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
