Obstetrics - General Flashcards
Define primary PPH
Minor
Major
Loss of blood estimated to be >500ml from the genital tract within 24 hours of delivery
Minor PPH – blood loss <1000mls
Major PPH – blood loss >1000mls
Aetiology of major PPH
The four Ts
- Tone – uterine atony, distended bladder
- Trauma – lacerations of the uterus/cervix/vagina
- Tissue – retained placenta or clots
- Thrombin – pre-existing or acquired coagulopathy
Aetiology of secondary PPH
• Endometritis (infection) o RF: CS PROM severe meconium staining in liquor long labour with multiple examinations manual removal of placenta mother’s age at extremes of the reproductive span low socio-economic status maternal anaemia prolonged surgery internal fetal monitoring GA
• RPOC (retained products of conception)
When does nausea + vomiting/hyperemesis gravidarum in pregnancy start + when does it end?
- NVP typically begins between the 4th and 7th week after the LMP and peaks at 9th weak
- Resolves in the second trimester/by 20th week
• Vomiting that begins after 12 weeks of gestation is unlikely to be caused by hyperemesis gravidarum – other pathological causes should be considered
Diagnostic criteria for hyperemesis gravidarum (RCOG)
• RCOG diagnostic criteria (requires all 3)
o >5% pre-pregnancy weight loss
o Dehydration*
o Electrolyte imbalance
*Dry mucous membranes
Postural dizziness
Tachycardia
Hypotension
Ketosis might also be present
What are the 6 questions in the PUQE-24 questionnaire?
Where is it being used?
Which PUQE-24 score indicates severe N+V?
1. In the last 24h, for how long have you felt nauseated or sick to your stomach? 1 - Not at all 2 - 1 hour or less 3 - 2-3 h 4 - 4-6 h 5 - >6 h
2. In the last 24h, have you vomited or thrown up? 1 - I did not throw up 2 - 1-2 3 - 3-4 4 - 5-6 5 - >7
3. In the last 24 hours, how many times have you had dry retching or dry heaves without brining anything up? 1 - No time 2 - 1-2 3 - 3-4 4 - 5-6 5 - >7
How many hours have you slept out of 24h? Why?
On a scale of 0-10, how would you rate your wellbeing?
Can you tell me what causes you to feel that way?
It is a scoring system used to quantify the severity of NVP
A score of 13 or more, indicates severe PUQE 24
Maternal and fetal complications of hyperemesis gravidarum
Maternal (major – VTE, Wernicke’s, hypokalaemia, hyponatraemia)
• Dehydration
• Wernicke’s encephalopathy (lack of B12)
• Central pontine myelinolysis (rapid [Na+] correction)
• VTE (dehydration)
• Acute tubular necrosis (dehydration)
• Mallory Weiss tear
• Spontaneous oesophageal rupture
Foetal
• IUGR
• PTL
• Termination
Define
- Hypertension
- Severe hypertension
- Chronic hypertension
- Gestational hypertension
- Pre-eclampsia
- Severe pre-eclampsia
- Eclampsia
- HELLP syndrome
in pregnancy
- Hypertension: BP of >140mmHg SBP or >90mmHg to 159/109mmHg
- Severe hypertension: SBP > 160mmHg or DBP >110mmHg
- Chronic hypertension: HTN that is present at the booking visit or before 20 weeks, or if the woman is already taking antihypertensive medication when referred to maternity services. Can be primary or secondary
- Gestational hypertension: New hypertension presenting after 20 weeks of pregnancy without significant proteinuria
• Pre-eclampsia: new onset hypertension (>140 mmHg SBP or >90 mmHg DBP) after 20 weeks of pregnancy + co-existence of 1 or more of the following new onset conditions
o Proteinuria (urine protein:creatinine ratio >30 g/mmol or albumin: creatinine ratio >8 mg/mmol or at least 1g/L [2+] protein on dipstick testing or >0.3g in 24 hours) or
o Other maternal organ dysfunction
Renal insufficiency (Cr > 90micromol/L, >1.02mg/100ml)
Liver involvement (raised transaminases – ALT or AST > 40IU/L) with or without RUQ or epigastric abdominal pain
Neurological complications (eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, persistent visual scotomata)
Haematological complications (thrombocytopenia (plt < 150.000/microleter), DIC, or haemolysis)
Uteroplacental dysfunction e.g. IUGR, abnormal umbilical artery doppler waveform analysis, stillbirth
• Severe pre-eclampsia: pre-eclampsia with severe hypertension that does not respond to treatment or is associated with
o Recurring severe headaches
o Visual scotomata
o N or V
o Epigastric pain
o Oliguria
o Severe hypertension
o Progressive deterioration in lab blood tests - raised Cr or liver transaminases, low platelet count
o Failure of fetal growth or abnormal doppler findings
- Eclampsia: occurrence of one or more convulsions superimposed on pre-eclampsia (>1 seizure in one with pre-eclampsia)
- HELLP syndrome: haemolysis, elevated liver enzymes, low platelets (severe form of pre-eclampsia)
- BP usually falls in the first half of pregnancy before rising back to pre-pregnancy levels before term
Pre-eclampsia
High RF 5
Moderate RF 6
• High RF o HTN disease during previous pregnancy o CKD o Autoimmune disease e.g. SLE or antiphospholipid syndrome o T1 or T2DM o Chronic HTN
• Moderate RF o First pregnancy o Pregnancy interval of >10 years o >40 y/o o BMI >35kg/m2 at first visit o FHx of pre-eclampsia o Multiple-fetal pregnancy
Complications of pre-eclampsia
• Baby o IUGR o LBW o Small for gestational age infants o PTL Half of women with severe pre-eclampsia will deliver before 36 weeks o Infant respiratory distress syndrome o Severe hypoxia – foetus and/or newborn may have neurological damage induced by hypoxia
• Mother o HELLP syndrome o DIC o AKI o ARDS o Pre-eclampsia can progress to eclampsia with epileptic fits + other neurological symptoms (incl. focal motor deficits, cortical blindness) • Cerebrovascular haemmorrhage
Define
Impaired Fasting glucose (IFG)
Impaired Glucose Tolerance (IGT)
Diabetes
In terms of fasting plasma glucose and OGTT
Impaired Fasting Glucose
Fasting plasma glucose 6.1-6.9 mmol/l
Impaired Glucose Tolerance
OGTT >7.8 and <11.1 mmol/l
Diabetes
Fasting plasma glucose >7.0 mmol/l
OGTT >11.1 mmol/l
Effect of pregnancy on diabetes
Nausea and vomiting (particularly early on)
Greater importance of tight glucose control
Increase in insulin dose requirements in second half of pregnancy
Increased risk of severe hypoglycaemia
Risk of deterioration of any retinopathy
Risk of deterioration of any nephropathy
Effect of diabetes on Pregnancy
Increased risk of miscarriage
Risk of congenital malformation / spina bifida
Risk of macrosomia
Increased risk of pre-eclampsia
Increased risk of stillbirth
Increased risk of infection
Increased operative delivery rate
Pre-existing diabetes during pregnancy complications
• Antenatal period
o Embryogenesis is affected by DM and so miscarriage risk is higher
o Midline deformities e.g. spina bifida – poor glycaemic control is teratogenic
o Growth restriction possible – macrocosmic babies can still be growth restricted
o Polyhydramnios – baby has osmotic diuresis – cord prolapse + placental abruption
o Higher infection + DKA risk in pregnancy
o Pregnancy induced hypertension, pre-eclampsia
o Thromboembolism
o Ketoacidosis
o Hypoglycaemia
o Progression of microvascular complications incl. retinopathy, nephropathy
o Spontaneous abortion
o Worsening nephropathy – can affect maternal BP
o Nephropathy with superimposed pre-eclampsia – most common cause of pre-term delivery in women with diabetes
• During birth
o Preterm labour
o Birth injury
o Fetal distress
o Respiratory distress syndrome
o Jaundice
o Congenital malformations – neurological and cardiac abnormalities
o Macrosomia
o Obstructed labour – associated with increased risk of macrosomia + shoulder dystocia + Erb’s palsy
o Late intrauterine death/Stillbirth risk – baby outgrowing supply of the placenta
o Hypoglycaemic risk for baby after cut cord – loss of glucose + high insulin levels
If the mother has high glucose, the glucose passes to the baby and the baby’s pancreas produces insulin (like IGF-1, a growth factor) and so the baby becomes macrosomic (insulin + fragmin are the two molecules that cannot cross the placenta)
• After birth
o Increased Perinatal mortality
o Postnatal adaptation problems (e.g. hypoglycaemia)
Why is there a risk of hypoglycaemia in pregnant women with pre-existing diabetes?
Insulin resistance increases throughout pregnancy (Increase dose of metformin or insulin during pregnancy)
Postnatally, insulin requirements return to normal levels - insulin should be adjusted accordingly
If glucose drops with insulin tx in pregnancy – bad because insulin resistance should go up
Human placental lactogen + steroids drive the diabetes in pregnancy so if insulin control gets better this means that the placenta isn’t working as well
Doppler USS will not detect this as it is a metabolic change
Check foetal movement and CTG measurements
Define gestational diabetes
• Any degree of glucose intolerance with its onset (or first diagnosis) during pregnancy
o Fasting plasma glucose level >5.6 mmol/L
o 2-h plasma glucose level (OGTT) >7.8 mmol/L
- Occurs 24-28w gestation
- Usually resolves after delivery
• Mild GDM
o Positive OGTT but fasting blood glucose <5.3mmol/L
Complications of gestational diabetes melitus /GDM
Complications are the same as DM in pregnancy but to a lesser degree (as effects of glucose occur for less time)
Maternal
• Hyperglycaemia – large-for-dates babies, adverse maternal + fetal outcomes
• Pre-eclampsia
• Preterm labour
• Increased risk of developing diabetes later in life
o GDM is a strong RF for diabetes + metabolic syndrome
o Most women will recover after the pregnancy but with about 50% of recurrence in a future pregnancy
Fetal • Shoulder dystocia • Birth injury e.g. bone fractures, nerve palsies • Large for gestational age • Delivery by C-section • Intensive neonatal care requirement • Hyperbilirubinemia • Hyperinsulinemia • Hypoglycaemia
• Long term outcomes in infants born to mothers with GDM
o Sustained impairment of glucose tolerance
o Subsequent obesity
o Impaired intellectual achievement
Ectopic pregnancy complications
- Tubal or uterine rupture (depending on the location of the pregnancy) - massive haemorrhage, shock, DIC, death, psychological sequalae
- Complications of surgery – bleeding, infection, damage to surrounding major vessels + organs (e.g. bowel, bladder, ureters
DDx of ectopic pregnancy
• Threatened miscarriage
o Vaginal bleeding is the predominant feature
o Pain may come later as the cervix dilates
o Dilated cervix
o In ectopic pregnancy, pain usually comes first and if vaginal bleeding occurs it is of much less significance
- Normal pregnancy – hCG doubles every 48 hours
- Miscarriage – hCG decreases
- Ectopic – hCG hovers around a single value
Ectopic pregnancy risk factors
• IVF
• PID – may cause tubal occlusion or delay the transport of the embryo so that implantation occurs in the tube
• Endometriosis – adhesions
• Infection – adhesions
• Previous tubal surgery – adhesions
• PMHx of ectopic
• IUCD or IUS use
o IUCDs reduce the risk of ectopic pregnancy compared to using no contraception
o Where an IUCD fails, the risk of pregnancy being ectopic is very high
• Women becoming pregnant whilst using POP
Placenta praevia vs low lying placenta
- Placenta praevia = when the placenta lies directly over the internal os [diagnosed at >32 weeks]
- Low lying placenta = >16 weeks gestation + placental edge is <20mm from the internal os on transabdominal or transvaginal screening
Placenta praevia complications
• Placenta accreta
o Morbidly adherent placenta
o Rare but important complication of placenta praevia esp. in women w a previous C-section
• Rare: placenta accreta/increta/percreta
- Maternal: APH, DIC, hysterectomy, death
- Fetal: Fetal haemorrhage, prematurity, intrauterine asphyxia, IUGR, birth injury, death
- Labour: PPH, blood transfusion
• Placenta praevia + anterior low-lying placenta - higher risk of massive obstetric haemorrhage + hysterectomy
o Indications for blood transfusion and hysterectomy should be reviewed + discussed with the woman
o Delivery should be arranged in a maternity unit with on-site blood transfusion services + access to critical care
- Potentially fatal hypovolaemic shock resulting from severe antepartum, intrapartum, postpartum bleeding
- VTE
• Other complications o 54.9% preterm birth o Antepartum (42.3%), postpartum (7.1%) haemorrhage o 35.6% low birth weight <2500g o 30% maternal anaemia o 4% co-existing placenta accreta o 5.2% hysterectomy o 1.5% fetal mortality
Placenta praevia grades
- Grade I or minor praevia is defined as a lower edge inside the lower uterine segment
- Grade II or marginal praevia as a lower edge reaching the internal os
- Grade III or partial praevia when the placenta partially covers the cervix
- Grade IV or complete praevia when the placenta completely covers the cervix
Vasa praevia definitions
• Velamentous cord insertion = placenta has developed away from the attachment of the cord and the vessels divide in the membrane
• Vasa previa
These exposed blood vessels cross the lower pole of the chorion
Foetal vessels course through membrane over the internal cervical os and below fetal presenting part, unprotected by placental tissue or umbilical cord
o This is fetal blood, therefore at rupture of membranes and as baby descends, there is a high risk of fetal haemorrhage and death (vs in placental abruption where there is maternal loss of blood)
- Type 1 VP = velamentous cord insertion in a single or bilobed placenta
- Type 2 VP = foetal vessels running between lobes of a placenta with 1 or more accessory lobes
- Benckaiser’s haemorrhage = the haemorrhage of blood when the vessels are ruptured
Vasa praevia complications, prognosis and ddx
Complications
• No major maternal risk but dangerous for the foetus
o Foetus – loss of relatively small amounts of blood can have major implications for the foetus = rapid delivery + aggressive resuscitation incl. use of blood transfusion if required
Prognosis
• Foetal mortality if presenting with haemorrhage is 60% but if identified antenatally it’s 3%
DDx
• Placental abruption
o Will present with pain
o It is maternal blood, therefore mum is in danger
What is Benckaiser’s haemorrhage?
the haemorrhage of blood when the vessels n vasa previa are ruptured
Placental abruption prognosis + complications
Complications • Foetal o Fetal anaemia, fetal compromise o Fetus exposed to severe hypoxia and acidaemia o Abnormalities of the fetal HR pattern If fetal heart rate cannot be heard on auscultation, then USS should be performed to exclude IUD o Birth asphyxia o IUD
• Maternal o Coagulopathy o DIC o Hypovolaemic shock o Renal failure o Catastrophic haemorrhage associated with postpartum DIC o Haemorrhage (APH, PPH)
• Labour – blood transfusion
Prognosis
• Maternal – 0.5% mortality in severe abruption
• Foetal – 3.3% mortality in severe abruption
Placental abruption ddx
DDx
• Labour
o Placental abruption should be considered when the pain is continuous
o Labour should be considered if the pain is intermittent
• Placenta praevia
o In placenta praevia the uterus is soft + non-tender, bleeding + no pain
o In placental abruption the uterus is tense (woody) + tender, bleeding + pain
Placental abruption definitions
Placental abruption >24 weeks, <24 weeks
Concealed haemorrhage
Revealed haemorrhage
Marginal haemorrhage
• The premature separation of a normally placed placenta before delivery of the fetus with blood collecting between the placenta and the uterus before delivery (>24 weeks)
o If <24 weeks – miscarriage
- As placenta separates, retroperitoneal bleeding results in further detachment
- One of the most important causes of antepartum haemorrhage (APH) (the other being placenta praevia)
Concealed (20% of cases) – haemorrhage is confined within the uterine cavity and is the more severe form. The amount of blood lost is easily underestimated
Revealed (80)% - where blood drains through the cervix, usually with incomplete placental detachment and fewer associated problems
Marginal haemorrhage – painless bleed and clot located along the margin of the placenta with no distortion of its shape. It is usually due to the rupture of a marginal sinus. Women should be admitted for observation and fetal monitoring
Placental abruption RF
• 70% occur in low-risk pregnancy
Maternal
• Previous abruption – the most predictive RF
• Previous C-section
• Intrauterine infections
• Pre-eclampsia
• Hypertension
• Thrombophilia e.g. FV leiden
• Advanced maternal age, low BMI
• Trauma – road traffic accident, domestic violence, iatrogenic (e.g. ECV)
• Smoking, cocaine or amphetamine use during pregnancy [MCQ]
• Pregnancy following assisted reproductive techniques, PPROM
Fetal
• Non-vertex presentations
• Threatened miscarriage earlier in current pregnancy, fetal growth restriction
• Multiple pregnancy, Multiparity, polyhydramnios,
Causes of APH during pregnancy
o The causes of APH include:
Placenta praevia
Placental abruption
Local causes e.g. bleeding form the vulva, vagina, cervix
Classification of pregnancy following an APH
Following APH from placental abruption or unexplained APH
Pregnancy should be classified as “high risk” and antenatal care should be consultant led
Serial USS for fetal growth should be performed
Causes of seizures in pregnancy
- Epilepsy
- Eclampsia
- Encephalitis or meningitis
- Cerebral malaria or toxoplasmosis
- CVA
- TTP
- SOL
- Toxic overdose
- Drug/alcohol withdrawal
- Metabolic abnormalities (e.g. hypoglycaemia)
Advice that should be given to women with epilepsy on AEDs wanting to become pregnant
o Prenatal screening + its implications
o Risks of self-discontinuation of AEDs – stress importance of compliance with medication
o Effects of seizures + AEDs on the fetus + on pregnancy, breastfeeding and contraception
o Explain risk of congenital malformations
o Explain risk from recurrent seizures
o Explain importance of pre-conceptional + antenatal folic acid 5mg
• Although they are likely to have healthy pregnancies, their risk of complications during pregnancy + labour is higher than for women + girls without epilepsy
risk of x to fetus
- Generalised tonic clonic seizure
- Status epilepticus
- Focal, absence, myoclonic seizures
Generalised tonic clonic seizure
o Fetus at relatively higher risk of harm
o Level of risk may depend on seizure frequency
o Miscarriage
o Trauma related to falls
o Fetal hypoxia and acidosis
- Status epilepticus High mortality rate for mother + fetus
- Focal, absence, myoclonic seizures no evidence that they affect the pregnancy or developing fetus adversely unless the mother falls and sustains an injury
• Complications that are more likely during the pregnancy of women with epilepsy
o Hyperemesis gravidarum o Gestational hypertension o Mild pre-eclampsia o Vaginal bleeding o Anaemia
• Complications during labour + delivery in women with epilepsy
o Premature labour
o Failure to progress
o Increased rate of caesarean sections
o Generalised seizures occurring during labour fetal bradycardia
Risk of seizures in a child born to an epileptic mother
• Increased risk of seizures in children of parents with epilepsy but the probability that the child will be affected is generally low – this will also depend on the family history
Counselling a mother with epilepsy about the risk of congenital abnormalities in her baby
- Risk of congenital malformations
- Risk of congenital malformations if mother is on AEDs
- The likelihood of a woman who is taking AEDs having a baby with no malformations
o 3-4% risk of developing congenital defects
o 1-2% in non-epileptic mothers
- most mothers have normal healthy babies + the risk of congenital malformations is low if they are not exposed to AEDs in the periconception period
- Increased risk of congenital abnormality caused by AEDs (2-3x increase)
• The likelihood of a woman who is taking AEDs having a baby with no malformations 90%
Which factors of AED use increase the risk of teratogenicity?
o Especially if used during the first trimester
o Especially if the patient takes two or more AEDs
Fetal abnormalities associated with AEDs
o Neural tube defects
o Facial clefts
o Cardiac defects
o Other abnormalities – developmental delay, nail hypoplasia, IUGR, midface abnormalities
can often be detected in anomaly scans
Fetal valproate exposure effect on fetus
o Associated with the highest risk of major + minor congenital malformations
o In particular neural tube defects
o Long-term neurodevelopmental effects
o Associated with an increased likelihood of difficulty with adaptive functioning
o Associated with ADHD
Which AEDs confer an increased risk of teratogenicity?
o Phenytoin o Primidone o Phenobarbital o Lamotrigine o Carbamazepine
o In utero exposure to carbamazepine + lamotrigine does not appear to adversely affect neurodevelopment of the offspring
o Levetiracetam + phenytoin limited evidence
• Topiramate increased risk of cleft palate if taken in the first trimester
Fetal anticonvulsant syndrome
- Children exposed to valproate have more distinctive facial features
- Bustle + distinctive facial phenotype is also seen in children exposed to carbamazepine
- Tall/broad forehead
- Trigonocephaly – premature fusion of the metopic suture, leading to a triangular-shaped forehead
- Medial deficiency of eyebrows
- Infraorbital grooves
- Epicanthic folds
- Broad nasal bridge
- Anteverted nose
- Abnormal philtrum
- Thin upper lip
- Everted lower lip
- Micrognathia
- Dysplastic ears
- Hypoplastic digits
- Arachnodactyly
- Clinodactyly
- Flat feet
- Hypoplastic nails
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Things to discuss with women with epilepsy during pregnancy planning
confirm dx fertility obtaining optimal seizure control risk of withdrawal from AEDs 9SUDEP, status epilepticus) drug regimen (withdrawal + substitution) folic acid supplementation 5mg per day teratogenic effect of AEDs effect of pregnancy on seizure control effect of epilepsy on fetus risk of child developing epilepsy
Things to discuss with pregnant women with epilepsy
pain control during labour
importance of taking medication into hospital
post natal exhaustion and seizure frequency
BF + AEDs
looking after the child
Define asymptomatic bacteriuria
o Presence of significant levels of bacteria (>10^5 colony forming units/ml) in the urine in a person without signs or symptoms
Why do we have to screen for + treat asymptomatic bacteriuria?
When does screening take place?
RF for pyelonephritis, premature delivery, LBW
Screening takes place <10w MC+S
Complications of UTI/asymptomactic bacteriuria in pregnancy
o Infection can progress upward acute urethritis, acute cystitis, acute pyelonephritis
o Adverse pregnancy outcomes if woman ends up developing kidney infection LBW, preterm labour
o Pyelonephritis (up to 45% of pregnant women with untreated asymptomatic bacteriuria will develop pyelonephritis)
Complications of pyelonephritis in pregnancy
- Preterm labour
- Severe infection
- ARDS
- Sepsis
- Aneamia
- Long-term infection
Physiological changes in thyroid hormones during pregnancy
- Pregnancy increases thyroid hormone requirements
- Required dose for levothyroxine may increase
• Physiological changes during pregnancy – these reverse postnatally
o Total T4 + T3 increase
o Free T4 + T3 remain within the normal range
o TSH doesn’t change
o Usual for the thyroid gland to hypertrophy in normal pregnancy
o Increased thyroid gland vascularity
o Increase in TBG + albumin due to increased hepatic synthesis
o Thyroid gland will need to produce 50% more thyroid hormone during pregnancy to maintain a euthyroid state
o Free T4 will then fall with advancing gestation
What is transient gestational hyperthyroidism?
• Associated with hyperemesis gravidarum
• Can arise from high levels of hcg which stimulate the TSH receptor resolves as hCG falls
o May occur in molar pregnancy
• Patients are not usually thyrotoxic – antithyroid drugs don’t help
How can presence of TRAbs (TSH-receptor antibodies - these are the antibodies in Grave’s disease) affect pregnancy?
Can cross the placenta – if current or previous hx of Graves’ disease
Can cause temporary hyperthyroidism in the baby during pregnancy and after birth
This is treatable – can be treated during pregnancy and after birth
This blood test can help predict whether the baby will be affected in this way
Normal values <130% (by measuring thyroid-stimulating immunoglobulins) of basal activity
If levels of antibodies are high baby to be reviewed by neonatology team monitor baby closely (seral ultrasonography)
Re-measure TRAb in the third trimester
• If TRAb remains high at 36 w neonate needs to have TFTs performed at birth + then repeated a few days later
Associated with an risk of fetal/neonatal morbidity + mortality if it is unrecognised and untreated
incidence of fetal/neonatal hyperthyrodisim is 1-5% in all women with active/PMHx of Grave’s hyperthyroidis)
What is post-partum thyroiditis?
• Abnormal TSH level within the first 12 months post-partum in the absence of a toxic thyroid nodule or thyroxin receptor antibodies
- Temporary inflammatory thyroid disorder
- Occurs following 5-10% of pregnancies
- ESR is normal
- Women with T1DM + women with thyroglobulin or thyroid peroxidase autoantibodies are at higher risk of these conditions
- Usually shows up in the mother within 6-12 months after birth
• Diagnosed based on 3 criteria
o Patient is <12 months after giving birth
o Clinical manifestations suggestive of hypothyroidism
o TFTs alone – no need to measure TPO antibodies
• Three stages – thyrotoxicosis hypothyroidism euthyroid
Hypothyroidism complications in pregnancy
Hypothyroidism complications o risk of 2nd trimester miscarriage o Foetal hypocalcaemia o Neonatal rickets o Management – vitamin D, oral calcium supplements, regular monitoring of calcium + albumin
• Overt hypothyroidism increased risk of infertility + subfertility
• Must be avoided during pregnancy to avert adverse effects on the fetus
o Suboptimal replacement is associated with developmental delay + pregnancy loss
- Corrected hypothyroidism has no influence on pregnancy outcome or complications
- Main complication of levothyroxine treatment over-replacement of thyroid hormone increased risk of osteoporosis and AF
• Sub-clinical hypothyroidism or the presence of thyroid antibodies risk of complications in pregnancy o PET o Gestational HTN o LBW o GDM o Pre-term delivery o Perinatal mortality o Recurrent miscarriage o Fetal neurological maldevelopment
• Presence of TPO (thyroid peroxidase) antibodies – indicate a degree of thyroid autoimmunity - increased risk of having a miscarriage/gestational thyroid dysfunction/predisposition to PPT
Effect on anti-thyroid drugs on fetus
• Antithyroid drugs
o Slight increased risk of baby having developmental abnormalities some patients choose to have definitive treatment for Graves’ disease with radioactive iodine or surgery to allow them to have a pregnancy without needing to take antithyroid drugs
o High dose underactive thyroid in baby goitre
o Do not stop taking antithyroid drugs before speaking to a doctor greater risk to the pregnancy from an untreated overactive thyroid gland than from taking antithyroid medication
Hyperthyroidism complications in pregnancy
- Negative impact of mild maternal thyrotoxicosis on the IQ of the offspring
- Relapse rate after a full course of therapy = 50-70%
- It is possible to discontinue treatment with antithyroid drugs in 20-30% of women in the last trimester of pregnancy
- Small risk of birth defects if carbimazole is taken in pregnancy
- Increased risk of miscarriage in the early stages if your hypothyroidism is not under control
Untreated hypothyroidism in pregnancy complications
• Untreated overt hypothyroidism in pregnancy Maternal o Miscarriage o Anaemia o PET o Placental abruption o PPH o Congestive HF o Megacolon o Adrenal crisis o Organic psychosis o Myxoedema coma o Hyponatremia due to SIADH
Fetal o Stillbirth o Adverse neonatal outcomes Preterm delivery LBW Neonatal respiratory distress Congenital abnormalities Congenital hypothyroidism Impaired fetal neurocognitive development
Untreated hyperthyroidism in pregnancy complications
o Miscarriage o Pregnancy-induced HTN o PET o Maternal heart failure o Thyroid storm o Preterm delivery o IUGR o LBW o Fetal death o Fetal goitre o Fetal hydrops and heart failure o Fetal or neonatal thyrotoxicosis In women with Grave’s disease May occur as a result of TRAbs (thyroid-stimulating hormone receptor antibodies) crossing the placenta + stimulating the fetal thyroid Incidence of fetal/neonatal hyperthyroidism is 1-5% in all women with active/PMHx of Grave’s hyperthyroidism Associated with an risk of fetal/neonatal morbidity + mortality if it is unrecognised and untreated • Subclinical hyperthyroidism GDM
Thyroid disease in pregnancy prognosis
- Fetal + neonatal hyperthyroidism
- For women who have previously had Graves’ disease
- PPT
• Fetal + neonatal hyperthyroidism
o 1-5% in all women with active/PMHx of Grave’s hyperthyroidism
o Associated with an risk of fetal/neonatal morbidity + mortality if it is unrecognised and untreated
• For women who have previously had Graves’ disease (but not had thyroid surgery or radioiodine) may relapse at any stage but the risk rises after giving birth + remains high for up to a year
• PPT -> 50% risk that you develop a recurrence of PPT in subsequent pregnancies
Normal cardiac responses in pregnancy
• Ejection systolic murmur o In 96% (more CO) o Can be normal in pregnancy esp. systolic murmur at the 2nd L ICS or along the sternal border which radiates. May occur at any stage in pregnancy + may come and go • 3rd heart sound o In 84% (more CO) • Forceful apex (more CO) • Peripheral oedema (more volume)
Puerperal cardiomyopathy + myositis/ Peripartum cardiomyopathy
- New onset cardiomyopathy + HF
- Can present one month before-five months after delivery
- Viral myositis
- RF – old age, greater parity, black race, multiple gestations
Define obstetric cholestasis
• Impaired flow of bile from the liver/ Flow is reduced or blocked – this causes a build-up of bile acids in the body
can be due to a functional impairment of the hepatocytes in the secretion of bile and/or due to an obstruction at any level of the excretory pathway of the bile
Obstetric cholestasis RF
- Past history of obstetric cholestasis – tends to recur in a more severe form in 45-90% of subsequent pregnancies
- Family history of obstetric cholestasis e.g. mother
- Multiple pregnancy
- Pruritis on COCP
- Ethnicity (south Asia, Chilean, Bolivian)
- Presence of gallstones
- Hepatitis C
Obstetric cholestasis complications
- Increased incidence of premature birth
- Increased likelihood of meconium passage, fetal distress, delivery by C-section, PPH
- In a hospital setting, the current additional risk of stillbirth above that of the general population has not been determined but is likely to be small
- IUD – intracranial haemorrhage
Obstetric cholestasis prognosis
• Condition should settle spontaneously following delivery
• Follow-up should be long enough to ensure normalisation of LFTs – reasonable to check LFTs at the 6 week PN check
o If not improvement at 6 months – further specialist input is required
• Significant risk of recurrence (45-90%)
• Increased risk of adverse fetal outcome
Acute fatty liver in pregnancy definition
• Pregnancy associated disorder characterised by fatty infiltration of the liver
- Rare condition – prevalence 0.005-0.01%
- Tends to occur late in pregnancy
• May be associated with a mutant gene producing a defect in mitochondrial fatty acid oxidation
o Infants born to mothers with AFLP should be screened for defects in this system
Acute fatty liver in pregnancy complications
• Maternal
o Life-threatening condition
o Can progress to acute liver failure within 1-2 weeks
o Haemorrhage, renal failure, hepatic encephalopathy, sepsis, pancreatitis
• Fetal – death
Acute fatty liver in pregnancy prognosis
Condition usually resolves after delivery with complete recovery
o No reports of spontaneous remission of AFL prior to delivery of the infant
• Maternal mortality 10-20%
• Perinatal mortality (still birth + early neonatal death (death of a live newborn <7 days)) 20-30%
Acute fatty liver in pregnancy ddx
• Obstetric cholestasis
o Obstetric cholestasis patients have pruritus
• Pre-eclampsia (PET)
o AST in acute fatty liver disease – mean elevation of 300 unis/L
o AST in PET – 60 units/L
• HELLP
o AST in HELLP – 150 units/L
Conditions that can cause jaundice during pregnancy
Acute fatty liver of pregnancy Hyperemesis gravidarum Acute viral hepatitis (most common cause of jaundice in pregnancy) cholelithiasis in pregnancy choric liver disease HELLP syndrome Autoimmune hepatitis
Prognosis of liver disease during pregnancy
• All liver diseases occurring during pregnancy can lead to increased maternal and fetal morbidity and mortality
HELLP syndrome maternal complications
Maternal • DIC 5-56% • AKI 7-46% • Placental abruption 9-20% • Eclampsia 4-9% • Severe ascites 4-11% • Cerebral oedema 1-8% • Pulmonary oedema 3-10% • Death 1-25%
HELLP syndrome fetal complications
Fetal • Perinatal death – 7-34% • IUGR – 38-61% • Preterm delivery – 70% • Neonatal thrombocytopenia – 15-38%
Define anaemia in pregnancy
• In pregnant women anaemia is defined as Hb <110 g/L throughout pregnancy
o Hb <110g/L – adequate in the first trimester
o Hb <105 g/L – adequate in the second and third trimesters
o Hb <70g/L – urgent referral
• Postpartum – anaemia is Hb <100g/L
Causes of anaemia in pregnancy
• Iron deficiency anaemia accounts for the majority of cases of anaemia – low MCV o Nutritional deficiency, blood loss, decreased absorption, haemolysis, increased use, low iron stores resulting from previous pregnancy or previous heavy menstrual loss o Hypochromic microcytic anaemia, o Pencil cells • Less common causes of anaemia in pregnancy o Folic acid deficiency Green leafy vegetables Lack increases neural tube defects Diet, demand, malabsorption, drugs Megaloblastic anaemia • Macrocytosis • Hypersegmented neutrophils • Leucopaenia • Thrombocytopenia o Vitamin B deficiency Vegans, poultry, dairy, eggs Lack increases neural tube defects Diet, malabsorption Megaloblastic anaemia • Macrocytosis • Hypersegmented neutrophils • Leucopaenia • Thrombocytopenia o Sickle cell disease o Beta thalassaemia o Haemoglobin sickle-C (HbSC), hereditary spherocytosis (chronic haemolysis), leukaemia, paroxysmal nocturnal haemoglobinuria o GI bleeding, coeliac disease, parasitic diseases (e.g. hookworm, schistosomiasis)
CV changes in pregnancy
• Haemoglobin in normal pregnancy
o Physiological reduction in Hb concentration occurs which does not represent anaemia
o Increased in red cell mass + plasma volume
o Plasma volume increase > red cell mass increase haemodilution fall in HCT from 40% to 33% on average
o This does not represent anaemia – Hb resulting from haemodilution is approx. 115 g/L
o Slight increase in MCV (by approx.. 4 femtolitres)
• Serum ferritin concentration in normal pregnancy
o In women with adequate iron stores at conception, serum ferritin concentration initially rises followed by a progressive fall by 32 weeks to about 50% pre-pregnancy levels
o This is due to haemodilution + mobilisation of iron
o Levels increase again mildly in the third trimester
• Requirements in pregnancy
o Physiological requirements for iron in pregnancy are 3x higher than in non-pregnant menstruating women
o Iron requirement increases as pregnancy advances
RF for anaemia in pregnancy
- Previous anaemia
- Multiparity >P3
- Multiple pregnancy
- Interpregnancy interval <1y
- Poor dietary habits
- Vegans/vegetarians
- Teenagers
- Recent history of clinically significant bleeding
Complications of sickle cell anaemia in pregnancy
Spontaneous abortion – up to 25%
Perinatal mortality – 15%
• Associated with preterm delivery + low birth weight (30% <2500g)
Stillbirth – 8-10%
• Thorough antenatal fetal testing is required to assess growth, incl. US of the umbilical artery
Sickle cell crisis, stroke, PE
Frequent UTIs – common + require prompt treatment
Pregnancy associated hypertension
Anaemia in pregnancy - complications
• Iron deficiency anaemia associated with
o Increased risk of maternal morbidity and mortality
o Increased risk of perinatal morbidity and mortality
o Has important implications for the future neuro-development of the infant
• Women with anaemia in pregnancy
o Maternal death
o Fetal death
o Premature delivery
o LBW
o HF
o Babies have subsequent developmental problems
o Poor work/capacity performance
o Susceptibility to infection
Pregnancy RF that predispose to DVT
- Venous stasis
- Maternal age >35 years
- Multiparity
- Gestation <36 weeks
- Instrument-assisted or C-section
- Haemorrhage
- Pre-eclampsia
- Prolonged labour
Complications of ix for PE + mx w heparin
• Women with suspected PE should be advised that
o V/Q scanning may carry a slightly increased childhood cancer
o CTPA is associated with a higher risk of maternal breast cancer
o Absolute risk of both is very small
• Management with heparin
o HIT – heparin induced thrombocytopenia
Usually happens 5 days – 2 weeks after the first dose of heparin
Can cause DVT or PE
o Heparin allergy
o Heparin induced osteoporosis
DVT scoring system in pregnancy
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DVT
PE
in pregnancy
ddx
- DVT – muscle strain, ruptured Baker’s cyst, cellulitis superficial thrombophlebitis, rupture plantaris tendon, trauma
- PE – chest infection, intra-abdominal bleed (look for abdominal signs, shoulder tip pain from diaphragmatic irritation, low JVP)
Define P-PROM
Preterm prematre rupture of membranes
• Rupture of membranes prior to the onset of labour <37 weeks
Define PROM
Premature rupture of membranes
• Rupture of membranes occurring prior to the onset of labour >37 weeks (absence of any uterine activity)
RF for P-PROM
• Smoking
• Previous preterm delivery/PPROM
• Multiple pregnancy/polyhydramnios
• Vaginal bleeding – at any time during the pregnancy
• Trauma
• Uterine abnormalities/cervical incompetence
• Lower genital tract infection
o UTI
o STI
• Previous P-PROM
• Around 1/3 of women with P-PROM have positive amniotic fluid cultures
P-PROM complications
• 3 main causes of neonatal morality associated with P-PROM
o Prematurity
o Sepsis
o Pulmonary hypoplasia
• Fetal o Chorioamnionitis o Umbilical cord prolapse o Limb contractures o Death
• Maternal
o Sepsis
o Placental abruption
o Increased incidence of retained placenta + primary + secondary PPH
Define oligohydramnios
- Amniotic fluid volume (AFV) <500ml at 32-36 weeks of gestation
- Maximum vertical pocket (MVP) <2 cm from late mid-trimester
- Amniotic fluid index (AFI) <5cm or <5th percentile from late mid-trimester
Source of amniotic fluid during pregnancy + clearance pathway
• Second half of pregnancy
o Excretion of urine by the fetus is the major source of amniotic fluid production
o Fluid secreted by the fetal respiratory tract
o In the first half of pregnancy – fetal skin
This becomes keratinised at 22-25 weeks of gestation, significantly reducing transfer
o In the last half of gestation – fetal swallowing
Oligohydramnios RF
• The mother’s fluid balance has a major effect on the AFV o Increased maternal fluid intake has been shown to increase the AFV in women with oligohydramnios • Secondary to either o An excess loss of fluid o Decrease in fetal urine production/excretion • Fetal causes o Chromosomal factors o Congenital factors o IUGR o Post-term pregnancy o PROM o Fetal demise • Placental causes o Abruption o Uteroplacental insufficiency o Twin-to-twin transfusion syndrome (TTTS) (monochorionic twins) • Maternal causes o Maternal dehydration o Hypertension o Pre-eclampsia o Diabetes (either pre-existing or gestational diabetes) o Chronic hypoxia o ROM o Post-pregnancy carry • Drug induced causes o Indometacin o ACEi o NSAIDs • Idiopathic
Oligohydramnios causes
• ROM
• Congenital absence of functional renal tissue or obstructive uropathy
o Conditions that prevent the formation of urine or entry of urine into the amniotic sac
o Fetal urinary tract malformations (incl. renal agenesis, cystic dysplasia, ureteral atresia)
• Decreased renal perfusion leading to reduced urine production
o As a sequela of hypoxaemia-induced redistribution of fetal cardiac output
o In growth-restricted fetuses, chronic hypoxia results in shunting of fetal blood away from the kidneys to more vital organs
o Anuria and oliguria lead to oligohydramnios
• Post-term gestation
o Cause of decreased AFV in post-term pregnancies is unknown
o The decreased deficiency of placental function has been proposed as a case – this has not been confirmed histologically
o reduced fetal renal blood flow + reduced fetal urine production have been demonstrated >42 weeks in pregnancies involving oligohydramnios
Oligohydramnios complications
• There is an association between oligohydramnios + IUGR + increased perinatal mortality • Fetus o Pulmonary hypoplasia o Fetal compression syndrome o Amniotic band syndrome o risk of fetal infection (by the presence of prolonged ROM) • Labour o incidence of CTG abnormalities o Meconium liquor o Emergency CS
Oligoyhydramnios prognosis
• The earlier in pregnancy that oligohydramnios occurs, the poorer the prognosis
• Fetal mortality in the second trimester is a result of
o Major congenital malformations
o Pulmonary hypoplasia
Secondary to PROM before 22 weeks of gestation
• Mid-trimester PROM
o Leads to pulmonary hypoplasia
The inspiration of amniotic fluid at regular intervals is probably needed for terminal alveolar development
o Fetal compression syndrome
o Amniotic band syndrome
• IUGR secondary to
o Decreased fetal blood volume renal blood flow fetal urine output
Polyhydramnios definition
- Abnormally large volume of amniotic fluid
- AFI >95th centile
- 2-3L fluid
- Deepest pool >8cm
Mechanisms affecting amniotic fluid volume
• Physiologically, the volume of fluid increases with gestation to a maximum at 36-37 weeks
• Purpose of the amniotic fluid
o Protects the fetus from trauma and infection
o Allows lung development
o Facilitates the development and movement of the limb + other skeletal parts
• Mechanisms affecting the amniotic fluid volume
o Fetal swallowing
By term, the fetus swallows 210-760ml of amniotic fluid per day
Polyhydramnios – Conditions which cause a problem with swallowing– atresia of the UGIT, fetal hypoxia, neuromuscular disorders, brain abnormalities
o Fetal urination
By term, urinary output is 700-900ml/day
Main source of amniotic fluid in the second half of pregnancy – there is almost no amniotic fluid in cases of renal agenesis or fetal urinary tract obstruction
Fetus regulates amniotic volume as it responds to changes by adjusting the amount of urination
Polyhydramnios – increases in fetal urination e.g. fetal anaemia => subsequent cardiac output
o Secretions of fetal lung fluid + fetal oral and nasal cavities
o Absorption via intramembranous and transmembranous pathways
This includes movement of fluid between the fetal blood + placenta
And across intrauterine membranes such as the amnion and chorion
Polyhydramnios RF
• Idiopathic – most common
Fetal factors
• Fetal macrosomia
• Fetal anaemia (1-11% of cases)
• Hydrops fetalis (excessive fluid in >1 fetal compartment e.g. the pleural space or abdominal space – common in rhesus haemolytic disease)
• Foetal polyuria – maternal diabetes, twin to twin transfusion syndrome
• Chromosomal abnormalities
• Congenital anomalies and genetic disorders (8-24%)– anomalies may be isolated or due to a genetic disorder
o Oesophageal or duodenal atresia
o CV defects
o Microcephaly or anencephaly
o Neural tube defects
o Renal defects (incl. Bartter’s syndrome – a rare inherited defect in the LoH of the renal tube)
• Genetic disorders
o Trisomy 21, 18, 13
o Pena-Shokeir syndrome (contractures of the joints (arthrogryposis), growth problems, underdeveloped lungs, facial deformities)
o Beckwith-Wiedemann syndrome (overgrowth disorder)
Maternal factors
• Maternal DM (5-26%)
• Increasing maternal age
• Multiple pregnancy (8-10%)
• Congenital infections (e.g. toxoplasmosis, parvovirus, rubella, CMV)
• Maternal substance abuse
• Maternal metabolic abnormalities e.g. hypercalcaemia
Polyhydramnios complications
• Pregnancy o Higher incidence of preterm labour + delivery o Higher incidence of C-section o PROM o Placental abruption o Malpresentation o PPH o Cord prolapse • Maternal o Increased Risk of UTI (Increased pressure on urinary tract) o Increased dyspnoea (Increased pressure on diaphragm) o Risk of hypertension during pregnancy • Fetus o Low birth weight o Low Apgar scores o Fetal death o Neonatal mortality
Polyhydramnios prognosis
• The more severe the polyhydramnios, the more likely the chance of finding an underlying cause
o 17% of pregnancies with mild polyhydramnios have a significant associated problem
o 91% of pregnancies with moderate-to-severe polyhydramnios have a significant associated problem
• Poor prognosis is associated with the more severe fetal or placental malformations
o The severity of the prognosis is dependent on the severity of the abnormality
Define
• Primary syphilis • Secondary syphilis • Latent syphilis o Early latent syphilis o Late latent syphilis • Tertiary syphilis
• Primary syphilis – solitary painless genital ulcer (chancre) in the anogenital or cervix area
• Secondary syphilis – appear 4-8w after primary syphilis infection
• Latent syphilis – positive serology in the absence of clinical features
o Early latent syphilis – acquired <1y (CDC) or <2y (WHO) previously
o Late latent syphilis – acquired >1y (CDC) or >2y (WHO) previously
• Tertiary syphilis – if syphilis remains untreated – chronic, end organ complications many years after initial infection
Which organisms causes syphilis? Describe its appearance
• Caused by Treponema pallidum - coiled spirochaete bacterium with a corkscrew appearance + motility
Syphilis complications
• Miscarriage (25%)
• PTL/LBW (13%)
• Stillbirth (10%)
• If untreated congenital syphilis
• Jarisch - Herxheimer reaction
o Reaction to treatment, common in early syphilis
o Acute febrile illness with headache, myalgia, chills, rigors
o Resolves within 24h
o Occurs in up to 44% of pregnant women with syphilis- Might cause fetal distress, premature labour, stillbirth
o Rx – antipyretics, reassurance
Parvovirus infectious period
• Infectious period
o 7-10 days before the rash develops, until 1 day after the rash appears
Parvovirus RF
- Schoolchildren
* Household exposure > Occupational exposure
Parvovirus complications
• Usually occur 3-5 weeks after onset of maternal infection
• Infection in the first 20 w IUD (9%)
• 9-20 weeks gestation hydrops fetalis (3% of cases, 50% of these die)
• After 20w rarely associated with developmental hydrops or fetal loss (<1%)
• Permanent congenital abnormality and/or congenital anaemia
• Non-immune hydrops fetalis
o Infection of fetal erythroid progenitor cells in the BM + liver anaemia, hypoalbuminaemia, HF, hydrops fetalis
o There may be associated hepatitis + myocarditis in the fetus
o Can cause fetal loss in about 50% cases if left untreated
o Spontaneous resolution in 50% with no long term sequalae
• Fetal death
o Spontaneously or as a consequence of hydrops fetalis
o 5-10% - overall fetal loss rate for those with maternal infection
o Usually occurs in the second trimester, rare in the first trimester
• Maternal pre-eclampsia-like syndrome (“mirror syndrome” – maternal sins reflect those present in the fetus)
o Rare, typically presents late in pregnancy
o Maternal peripheral oedema, HTN, proteinuria, anaemia during conservative management of hydrops fetalis
Antenatal screening for infections includes
- Hepatitis B
- HIV
- Syphilis
What type of disease do the following cause
- HHV-1, HHV-2
- HHV-3
- HHV-4
- HHV-5
- HHV-6
- HHV-7
- HHV-8
- HHV-1, HHV-2 (HSV 1 and 2)
- HHV-3 (VZV)
- HHV-4 (EBV)
- HHV-5 (CMV)
- HHV-6 (Roseolovirus)
- HHV-7 (Roseolovirus)
- HHV-8 (Kaposi’s sarcoma-associated HIV)
What is GBS
- Gram +ve streptococcus characterised by presence of Group B Lancefield antigen (streptococcus agalactiae)
- Gram +ve cocci in chains
- Most common cause of early onset infection in neonates <7d old
• Commensal bacterium of vaginal and rectum
Early onset vs late onset GBS
Early-onset GBS (EOGBS)
• Most babies who develop GBS infection become unwell in the first week of life, usually within the first 12h after birth
Late onset GBS
• Affects babies between 7 days and 3 months after birth
o Infection in babies older than 1 month – very uncommon
o Very rare after the age of 3 months
• Less common than EOGBS
GBS aetiology
- GBS is carried in the vagina and bowel of about 30% of women in the UK
- The likelihood of maternal GBS carriage in pregnancy is 50%
- If GBS was found in a previous pregnancy but baby unaffected, then there is a 50% chance that the mother will be carrying GBS in any future pregnancy
- Up to 1/3 of GBS infections in babies are late onset
- GBS is the most common cause of severe infection in newborn babies
- It is the most common cause of meningitis in babies <3 months
- In the UK, about 1 in 2,000 newborn babies are diagnosed with EOGBS
- Majority of babies who come into contact are not affected (some become colonised, minority become ill)
GBS complications
• Can rarely cause serious infections in babies incl. sepsis, pneumonia, meningitis, osteomyelitis, septic arthritis
GBS prognosis
• Delay in treating baby can be very serious or even fatal
o 1 in 20 babies die
o 1 in 14 survivors will have a long-term disability
• IAP reduce the risk of EOGBS from 1 in 400 to 1 in 4000
• The chance the baby will develop infection after 12h is very low and neither the mother nor the baby will need abx after this time unless they become unwell
• If you’ve had a baby affected with GBS there is an increased risk that any future baby will also be affected
• In average in the UK, every month
o 43 babies develop EOGBS
o 38 babies make full recovery
o 3 babies survive with long-term physical or mental disabilities
o 2 babies die from their EOGBS
How long is chickenpox infectious for?
How long is shingles infectious for?
- Chickenpox is infectious from 2 days before the spots first appear until they have all crusted over this is commonly about 5 days after the spots appear
- Shingles is infectious from when the rash appears until all the affected areas have crusts on them
Maternal complications of chickenpox in pregnancy
• Most pregnant women who have chickenpox recover fully and their babies are fine
Maternal
• Likely to make full recovery however serious complications occur in a small number of cases
• Pneumonia (5x greater, 10%, death in 1% of these 10%)
• Hepatitis
• Encephalitis + ataxia (uncommon but very serious)
• Death
• Other – myocarditis, glomerulonephritis, appendicitis, pancreatitis, arthritis, inflammation of various parts of the eye, hepatitis, bleeding, DIC, thrombocytopenia
Fetal complications of chickenpox during pregnancy
• Maternal infection occurs in the last 4 weeks of pregnancy – significant risk of varicella infection of the newborn
o Delay delivery until 7 days after the onset of the rash
• Risk of spontaneous miscarriage does not appear to be increased if chickenpox occurs in the first trimester
• FVS (fetal varicella syndrome) – if the pregnant woman develops varicella or shows serological conversion in the first 28 weeks of pregnancy
o <12 weeks – 1 in 200 chance of FVS
o 13-20 weeks – 1 in 50 chance of FVS
o Small number of cases between 20-28 weeks, none following 28 weeks
o Features of FVS – skin scarring, eye defects (microphthalmia, chorioretinitis cataracts), limb hypoplasia, microcephaly, learning disabilities, IUGR
• Severe neonatal varicella – (VZV intra-/post-partum)
o If the mother develops a rash between 5 days before and 2 days after birth (or within 7 days before or after giving birth)
o Mild disease, disseminated skin lesions (purpura fulminans), pneumonia, visceral infections (i.e. hepatitis)
o May be fatal to the newborn child in around 20% of cases
• Shingles in infancy
o 1-2% risk if maternal exposure in the 2nd or 3rd trimester
o If the baby catches the chickenpox from the mother before they are born
VZIG – might prevent chickenpox from developing or make it a much less serious infection if it does develop
List some other PSE – potential sensitising events
• Invasive fetal procedures
o Intrauterine transfusion/surgery/insertion of shunts/laser
o Intra-operative cell salvage
• Medical intervention
o Chorionic villus sampling
o Amniocentesis
o ECV
• Gynae
o Ectopic pregnancy
o TOP (any method, any GA), IUD, stillbirth, molar pregnancy
o Miscarriage, Threatened miscarriage
o Evacuation of molar pregnancy
• APH/PV bleed in pregnancy (>12w, prolonged and <12w)
• Abdominal trauma (sharp/blunt, open/closed)
• Placental trauma
• Previous blood transfusion (rare if in UK)
• Delivery
o Traumatic deliveries
o Sickle cell disease
o CS
o Instrumental
o Normal delivery of a Rh+Ve baby
• Over 99% have an FMH of <4ml at deliver – Large FMH RF
o Traumatic deliveries incl. C-section
o Manual removal of the placenta
o Stillbirths + IUD
o Abdominal trauma during the 3rd trimester (26-37w)
Which parameters do you need to assess on a CTG? (+normal values)
DR - define risk – high or low risk pregnancy
C - contractions (in labour should be 4-5 in 10, 1 big square = 1 min)
• Number of contractions in a 10-minute period (no. of contractions within 10 big squares)
• How long do they last?
• How strong are they? (assess using palpation – height of the wave does not correlate with strength of contraction
BR - Baseline HR - Normal FHR = 110-160
Variability = normal variability 5-25 bpm3
• Calculated by assessing how much the peaks and troughs of the FHR deviate from the baseline rate (in bpm), excluding accelerations + decelerations
Accelerations - abrupt increase in baseline FHR >15 bpm for >15s, reassuring
• Normal = >2 accelerations on a 20-30 mins CTG trace
Decelerations - abrupt decrease in baseline FHR >15 bpm for >15s,
Normal = no decelerations
Overall impression
Define
- Normal CTG
- Suspicious CTG
- Pathological CTG
- Need for urgent intervention CTG
- Normal CTG = all features are reassuring
- Suspicious CTG = 1 non-reassuring feature + 2 reassuring features
- Pathological CTG = 1 abnormal feature or >2 features are non-reassuring features
- Need for urgent intervention CTG = acute bradycardia or a single prolonged deceleration for >3 mins
• When describing decelerations in FHR specify
• When describing decelerations in FHR specify
o their timing in relation to the peaks of the contractions
o the duration of the individual decelerations
o whether or not the fetal heart rate returns to baseline
o how long they have been present for
o whether they occur with over 50% of contractions
o the presence or absence of a biphasic (W) shape
o the presence or absence of shouldering
o the presence or absence of reduced variability within the deceleration
• Concerning characteristics of variable decelerations
o >60s o Reduced baseline variability within the decelerating o Failure to return to baseline o Biphasic W shape o No shouldering
• 4 types of decelerations
• 4 types of decelerations o Early decelerations – physiological o Late decelerations o Variable decelerations o Prolonged decelerations
o Reassuring
o Non-reassuring
o Abnormal
variability
o Reassuring 5-25 bpm o Non-reassuring <5bpm form between 30-50 mins >25 bpm for 15-25 mins o Abnormal <5bpm for >50min >25 bpm >25min Sinusoidal
o Reassuring
CTG
FHR
110-160
Baseline variability
5-25
Decelerations
• None or early
• Variable decelerations with no concerning characteristics for <90 mins
o Non-reassuring
CTG
FHR
100-109
Or
161-180
Baseline variability
<5 for 30-50min
Or
>25 for 15-25 min
Decelerations
• Variable decelerations with no concerning characteristics for >90 mins
• Variable decelerations with any concerning characteristics in <50% of contractions >30 mins
• Variable decelerations with any concerning characteristics in >50% of contractions for <30 mins
• Late decelerations in >50% of contractions for <30 minutes, with no maternal or fetal clinical risk factors such as vaginal bleeding or significant meconium
o Abnormal
CTG
FHR
<100
>180
Baseline variability <5 for >50min Or >25 for >25min Or sinusoidal
Decelerations
• Variable decelerations with any concerning characteristics in >50% of contractions for 30 minutes (or less if any maternal or fetal clinical risk factors)
• Late decelerations for 30 minutes (or less if any maternal or fetal clinical risk factors)
• Acute bradycardia
• Single prolonged deceleration lasting >3 mins
Early deceleration
- Physiological + non-pathological (uniform in depth, length, shape)
- Start when the uterine contraction begins + recover when the uterine contraction stops
- Due to increased fetal intracranial pressure causing increased vagal tone
- https://geekymedics.com/wp-content/uploads/2011/05/CTG-Early-Decelerations-3-770x433.jpg
Late deceleration
• Begin at the peak of the uterine contraction + recover after the contraction ends
• Decelerations occur during the contractions + persist after the end of the contraction
• Indicates that there is insufficient blood flow to the uterus + the placenta
• Blood flow to the fetus is significantly reduced fetal hypoxia + acidosis
• Caused by contractions in the presence of hypoxia – they will occur with each contraction + the fetus is already hypoxic
•
https://geekymedics.com/wp-content/uploads/2011/05/CTG-Late-Decelerations-2-770x433.jpg
Variable deceleration
• Rapid fall in baseline FHR with a variable recovery phase
• Variable in their duration, may not have any relationship to uterine contractions
•
• Most often seen during labour + in patient’s with oligohydramnios
• Usually caused by umbilical cord compression
• Shoulders of deceleration = acceleration before + after variable deceleration
o Indicate that fetus is not yet hypoxic + is adjusting to reduced blood flow
o Variable decelerations without the shoulders are more worrying – suggests that the fetus is becoming hypoxic
• Variable decelerations can sometimes resolve if the mother changes position
• Presence of persistent variable decelerations indicates the need for close monitoring
• Concerning characteristics of variable decelerations
o >60s
o Reduced baseline variability within the decelerating
o Failure to return to baseline
o Biphasic W shape
o No shouldering
https://geekymedics.com/wp-content/uploads/2011/05/CTG-Variable-Decelerations-2.jpg
Prolonged deceleration
• Deceleration that lasts >2 mins
• Non-reassuring = 2-3 minutes
• Abnormal = >3 mins•
https://geekymedics.com/wp-content/uploads/2011/05/CTG-Prolonged-Deceleration-770x433.jpg
What is the most common cause of variable decelerations on CTG during labour?
What is the most common cause of variable decelerations on CTG during labour?
• Usually caused by umbilical cord compression
o Umbilical vein occluded first acceleration in FHR
o Then umbilical artery is occluded causes a subsequent rapid deceleration
o Pressure on the cord is reduced another acceleration occurs baseline then returns
Causes of late decelerations
• Always abnormal
• Suggest fetal hypoxia
• Late decelerations indicate that there is insufficient blood flow to the uterus + placenta
• As a result, blood flow to the fetus is significantly reduced, causing fetal hypoxia + acidosis
• Causes of reduced uteroplacental blood flow
o Maternal hypotension
o PET
o Uterine hyperstimulation
What is a sinusoidal pattern on CTG and what does it indicate?
• Rare, very concerning • Associate with high rates of fetal morbidity + mortality • Characteristic o Smooth, regular, wave-like pattern o Frequency of around 2-5 cycles/min o Stable baseline rate of 120-160bpm o No beat to beat variability • Indicates o Severe fetal hypoxia o Severe fetal anaemia (Hb <50gm/L2) o Fetal/maternal haemorrhage
What causes FHR decelerations on CTG?
• Hypoxic stress
o FHR is controlled by the ANS + SNS – in response to hypoxic stress, the fetus reduces its HR to preserve myocardial oxygenation + perfusion
• Deceleration = the reduction in HR to reduce myocardial demand
Reduced variability causes
• Fetal sleeping
o Most common cause
o Shouldn’t last >40 mins
o Preceded and followed by a normal CTG trace
o Heart rate decreases with quiet sleep – baby shouldn’t be tachycardic
• Fetal hypoxia
• Fetal infecition
• Fetal acidosis (due to hypoxia)
o More likely if late decelerations are also present
• Fetal tachycardia
• Drugs
o Opiates, BDZ, methyldopa, MgSO4
• Prematurity
o Variability is reduced at earlier gestation (<28w)
How would you recognise uterine hyperstimulation on a CTG and why is it dangerous?
- > 5 in 10 contractions
- Fetal heart rate abnormalities
- Uterine contractions reduce blood flow to the placenta thus reducing fetal oxygenation
- A period of 60-90s is required between contractions to allow fetal oxygenation to recover to fetal norms
List some IP RF that would require IP monitoring
• IOL PG / oxytocin
• Abnormal auscultation or CTG
• Oxytocin augmentation
• Regional analgesia e.g. epidural or spinal, paracervical block
o Following a decision to insert an epidural block, a CTG should be commenced to establish baseline features prior to the block’s insertion
• Abnormal vaginal bleeding in labour
• Maternal pyrexia > 38°C
• Meconium or blood stained liquor
• Absent liquor following amniotomy
• Active first stage of labour >12 hours (i.e. after diagnosis of labour)
• Active second stage (i.e. pushing) >1 hour where birth is not imminent
• Preterm labour less than 37 completed weeks
• Tachysystole (more than 5 active labour contractions in 10 minutes, without fetal heart rate changes)
• Uterine hypertonus (contractions lasting more than 2 minutes or occurring within 60s of each other, without fetal heart rate changes)
• Uterine hyperstimulation (tachysystole/hypertonus with fetal heart rate changes)
What are some reasons for which a pregnancy might be considered high risk/ AN RF requiring intrapartum monitoring?
• Maternal medical illness o GFM, HTN, asthma o Maternal age >42 • Obstetric complications • Maternal o Multiple gestation o Post-date gestation (>42w) o Previous CS o APH o PET • Fetal o IUGR o Oligohydramnios/ polyhydramnios o RFM o Preterm o Breech o PROM o Prolonged rupture of membranes (>24h) o Congenital malformations o Meconium stained liquor • Intrapartum o IOL w PG/ Oxytocin o Oxytocin induction/augmentation of labour o Abnormal auscultation or CTG o Epidural anaesthesia o Maternal pyrexia • Antenatal RF o Absence of prenatal care o Abnormal AN CTG o Abnormal doppler umbilical artery velocimetry o Abnormalities of maternal serum screening associated with an risk of poor perinatal outcomes e.g. low PAPP-A <0.4MoM o Smoking o Drug abuse
What are some causes of fetal bradycardia?
- Prolonged cord compression
- Cord prolapse
- Epidural + spinal anaesthesia
- Maternal seizures
- Maternal sedation
- Rapid fetal descent
- Hypotension
- Post-maturity
- Hypoxia
- Fetal distress due to placental abruption or uterine rupture
How often should the CTG be assessed?
- Every hour or more frequently if there are concerns
* Do not make any decision about a woman’s care in labour on the basis of CTG findings alone
Why do we use CTG?
How do you commence a CTG?
• Fetal heart rate
• Uterine contractions
• Mostly used in the third trimester to monitor fetal well-being + allow early detection of fetal distress
• Two transducers
o One records the FHR using US
o One monitors the uterine contractions measuring the tension of the maternal abdominal wall (indirect indication of intrauterine pressure)
- Determine indication for fetal monitoring
- Discuss fetal monitoring with the woman and obtain permission to commence
- Perform abdominal examination to determine lie and presentation
- Give the woman the opportunity to empty her bladder
- The woman should be in an upright or lateral position (not supine)
- Check the accurate date and time has been set on the CTG machine, and paper speed is set at 1cm per minute
- Label CTGs the mother’s name, UR number and date / time of commencement
- Maternal HR must be recorded on the CTG at commencement of the CTG in order to differentiate between maternal and fetal heart rates
Which feature on a CTG might indicate severe hypoxia?
Which situations commonly cause a lower baseline fetal heart rate (100-120bpm)?
Which feature on a CTG might indicate severe hypoxia?
• Severe prolonged bradycardia (<80 bpm for >3m)
Which situations commonly cause a lower baseline fetal heart rate (100-120bpm)?
• Postdate gestation
• Occiput posterior or transverse presentations
Difference between multigravida + multipara
A multigravida is a woman who has been pregnant at least once before the current pregnancy
A multipara is a woman who has previously given birth to live babies at least twice before now.
What is a partogram?
- Graphical record of key maternal + fetal data during labour entered against time on a singe piece of paper
- Intended to provide an accurate record of the progress in labour, so that any delay or deviation from normal may be detected quickly + treated accordingly
- Tool for monitoring maternal + fetal wellbeing during the active phase of labour + a decision making aid when abnormalities are detected
Which parameters are recorded on the partogram?
• Hours + Time
o Hours = the number of hours since you began monitoring the labour
o Time = time on the clock
o Recorded at an interval of 1 hour
o Start recording on the partograph when the labour is in active first stage (>4cm)
• Initially + Every 30 mins
o Contractions per 10 mins
Assess strength + duration through palpatin
o FHR (counted for 1 full minute)
Recorded every 30mins in the first stage of labour (if every count is within the normal range) + every 5 minutes in the second stage
Each square for the FHR on the partograph represents 30 mins
o Maternal Pulse
• Initially + Every 2 hours
o Maternal temperature
• Initially + Every 4 hours
o Liquor (record the colour, if the membranes have ruptured)
o Moulding (the extent to which the bones of the fetal skull are overlapping each other as the baby’s head is forced down the birth canal)
o Cervical dilation (as determined by vaginal examination, might need more frequent monitoring in multigravida/multipara mother)
o Descent of head (by measuring the station of the fetal head or by palpating the abdomen)
o Degree of moulding or caput
o Maternal BP
• Oxytocin (conc. + dose) / drugs given and IVF
• Temperature
• Urinalysis – protein + acetone + volume
What do the two lines in the section of cervical dilation + fetal head descent indicate?
Alert line
• Starts at 4cm of cervical dilation + ends 10cm (point of expected full dilation) at a rate of 1cm per hour
• If the marks recording cervical dilation cross over the alert line, this indicates that cervical dilation is proceeding too slowly – less than 1cm per hour
• Refer woman to hospital/ move to labour ward
Action line
• 4 hours to the R of the alert line
• If the dilation curve crosses this line, decisions must be made – augmentation of labour, artificial rupture of membranes CS etc
o CS if fetal distress/ obstructed labour
o Augmentation with IV oxytocin if there are no contraindications
Between alert + action lines
• Transfer to a hospital with facilities for a CS
o Unless almost fully dilated
o Observe labour progress for short period before transfer
• Continue routine observations
• ARM may be performed if membranes are still intact
Red flags on partogram
• Slow rate of cervical dilation
o Cervical dilation mark crosses alert line on partograph + is now on the R of the alert line
• +3 moulding of fetal skull with poor progress of labour indicates labour obstruction
• FHR <100/min or >160/min for >10min
• Meconium-stained liquor (even if N FHR) unless labour is progressing fast
o M1 in latent first stage of labour
o M2 in early active stage of labour
o M3 in any stage of labour
Latent phase (<4cm dilation) >8h
Good progress in the first active stage of labour is indicated by
How quickly should the cervix be dilating during active labour?
G
• A rate of dilation of the cervix that keeps it on or to the L of the alert line – 1cm/h cervical dilation
• Evidence of fetal descent coinciding with cervical dilation - 1cm descent in 4 hours
• Contractions which show a steady increase in duration + number in 10 mins
• 1cm per hour
• Often quicker in multigravida mothers
Describe the stages of labour
• First stage o Latent – cervical dilation up to 4cm At least 2 in 10 contractions, each lasting >20s o Active – cervical dilation from 4cm to 10cm 1cm dilation every 1h 1cm descent in 4h At least 3 in 10 contractions, each lasting >40s Nullips – 8-12h Multiparous – 5h • Second stage o 4-5 in 10 contractions o Nullips – <3h o Multiparous – <2h • Third stage o Active mx – within 30 mins o Physiological mx – up to 1h for separation to occur, only takes a few mins to push it out
How do you describe the fetal membranes on the partogram?
• I = intact membranes • If membranes have ruptured o A = absent o C = clear liquor o B = blood stained o M = meconium-stained M1 – lightly stained M2 – little bit thick M3 – very thick liquor, like soup
How do you assess descend of the fetal head?
Abdominal examination
• It should be assessed by abdominal examination immediately before doing a vaginal examination, using the rule of fifth to assess engagement
• When 2/5 or less of fetal head is felt above the level of symphysis pubis, this means that the head is engaged, and by vaginal examination, the lowest part of vertex has passed or is at the level of ischial spines
Vaginal examination
- Assess station through vaginal examination
- By reference to the position of the presenting part of the fetal skill relative to the ischial spines in the mother’s pelvic brim
- At station +3 the baby’s head is crowining – visible at the vaginal opening even between contractions, the cervix should be fully dilated at this point
When is the fetus considered engaged?
• When >50% of the presenting part (usually the head) has descended into the pelvis
What does crowning mean and what does it tell you?
- Crowning means that the presenting part of the baby’s head remains visible between contractions
- This indicates that the cervix is fully dilated
What makes the fetal skull so flexible?
- The 5 separate bones of the fetal skull are joined together by sutures which are quite flexible during birth, and there are also 2 larger soft areas called fontanels
- Movement in the sutures + fontanels allows the skull bones to overlap each other to some extent as the head is forced down the birth canal by the contractions of the uterus
What is moulding?How do you assess moulding ?
- The extent of overlapping of fetal skull bones
- Usually disappears within 1-3d after the birth
- 0 – bones are separated and the sutures can be felt easily
- +1 moulding – sutures apposed – adjacent skull bones are touching each other but are not overlapping
- +2 moulding – sutures overlapped but reducible – bones overlapping but can be separated easily with pressure by your finger
- +3 moulding – sutures overlapped but not reducible – bones overlapping but cannot be separated easily with pressure by your finger
What is the significance of degree 3 moulding?
- If found along with poor progress of labour, may indicate that the labour is at increased risk of becoming obstructed
- Red flag, needs urgent intervention
Which skull bones are most likely to overlap?
• Parietal bones which are joined by the sagittal suture + have the anterior + posterior fontanels to the front + back
What is caput?
- Swelling in baby’s skill in the area that was pressed against the cervix during labour + delivery
- Common
How do you assess maternal wellbeing duHow do you assess maternal wellbeing in the immediate postpartum period?ring labour?
- Pulse – every 30mins
- T – every 2h
- BP – every 4h
- Urine output – every time it is passed
- Vital signs (HR, BB, RR, T), blood loss, uterine retraction
- Bn Hr 0 + Hr 2 – every 15/30 mins
- Bn Hr 2 + Hr 4 – every hour
- Verify that the woman drinks + urinates
How can you assess the fetal welling during labour and delivery?
• CTG
• Partogram
o FHR 100-160 (except for slight changes lasting <10mins)
o Moulding of not more than +2
o Clear or only lightly stained liquor (C or M1) (if membranes have ruptured)
Lightly stained amniotic fluid may not necessarily indicate fetal distress unless it is accompanied by persistent FHR deviations outside the normal range
o Moulding
• Suspect fetal distress if persistent (>10mins) fetal bradycardia or tachycardia
• One you detect any FHR abnormality count it more frequently + refer quickly if it persists for >10mins
• Count every 5 mins if the liquor contains thick green or black meconium
Can you give reasons for fetal heart rate deviating from the normal range?
• Placental blood flow to the fetus is compromised
• Commonly occurs when there is
o HTN disorder in pregnancy
o Maternal anaemia
o Hypovolaemia due to blood loss or body fluid through V+D
o Maternal hypoxia due to hear/lung disease or living in a very high altitude
o Aged placenta
o Oligohydramnios – can prevent the fetus from moving easily the umbilical cord may become compressed against the uterine wall by the baby’s body
o Cord compression either due to prolapse or entanglement around the baby’s neck
o Placental abruption
Causes of prolonged labour
Causes of obstructed labour
- Macrosomic baby
- Weak contractions
- Epidural
- Malposition
- Malpresentatio
- Cephalo-pelvic disproportion (incl. small pelvis)
- Cephalo-pelvic disproportion (incl. small pelvis)
- Malpresentation
- Malprosition
Complications of obstructed labour
- Sepsis
- Stillbirth
- PPH
- Uterine rupture
- Maternal death
Asthma in pregnancy complications
• Risks of complications are small in those with well-controlled asthma
• Maternal
o Pre-eclampsia
o C-section
o GDM
o Complicate labour
• Foetal
o Premature birth
o Low birth weight
o Cleft lip or palate – oral CS use in first trimester increases this risk
o Prolonged hypoxia – FGR, foetal brain injury
• Prognosis
o Severity of asthma remans stable in 1/3, worsens in another 1/3, improves in 1/3
Which infections are screened for during AN screening?
- Hepatitis B
- HIV
- Syphilis
infections presenting with maculopapular rash/ Non-vesicular vs vesicular rashes
Maculopapular rash/ Non-vesicular
• Measles
• Rubella
• Parvovirus B19
Vesicular rash
• Chicken pox
• Shingles
Rubella complications if contracted at
o 8-10w o 12-20w 11-16w 16-20w o >20 weeks
o 8-10w – 90% risk of congenital rubella syndrome(CRS) + a high likelihood of multiple defects, microcephaly, miscarriage (20%)
o 12-20w - sensorineural hearing loss, chorioretinitis cataracts
11-16w – 10-20% risk of CRS, with single defects being most common
16-20w – low chance of deafness occurring
o >20 weeks – no published care reports of CRS
Rubella complications in mum
Maternal • Miscarriage • Pneumonia • Arthropathy • Encephalitis • ITP
• Maternal
o Usually a mild, self-limiting viral infection
o May cause first-trimester miscarriage
Rubella complications in baby
Fetal
• Death
• Congenital rubella syndrome
Transient
o IUGR
o Thrombocytopenic purpura (25% - blueberry skin), haemolytic anaemia, hepatosplenomegaly, jaundice
o Radiolucent bone disease (20%)
o Meningoencephalitis (25%) +/- neurological sequelae
Developmental
o Sensorineural deafness (80%, variable, unilateral or bilateral)
o General learning disability (55%)
o Insulin-dependent diabetes (20% - immune-related but often delayed to adolescence or adulthood)
o Late onset disease at 3-12 months – rash, diarrhoea, pneumonitis – high mortality
Permanent
o Congenital heart disease (patent ductus arteriosus or peripheral pulmonary artery stenosis)
o Eye defects – cataracts, congenital glaucoma, pigmentary retinopathy (50% “salt and pepper”), severe myopia, microphthalmia , chorioretinitis, blindness
o Microcephaly
• TORCH viruses (toxoplasmosis, rubella, CMV, herpes simplex) have the following common features
o Preterm delivery
o LBW
o Anaemia
o Thrombocytopenia
o Hepatitis with jaundice + hepatosplenomegaly
• Microcephaly, mental handicap, seizures, failure to thrive
• It’s the leading non-genetic cause of sensorineural hearing loss (SNHL)
CMV
Transmission of CMV to the baby
AN
IP
PN
o AN Transplacental route
o IP During labour and delivery through contact with cervicovaginal secretions and blood
o PN through breast milk
- Infection earlier in the pregnancy is associated with greater risk of more severe harm to the fetus/neonate
- Risk of vertical transmission increases with gestation
CMV infection in pregnancy - complications + prognosis
• Increased risk of miscarriage + still birth
• Most common sequalae
o Sensorineural hearing loss
o Mental retardation
o Cerebral palsy
• Other complications of congenital CMV
o IUGT, microcephaly periventricular calcifications, blindness, hepatosplenomegaly, skin rash, pneumonitis
• Cytomegalic inclusion disease complications
o Moderate to severe LD
o Neurological abnormalities
o Hearing loss
- Babies born with cytomegalic inclusion disease – poor prognosis
- Rate of transmission to fetus 40% - 10% will develop congenital syndrome
- In about 10-20% of cases, F/U shows neurological damage
- Significant morbidity especially in infants who are symptomatic in the neonatal period – 90% will later have neurodevelopmental problems
- Main sonographic prognostic indicator fetal cerebral anomalies
Listeria infection in pregnancy sources
• Found in soil, decayed matter and animals
• Infection may be foodborne or from direct contact with animals (faeco-oral transmission)
o Soft cheese and meat-based pate
o Raw foods incl. vegetables, uncooked meats, processed foods
o Eating cooked food that has been refrigerated and recooked
• Spread from mother to fetus can occur in utero (transplancental) or during birth (vertical transmission)
Listeria infection in pregnancy complications + prognosis
• In immunocompromised patients – severe illness, severe sepsis, meningitis, encephalitis
• Listeriosis in pregnancy
o Miscarriage or stillbirth
o Premature delivery
o Chorioamnionitis
o Severe illness in a newborn child
• Infants who survive listeriosis
o May have long-term neurological damage and delayed development
• Most cases of listeriosis in healthy adults + children mild and of short duration with complete recovery
• Invasive infection – fatality can be as high as 30% in specific high risk populations e.g. elderly, immunocompromised, fetuses, newborns
o Listeriosis in pregnancy Around ½ of infected infants at or near term will die
• Good if treated
• Poor – sepsis, meningitis or neonatal infection – mortality of 50%, 70%, 80%
Toxoplasmosis complications + prognosis
• Miscarriage
• Fetal anomalies
• Choroidoretinitis
• (any condition with chorioretinitis can progress to cataracts (it’s just rubella is most commonly associated)
o Rubella
o Toxoplasmosis
o CMV
o VZV
o HS
• The risk of maternal-fetal transmission increases as the pregnancy proceeds but the consequences become less severe
• Mother – if there are symptoms they normally get better on their own within about 6 weeks
• Once you’ve had toxoplasmosis you cant catch it again
neonatal herpes vs congenital herpes
Consider the dx in any infant in the first weeks of life who develops vesicles, seizures or sepsis
• Neonatal herpes – refers to infection acquired around the time of birth - classified into 3 subgroups
o Disease localised to skin, eye and/or mouth (30%)
o Local CNS disease (encephalitis alone) (70%)
o Disseminated infection with multiple organ involvement
• Appear 2 days – 6 weeks after delivery
• Nonspecific signs + no mucocutaneous involvement
• Rarely a hx of maternal infection
• Congenital herpes – refers to infection acquired in utero (very rare)
Congenital HSV infection – if lesions appear within 48h of brith, congenital infection is the cause
• Rare but more likely in mothers who have disseminated herpes infection
• IU transmission is greatest during the first half of the pregnancy
• Most congenital herpes infections are due to HSV-2
• Can cause miscarriage, stillbirth, microcephaly, hydrocephalus, chorioretinitis, vesicular skin lesions
• High perinatal mortality (50%)
Greatest risk of neonatal HSV infection - when?
- Greatest risk of neonatal infection third trimester primary presentation – viral shedding may persist + the baby is likely to be born before the development of protective maternal antibodies
- Infants born to women who have not completed HSV seroconversion during pregnancy (i.e. infants born before the development of protective maternal antibodies) (most commonly in third trimester, within 6 weeks of delivery) highest risk
- Primary genital infection with lesions present at the time of delivery + delivery is SVD risk of neonatal transmission of HSV is 41%
- Recurrent herpes Risk of neonatal herpes with vaginal delivery 0-3%
Factors associated with transmission of HSV from mother to fetus
actors associated with transmission
o The type of maternal infection (primary or recurrent)
Risks are greatest when a woman acquires primary genital herpes in the third trimester (particularly within 6 weeks of delivery) – viral shedding may persist + the baby is likely to be born before the development of protective maternal antibodies
Recurrent herpes
• Associated with a very low risk of neonatal herpes
• But recurrent herpes at the time of delivery (commonly asymptomatic or unrecognized) may cause the localised forms of neonatal herpes – both skin, eye and mouth infection and local CNS disease
o The presence of transplacental maternal neutralising antibodies
Transplacentally acquired HSV antibodies do not prevent herpes virus spreading to the brain of the neonate
o The duration of rupture of membranes before delivery
o The use of fetal scalp electrodes
o The mode of delivery
• I
HSV in pregnancy complications + prognosis
• Primary genital herpes in the first trimester No evidence of an increased risk of spontaneous miscarriage or congenital abnormalities
• Primary genital herpes acquisition in the third trimester Some evidence of increased perinatal morbidity (PTL, LBW) together with stillbirth
• Recurrent herpes
o No increased risk of PTL, PPROM, FGR
o Incidence of congenital abnormalities is not increased
• Genital herpes infection in mum – can last up to 4 weeks if not treated
• Disease localised to the skin, eye or mouth alone
o Best prognosis
o With appropriate antiviral treatment, neurological and/or ocular morbidity is <2%
• Local CNS disease
o 6% mortality
o Neurological morbidity is 70% (may be lifelong)
• Disseminated disease
o Have the worst prognosis
o 30% mortality with appropriate antiretroviral treatment
o 17% have long-term neurological sequelae
o More common in preterm infants, occurs almost exclusively as a result of primary infection in the mother
• The poor outcomes of disseminated and local CNS disease have been attributed to delays between symptoms onset and treatment
• Congenital herpes
o Skin, eyes, CNS
o FGR or IUD
o Can cause miscarriage, stillbirth, microcephaly, hydrocephalus, chorioretinitis, vesicular skin lesions
o High perinatal mortality (50%)
• Women with recurrent herpes
o Risk of neonatal herpes is low, even if lesions are present at the time of delivery (0-3%)
o No increased incidence of congenital abnormalities
2 important complications of HDN
haemolytic disease of the newborn
Anaemia
Kernicterus
o If rate of red cell destruction > red cell rate of production = fetal anaemia
If severe heart failure, fluid retention, swelling (hydrops) – hydrops fetalis
Red cell break breakdown = bilirubin release
• Not a problem during fetal life as it is cleared by the placenta
• At birth – immature neonatal liver is not capable of handling a high bilirubin load severe neonatal jaundice
• High levels of jaundice if untreated permanent brain damage (kernicterus) (because of deposition of bilirubin in certain areas of the neonatal brain)
• This can lead to neurodevelopmental problems cerebral palsy, deafness, motor and speech delay
how does anti-D work?
• The anti-D immunoglobulin administered neutralises the fetal RhD antigen in the maternal circulation
o Mechanism – baby Rh +ve cells in mother’s circulation coated in exogenous anti-D which is removed by reticuloendothelial system prior to any sensitisation
Sensitising events (RF for HDN haemolytic disease of the newborn, rhesus disease)
• Alloimmunization/Sensitization during first/second/subsequent pregnancy
o Results in large amounts of anti-D antibodies being produced in subsequent pregnancies
o Risk increases with each gestation
o The risk of sensitisation is greatest in the first pregnancy and decreases with each subsequent pregnancy
o Once sensitisation has occurred it is irreversible
• Failed prophylaxis
• Invasive fetal procedures
o Intrauterine transfusion/surgery/insertion of shunts/laser
o Intra-operative cell salvage
• Medical intervention (chorionic villus sampling, amniocentesis, ECV)
• Gynae
o Ectopic pregnancy
o TOP, IUD, stillbirth, molar pregnancy
o Therapeutic TOP(any GA, any method)
o Threatened miscarriage
o Spontaneous miscarriage
o Evacuation of molar pregnancy
• APH/PV bleed in pregnancy (>12w, prolonged and <12w)
• Placental trauma
• Previous blood transfusion (rare if in UK)
• Delivery
o Traumatic deliveries
o Sickle cell disease
o CS
o Instrumental
o Normal delivery of a Rh+Ve baby
• Over 99% have an FMH of <4ml at deliver – Large FMH RF
o Traumatic deliveries incl. C-section
o Manual removal of the placenta
o Stillbirths + IUD
o Abdominal trauma during the 3rd trimester (26-37w)
o Multiple pregnancies (at delivery)
o Unexplained hydrops fetalis
HDN haemolytic disease of the newborn, rhesus disease maternal complications
• Maternal
o No long-term adverse health consequences associated with the presence of red cell antibodies
o Anti-D
Small risk of localised or generalised allergic reaction
Transmission of blood-borne infections
• Extracted form donor blood + carefully screened for transmissible infection but there is always a small risk
HDN haemolytic disease of the newborn, rhesus disease fetal complications + neonatal complications
• Fetal
o Consequence of Rh disease is severe fetal anaemia which can result to hydrops fetalis (collection of fluid in serous compartments) and death
o Infants may experience anaemia persisting for a few weeks following birth
o Some infants may develop late anaemia which is usually due to hyporegenerative anaemia
o Kernicterus (bilirubin encephalopathy) – extrapyramidal, auditory, visual abnormalities, cognitive deficit)
o Graft vs host disease
o Infections
o Metabolic abnormalities
• Neonates
o Exchange transfusion – portal vein thrombosis, portal hypertension
o Kernicterus (permanent brain damage from large amounts of bilirubin) – neurodevelopmental problems cerebra palsy, deafness, motor and speech delay – phototherapy and exchange transfusion
Anti-D administration checklist
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Amnionicity vs Chorionicity
Amnionicity
• Number of amnions (inner membranes) that surround babies in a multiple pregnancy
• 1 amnion – all babies share an amniotic sac
Chorionicity
• Number of chorionic (outer) membranes that surround babies in a multiple pregnancy
• Monochorionic twin pregnancies + monochorionic or dichorionic triplet pregnancies – carry higher risks because babies share a placenta
Monochorionic twin or triplet pregnancy = a pregnancy in which any of the babies share a placenta and a chorionic (outer) membrane This includes monochorionic twins and dichorionic or monochorionic triplets
**Monochorionic triplet pregnancy includes dichorionic or monochorionic triplets
In dizygotic multiple pregnancies each fetus has its own placenta, amnion and chorion
In monozygotic multiple pregnancies, this depends on the timing of the division of the ovum
Multiple pregnancy RF
- Previous multiple pregnancy
- Family history (maternal side)
- Increasing maternal age (>45 are most likely to have a multiple birth)
- Racial origin (more common in West Africa, less common in Japan)
- Assisted reproductive techniques (ART) – might implant 2 ovuums
Twin to twin transfusion syndrome what is it TTTS
• Complication of monochorionic multiple pregnancies (monochorionic twins and monochorionic or dichorionic triplets) arising from shared placental circulation
• Pathogenesis
o When blood moves from one baby to another
o Donor = baby that loses blood / SGA / oligohydramnios
o Recipient = baby that receives blood / LGA / polyhydramnios
o Disproportionate blood supply between the fetuses leads to unequal levels of amniotic fluid between each fetus + usually leads to death of the undersupplied twin and without treatment, usually death or a range of birth defects or disabilities in for a surviving twin (underdeveloped/damaged/missing limbs/digits/organs, cerebral palsy)
o Sometimes, one fetus dies and forms a mummified fetus papyraceous or is reabsorbed (“the disappearing twin” syndrome)
o Risk to recipient baby > donor baby – more blood – more cardiac strain – hydrops fetalis
• Symptoms
o Sudden abdomen size increase, SOB
Twin anaemia polycythaemia sequence (TAPS) what is it
- Complication affecting monochorionic twin or triplet pregnancies
- Chronic form of feto-fetal transfusion caused by the joining for fine blood vessels connecting the fetal circulations of the placenta
- Occurs without the differences in levels of amniotic fluids between the fetuses (polyhydramnios and oligohydramnios) that is usually seen in FFTS
- Donor – at risk of progressive blood loss (anaemia)
- Recipient – at risk of successively increasing blood count (polycythaemia)
Multiple pregnancy maternal complications
• Hypertension
o At each AN appointment – measure BP + test urine for proteinuria
o (If at high risk of pre-eclampsia (>1 high risk factors) or if >2 moderate RF) - aspirin
o If there is presence of >2 RF for hypertension (multiple fetal pregnancy is already a moderate RF so you only need 1 more high or moderate RF for hypertension to prescribe aspirin)
Low dose aspirin (75-150mg) daily from 12 weeks until birth
o High risk factors
HTN disease during previous pregnancy
CKD
Autoimmune disease e.g. SLE or antiphospholipid syndrome
T1 or T2DM
Chronic HTN
o Moderate RF
First pregnancy
Pregnancy interval of >10 years
>40 y/o
BMI >35kg/m2 at first visit
FHx of pre-eclampsia
Multiple-fetal pregnancy
• Anaemia
o Higher incidence in women with a multiple pregnancy
o FBC at 2 at booking + 20 + 24 + 28 to identify need for early supplementation with iron or folic acid
• Indications for referral to a tertiary level fetal medicine centre
o Pregnancies with a shared amnion
o Pregnancies complicated by any of the following
Fetal weight discordance (>25%) and an EFW of any of the babies <10th centile for GA
Fetal anomaly (structural or chromosomal0
Discordant fetal death
Feto-fetal transfusion syndrome
TRAP – twin reverse arterial perfusion sequence
Conjoined twins or triplets
Suspected TAPS
• Triple pregnancy – before offering screening for those conditions, inform the woman about
=increased
o likelihood of these conditions in triple pregnancy
o Different options for screening
o false positive rate of screening tests in triplet pregnancy
o likelihood of being offered invasive testing
o likelihood of complications of invasive testing
o The physical risk + psychological implications in the short and long-term relating to selective fetal reduction
o Calculate the chance for each fetus
Multiple pregnancies prevention
Primary prevention
• Limiting the number of embryos transferred in IVF
• Close counselling/monitoring of those using ovulation-induction therapies
• HFEA – has criteria for single embryo transfer
o If the woman does not fulfil them, a maximum of 2 embryos can be transferred per cycle
Secondary prevention
• Multifetal pregnancy reduction (MFPR)
o Not acceptable to all – particularly those with a past hx of infertility
o Preformed early in pregnancy – usually between 9-12 weeks
o TA or TV US-guided injection of KCl into the heart of selected fetuses – heart stops and fetus dies
o Generally the fetal material is reabsorbed into the woman’s body
o Usual practice is to reduce higher-order pregnancies to a twin pregnancy, although some favour reduction to a singleton pregnancy
o Risks
Miscarriage of remaining fetuses
Emotional consequences to parents
Infections
Multiple pregnancies complications for the baby
o Stillbirth
Singletons 5 per 1,000
Twins – 12.3 per 1,000
Triplets 31.1 per 1,000
o IUD
For dizygotic twins, the other twin will be fine
For monochorionic monozygotic twins this can be bad BP will drop in the surviving twins’ placenta neurological damage in the surviving twin in 25%
o PTL
neonatal mortality rate
chance of long-term morbidity (neurodevelopmental delay, chronic lung disease)
o FFTS
Most common in monochorionic twins
Also occurs in monochorionic or dichorionic triplets
Accounts for 20% of the stillbirths in multiple pregnancy
o risk of umbilical cord entanglement – mainly in monochorionic monoamniotic twin pregnancies
o IUGR
And discordant IUGR – when one baby is SGA + the other normal or LGA
Monitored with EFW discordance (not SFH) difference in size >25% - indicator of IUGR
o Congenital abnormalities
• Language and speech delay, more general cognitive delay or motor problems, behavioural problems and difficulty in parent-child interactions all appear to be more common in multiple birth children
Risk higher in monozygotic twins (2X)
In dizygous twins the risk is close to that in singleton pregnancy
o DS
Greater absolute risk as same risk per baby so increased total risk
Multiple pregnancies complications for the baby
o Miscarriage
o Anaemia, thrombocytopenia
o Pre-eclampsia
More risk of abnormal vasculature development
Always check at every antenatal appointment – BP, urine dip for protein
Follow normal pre-eclampsia pathways
o APH, PPH (stretched uterus)
o Operative delivery
o Severity of symptoms of pregnancy – N, V SOB, heartburn
o Hyperemesis gravidarum (more bHCG)
o GDM (more placental lactogen and placental steroids so more likely to tip into diabetes)
o Polyhydramnios
o Postnatal illness
o Death (maternal mortality is 2.5x higher for twin pregnancy than singleton pregnancy)
• Risks to the fetus/baby – increased risk of
What should multiple pregnancies be monitored for?
• Multiple pregnancies should be monitored for IUGR + FFTS
Small for dates definition
• An infant born with a birth weight <10th centile
LBW definition
• LBW = birth weight <2500 g
SGA vs FGR
• Fetal growth restriction (FGR) is not synonymous with SGA
o FGR implies a pathological restriction of the genetic growth potential
FGR fetuses may manifest evidence of fetal compromise – abnormal Doppler studies, reduced liquor volume
Clinical definition and applies to neonates born with clinical features of malnutrition and IUGR, irrespective of their birth weight percentile
o SGA is not always pathological, but it can be
Used in neonates whose birth weight is <10th percentile for that GA or 2 S.D. below the population norms on the growth charts
The definition considers only the birth weight without any consideration of the in-utero growth and physical characteristics at birth
• Some growth restricted fetuses are SGA
• A baby may not be SGA (birth weight >10th percentile) but still be considered IUGR if they have features of in-utero growth restriction and malnutrition at the time of birth
• A baby may be SGA (birth weight <10th percentile) but not considered IUGR (no features of malnutrition)
o The likelihood of FGR is higher in severe SGA infants
• Small fetuses are divided into
o Normal (constitutionally) small
Babies whose growth at all GAs has been low
They are SGA but otherwise healthy
50-70% constitutionally small – fetal growth appropriate for maternal size and ethnicity
o Non-placenta mediated growth restriction
E.g. structural or chromosomal anomaly, inborn errors of metabolism, fetal infection
Symmetrical
o Placenta mediated growth restriction
Growth is normal in the early part of pregnancy but slows in utero by at least 2 measurements (normally from US assessments)
Due to IUGR
Newborn baby has a wasted appearance with little SC fat + a greater risk of complications
Asymmetrical (head circumference is spared, AC smaller than it should be)
Serial growth scans needed every 2 weeks
Doppler USS 2ice a week
risk of fetal death
SGA RF
• Maternal factors can affect placental transfer of nutrients o Low pre-pregnancy weight o Under nutrition o Substance abuse o Severe anaemia • Medical conditions can affect placental implantation and vasculature and hence transfer o Pre-eclampsia o Autoimmune disease o Thrombophilia o Renal disease o Diabetes o Essential hypertension
• Fetal
o Chromosomal abnormalities (symmetrical IUGR)
o Infection (CMV, toxoplasmosis, syphilis, malaria)
• Other
o Placental insufficiency (any conditions that result from malfunctioning of the placenta – includes pre-eclampsia) (asymmetrical IUGR)
Major • Age >40 • Smoker >11 cigarettes per day • Cocaine • Daily vigorous exercise • Previous SGA baby • Previous stillbirth • Maternal SGA • Paternal SGA • Chronic hypertension • Severe pregnancy induced hypertension • Diabetes with vascular disease • Renal impairment • APL syndrome • Threatened miscarriage – heavy bleeding similar to menses • Unexplained APH • Low maternal weight gain • PAPP-A <0.415 MoM • Fetal Echogenic bowel o Has been shown to be independently associated with an SGA neonate and fetal demise
Minor • Age >35 • Nulliparity • BMI <20 or >25 • Smoker 1-10 cigarettes per day • IVF singleton pregnancy • Low fruit intake pre-pregnancy • Pre-eclampsia • Mild pregnancy induced hypertension • Placental abruption • Pregnancy interval <6 months or >60 months • Caffeine >300 mg/day in third trimester
Define lie + unstable lie
- The relationship between the long axis of the fetus and the mother
- Longitudinal, transverse, oblique
Unstable lie = where the presentation of the fetus changes between transverse/oblique/breech and back
Define presentation + malpresentation
- The fetal part that first enters the maternal pelvis
- Cephalic vertex, breech, shoulder, face, brow
Malpresentations = all presentations of the fetus other than vertex (brow, face, shoulder, breech, variable lie)
Variable lie = when the head is completely unengaged and floating (seen mostly in cases of severe polyhydramnios and prematurity)
Define position + malposition
- The position of the fetal head as it exits he birth canal
- Occipito-anterior, occipito-osterior, occipito-transvrse
Malposition = abnormal position of the vertex of the fetal head relative to the maternal pelvis
Define vertex
Vertex = head is flexed and the occiput leads the face
define denomnator
Denominator = the bony landmark on the presenting part used to denote position
Vertex = occiput
Face = mentum (chin)
Breech = sacrum
Define attitude
Attitude = relation of different parts of the fetus to one another
Malpresentation + malposition RF
• Maternal factors o Abnormalities of the uterus e.g. fibroids o Obstructed lower segments (fibroids, pelvic abnormalities) o Uterine malformations o Partial septate uterus o Multiparity (uterine laxity) o Multiple pregnancy • Fetal factors o Prematurity o Fetal anomaly (CNS malformations, chromosomal disorders) o Macrosomia • Pregnancy factors o Placenta praevia o Poly/oligohydramnios
Presentation
Attitude
Engaging diameter
Denominator in
Vertex
Occipitoposterior
Brow
Face
presentations
https://i.pinimg.com/736x/a0/56/0b/a0560b951317b0814280ad95b21dc061.jpg
RF for breech presentation
Multiparity
Uterine malformations (e.g. septate uterus)
Fibroids
Placenta praevia
prematurity macrosomia polyhydramnios twin pregnancy abnormality
Different types of breech
• Complete (flexed) breech
o Both legs are flexed at the hips and the knees
• Frank (extended breech)
o Both legs are flexed at the hips and extended at the knee
o Most common type of breech presentation
• Incomplete/Footling breech
o One or both legs extended at the hip
o Foot is the presenting part
o Can become footling breech
What is a brow presentaiton
Brow position
• Fetal head stays between full extension and full flexion
• The biggest diameter (mento-vertex) presents
• Occurs in 0.14% of deliveries
• Usually only diagnosed when labour is well established
• Anterior fontanelle and supra-orbital ridges or base of nose are palpable on vaginal examination
which positions are considered malpositions?
Occipito-posterior position
• Most common malposition
• Head initially engages normally but then the occiput rotates posteriorly rather than anteriorly
• Results from
o Poorly flexed vertex
o Weak uterine contractions which may not push the head down into the pelvis with sufficient strength to produce correct rotation
o Flat sacrum
• Anterior fontanelle felt anteriorly (4 radiating sutures)
• Posterior fontanelle palpated posteriorly (3 radiating sutures)
Occipito-transverse position
• Head initially engages correctly but fails to rotate + remains in a transverse position
Breech presentation vaginal delivery information to be given to the woman
o Woman’s choice
o Maternal complications are least with successful vaginal birth (ELCS carries a higher risk)
o 40% risk of needing an EMCS
EMCS carries the highest risk out of planned vaginal breech or ELCS
Risks of breech SVD
o Risks
Low Apgar scores
Serious short-term complications
• fetal head entrapment
o due to delivery of the trunk through an incompletely dilated cervix – occurs in up to 14% of vaginal deliveries
o incisions in the cervix (vaginal birth) or vertical uterine incision extension (C-section) may be used
• birth asphyxia – usually secondary to delay in delivery
• Birth trauma
• intracranial haemorrhage – as a result of rapid compression of the head during delivery
Has not been shown to increase the risk of long-term morbidity
o Risk of perinatal mortality with a planned breech vaginal delivery – 2/1000
Compares to approx. 1/1000 with planned cephalic birth
Breech complications
• Major complication cord prolapse (= the umbilical cord drops down below the presenting part of the baby and becomes compressed as the head enters the pelvis – likely to be better tolerated by a fetus that is not hypoxic)
o Incomplete or footling breech 15-18% risk of cord prolapse
o Complete breech 4-6% risk of cord prolapse
o Frank breech 0.5% risk of cord prolapse
• higher perinatal mortality and morbidity due to
o premature rupture of membranes
o fetal head entrapment
o birth asphyxia – usually secondary to delay in delivery
o Birth trauma
o intracranial haemorrhage – as a result of rapid compression of the head during delivery
o increased incidence of congenital malformations
• term babes presenting by the breech have worse outcomes than cephalic ones, irrespective of the mode of delivery
• Perinatal morbidity and mortality is higher in cases of planned vaginal breech birth compared to CS in term babies
• Breech presentation is associated with an risk of developmental dysplasia of the hip USS of the hips should be performed in all babies who were breech at 36 weeks irrespective of their presentation at delivery or mode of delivery
• Breech presentation has a significant recurrence risk
• Look at risks/complications of each mode of delivery for breech presentation
Transverse lie complications
Transverse lie
• Associated with a risk of cord prolapse of up to 20%
Define high risk pregnancy
• Pregnant women who have a medical condition or complications in their current or previous pregnancy • Women who have had no antenatal care • Includes women with o Existing medical conditions o Heart disease o Asthma o Long-term systemic steroids o Bleeding disorders o SAH or arteriovenous malformation of the brain o AKI or CKD o Obesity o Obstetric complications or no antenatal care o Pyrexia o Sepsis o IPH o Breech presentation in labour o Small for gestation age baby o Large for gestational age baby o No antenatal care o Previous CS o Labour after 42 weeks of pregnancy
RF for high risk pregnancy
- Age <15yo or >35yo
- Pre-pregnancy weight under 45kg or obese
- Height under 5 ft (1.5m)
- Incompetent cervix
- Uterine malformations
- Small pelvis
- Being single
- Smoker or alcohol
- Illicit drugs
- No access to early prenatal care
- Low socioeconomic status
- Previous obs hx for recurrent miscarriages
- Hypothyroid
- Hyperthyroid
Define prolonged pregnancy
• Pregnancy which progresses beyond 42 weeks
Risks of prolonged pregnancy
• Risks associated with continuing pregnancy beyond 41+0 weeks:
o increased likelihood of CS
o increased likelihood of the baby needing admission to NICU
o increased likelihood of stillbirth + neonatal death
Maternal risks • Obstructed labour • Perineal damage • Instrumental vaginal delivery • CS • PPH • Infection
• Fetal risks due to o Utero-placental insufficiency o Meconium aspiration o Intrauterine infection • Increased risk of stillbirth + neonatal death • Increased risk of death in the first year of life • Meconium aspiration • Macrosomia + larger babies – prolonged labour, cephalo-pelvic disproportion, shoulder dystocia, birth injury (brachial plexus damage, cerebral palsy) • Neonatal acidaemia • Low 5 minute Apgar scores • Neonatal encephalopathy • Neonatal seizures • IUGR due to placental insufficiency
IOL before uterus or cervix are in a favourable state • Need for CS • Prolonged labour • PPH • Traumatic delivery
Prolonged pregnacny RF
- Previous post-term pregnancies
- Primigravity
- High maternal BMI
- Genetic factors
- Advanced maternal age
Define obesity in pregnancy
BM > 30 kg/m2
Shoulder dystocia RF
• Maternal o High maternal BMI o DM o GDM o Short stature o Multiparity • Fetal o Macrosomia o Post-term gestation • Labour o Prolonged 2nd stage of labour • Previous hx of shoulder dystocia • Previous large infant
