Control of blood pressure – IV labetolol, hydrallazine (if > 160/110) Avoid fluid overload – aim for 80mls/hour fluid intake
131
What is the prophylaxis for PET in subsequent preg?
Low dose Aspirin from 12 weeks till delivery Women with PET at a higher risk to develop hypertension in later life
132
What are the characteristics of gestational diabetes?
- carbohydrate intolerance with onset (or first recognised) in pregnancy - abnormal glucose tolerance that reverts to normal after delivery - however, more at risk of developing type II diabetes later in life
133
Why do insulin requirements of the mother increase in preg?
Human placental lactogen, progesterone, human chorionic gonadotrophin, and cortisol from the placenta have anti-insulin action
134
How does fetal hyper-insulinemia occur?
Maternal glucose crosses the placenta and induces increased insulin production in the fetus. The fetal hyperinsulinemia causes macrosomia Post delivery – more risk of neonatal hypoglycaemia and increased risk of respiratory distress
135
What does diabetes increase the risk of in preg?
Fetal congenital abnormalities e.g – cardiac abnormalities, sacral agenesis (especially if blood sugars high peri-conception) Miscarriage Fetal macrosomia, polyhydramnios Operative delivery, shoulder dystocia Stillbirth, increased perinatal mortality
136
What are some complications of diabetes in preg?
Increased risk of pre-eclampsia Worsening of maternal nephropathy, retinopathy, hypoglycaemia, reduced awareness of hypoglycaemia Infections Neonatal - Impaired lung maturity, neonatal hypoglycemia, jaundice
137
How should diabetes be managed preconception?
- better glycemic control, ideally blood sugars should be around 4 – 7 mmol/l pre-conception and HbA1c < 6.5% ( < 48 mmol/mol) - folic acid 5mg - dietary advice - retinal and renal assessment
138
How should diabetes be managed during pregnancy and what should be watched out for?
- optimise glucose control – insulin requirements will increase - Could continue oral anti-diabetic agents (metformin) but may need to change to insulin for tighter glucose control - should be aware of the risk of hypoglycemia – provide glucagon injections/ conc. glucose solution - watch for ketonuria/ infections - repeat retinal assessments 28 and 34 weeks - watch fetal growth
139
What management should be taken for diabetes in labour?
- observe for PET - labour usually induced 38-40 weeks, earlier if fetal or maternal concerns consider elective CS if significant fetal macrosomnia maintain blood sugar in labour with insulin – dextrose insulin infusion continuous CTG fetal monitoring in labour Early feeding of baby to reduce neonatal hypoglycemia Can go back to pre-pregnancy regimen of insulin post delivery
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What are some risk factors for GDM that may cause you to consider screening for GDM?
Increased BMI >30 Previous macrosomic baby > 4.5kg Previous GDM Family history of diabetes Women from high risk groups for developing diabetes – eg. Asian origin Polyhydramnios or big baby in current pregnancy Recurrent glycosuria in current pregnancy GDM associated with some increase in maternal complications (eg PET) and fetal complications (macrosomia) but much less than with type I or II diabetes
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How is GDM screened for?
If risk factor present, offer HbA1C estimation at booking, if > 6% (43 mmol/mol), 75gms OGTT to be done. If OGTT normal, repeat OGTT at 24 -28 weeks Can also offer OGTT at around 16 weeks and repeat at 28 weeks if significant risk factors (eg. Previous GDM) present
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How is GDM managed?
control blood sugars – diet - metformin/ insulin if sugars remain high Post delivery – check OGTT 6 to 8 weeks PN Yearly check on HbA1C/ blood sugars as at a higher risk of developing overt diabetes
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What is Virchows triad for VTE?
- Stasis - Vessel wall injury - Hypercoagulability ===THROMBOSIS
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Why does the risk of thromboembolism increase in preg?
- pregnancy a hypercoagulable state (to protect mother against bleeding post delivery) - increase in fibrinogen, factor VIII, VW factor, platelets - decrease in natural anticoagulants – antithrombin III - decrease in fibrinolysis Increased stasis – progesterone, effects of enlarging uterus May be vascular damage at delivery/ caesarean section
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What is the VTE prophylaxis used in preg?
TED stockings Advice increased mobility, hydration Prophylactic anti-coagulation with 3 or more risk factors (may be indicated even with one risk factor if significant risk), may need to continue 6 weeks postpartum
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What are the signs/symptoms of VTE?
Pain in calf, increased girth of affected leg, calf muscle tenderness, breathlessness, pain on breathing, cough, tachycardia, hypoxic, pleural rub, etc
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What investigations are carried out if there is suspicion of VTE?
- ECG, Blood gases, doppler V/Q (ventilation perfusion) lung scan CTPA (computed tomography pulmonary angiogram) Appropriate treatment with anticoagulation if VTE confirmed
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How is DVT investigated for?
Dopplers