Olivia RANZCOG content Flashcards
What are the criteria for RMI?
RMI = U x Ca125 x menopausal status
Ultrasound findings - 0 points for no findings, 1 point for 1 finding, and 3 points for 2 or more findings. Findings include multiloculated, solid areas, metastases, ascites, bilateral lesions.
Pre menopausal = 1
Post menopausal = 3
2/3 of people will have a malignancy if their RMI is >200
Sens 78
Spec 87
What are the characteristics of a good screening test?
- Common disease in the screened population
- Natural history known, and “latent phase” where intervention will improve outcomes - detect disease in a preclinical stage
- High sensitivity and specificity
- Acceptable test to patient and easy to administer
- Affordable
- Treatment for the disease is available
- Will ultimately reduce the morbidity and mortality of that disease
qSOFA score involves what?
For screening for sepsis in clinical use. Score 0 or 1 -SBP ≥90 or <90 - RR <25, ≥25 - Alert or not alert
≥2 = greater risk of mortality
Obstetric modified SOFA score involves what parameters?
Screens for end organ dysfunction
Respiration (PaO2), coagulation (platelets), liver (bilirubin), cardiovascular (MABP), CNS (alert), Renal (cr)
Septic shock: complication of sepsis and is diagnosed when, despite adequate fluid resuscitation, there is hypotension and a requirement for vasopressors. Associated with high lactate and has increased mortality.
Sepsis: life threatening organ dysfunction caused by a dysregulated host response to infection
2 endpoints that give septic shock:
- Hypotension requiring vasopressor therapy to maintain MAP >65mmHg
- Serum lactate >2mmol/L after adequate resuscitation
Fever as a teratogen can cause?
NTDs
Micropthalmia and microcephaly
Cardiac defects
Orofacial defects
Most vulnerable period 4-5 weeks
Rates of death secondary to puerperal sepsis
severe sepsis with acute organ dysfunction has a mortality rate of 20-40%, rising to 60% if shock occurs
Risk factors for maternal sepsis as identified by the confidential enquiries into maternal deaths
obesity IGT / diabetes Impaired immunity Anaemia Vaginal discharge History of pelvic infection Amniocentesis and other invasive procedures cervical cerclage Prolonged ROM Vaginal trauma, CS, wound haematoma RPOC GAS infection in close contacts / family members Black or minority ethnic groups
Most commonest casue of maternal bacterial infection?
And most common cause of death from sepsis?
E. coli (second most common cause of maternal death)
GAS - Pregnant women and postpartum women 20 fold increase in the incidence of GAS. Found in 5-30% of general population as asymtpoamtic carriers. Can cause rheumatic fever, scarlet fever, bacteraemia, streptococcal shock syndrome, nec fasc
Presents with non specific symptoms - fever, sore throat, vomiting, diarrhoea
GBS also common
(S. aureus: mastitis most common)
Community acquired sepsis antibiotic regimen
Cefuroxime 1.5g IV 8hourly, PLUS Gent 4-7mg/kg IV, PLUS Metronidazole 500mg IV 12hourly
Vanc if MRSA
GAS: ADD Clindamycin 600mg IV q8h, PLUS consider normal immunoglobulin 1-2g/kg/IV for up to 2 doses
Clindamycin switches off exotoxin production with significantly decreased mortality. Inhibits production of TNF and IL
Hospital acquired sepsis - source not apparent - treatment
Cef, Gent, Met
At risk of MRSA: vanocmycin
At risk of multidrug resistant gram negative organisms: meropenem ALONE
At risk of GAS: Clindamycin 600mg IV q8hourly plus consider IV Immunoglobulin 1-2g/kg IV
Wound infection post CS Abx
Episiotomy wound infection Abx
CS: fluclox 2g 6hourly
(Suspect MRSA Vanc)
episiotomy: Fluclox and metronidazole
CAP: cef and azithromycin
Influenza antiviral treatment
oseltamivir: prophyactic dose 75mg orally, take for 7-10 days after exposure
Should start within 48h
Vacc reduces infection rates by 35%. rates in infants by 60%, 45% reduction in hospitlizations
What are the criteria for staphylococcal toxic shock syndrome?
- Fever ≥39.9
- Rash: diffuse macular erythema
- Desquamation: 10-14 days after onset of illness, especially palms and soles
- Hypotension: systolic BP <90mmHg
- Multisystem involvement (3 or more systems affected)
4/5 = probable staphylococcal toxic shock syndrome
5/5 confirmed
What are the chances of cancer progression in VIN? (uVIN and dVIN)
uVIN: 10% (recurrence of uVIN after treatment 50%)
dVIN: 33-86%
6 monthly inspection / colposcopy required
Rates of pregnancy outcomes following non obstetric surgery
Maternal death 0.06%
Miscarraige 5.8% all trimesters, 10.5% first trimester
Premature labour 3.5%
Fetal loss 2.5%
Prematurity 8.2%
Major birth defects ass with surgery in 1st trimester - 3.9% (1-3% gen popn)
SOMANZ
What are the criteria for Streptococcal toxic shock syndrome?
- Isolation of Streptococcus from a normally sterile site such as blood, CSF, peritoneal fluid, tissue biopsy
- Isoaltion from a non sterile site such as throat, vagina, sputum
AND
Multiorgan involvement characterised by hypotension and two of
- renal impairment
- coagulopathy
- liver involvement
- ARDS
- generalised erythematous macular rash
- soft tissue necrosis
Definite case= GAS from a sterile site, probable from a non sterile site
Any widespread rash should suggest early toxic shock syndrome, especially if conjunctival hyperaemia or suffusion present. More common in staphylococcal toxic shock syndrome than streprotococcal
People at home may have pharyngitis, fever etc
PResentation with sepsis <12h post birth - most likely GAS
IF EITHER THE MOTHER OR THE BABY IS INFECTED WITH GAS IN THE PP PERIOD BOTH SHOULD BE TREATED WITH ABX. ALWAYS CHECK THE BABIES UMBILICUS AND INVOLVE A PAEDIATRICIAN
Staphylococcal toxic shock syndrome
Confirmed case if all 5 are present, probable if 4/5
Fever
Rash: diffuse macular erythema
Desquamation 10-14 days after onset of illness, especially palms and soles
Hypotension
Multisystem inovlvement: 3 other organ systems affected
Rates of perinatal depression and anxiety
10%
Rate of baby blues
80%
DSM Fifth Edition criteria for depression
5 or more symptoms for at least 2 weeks with at least one of the first two symptoms
- Depressed mood AND / OR
- Anhedonia
- Significant change in weight or appetite
- Markedly increased or decreased sleep
- Psychomotor agitation or retardation
- Fatigue or loss of energy
- Feelings of worthlessness or guilt
- Reduced concentration
- Recurrent thoughts of death or suicide
Scores for edinburgh postnatal depression score
<8 = depression not likely
9 - 11 = depression possible
12 - 13 = fairly high possibility of depression
≥ 14 = probable depression
Positive score on question 10 - suicide - immediate dicussion required.
RANZCOG states to seek help for someone with score ≥13
Main cardiac physiological changes in pregnancy
CO = SV x HR (all 3 increase)
Increased oxygen requirement
Decreased systemic vasodilation - peak 14/40, max 40%
CO increases significantly
- 4L/min pre pregnancy
- 6L/min by 24/40
- increases another 15% first stage of labour, 50% second stage, 60-80% immediately after birth. Decreases to pre-labour levels by 1 hour and prepregnancy levels by 2 weeks
BP decreases, nadir 24/40
Cardiac muscle hypertrophy
Increased HR - 25% increase.
Blood volume increases (30% increase red cell mass, 50% plasma volume (oestrogen –> renin angiotensin system –> aldosterone –> Na+ an H20 reabsorption) , 45% increase overall)
Main anatomical cardiac changes in pregnancy
Heart displaced upwards and left
Cardiac muscle hypertrophy
Compression on IVC / iliac veins
Main ECG changes pregnancy
Sinus tachycardia
Left axis deviation
Atrial and ventricular ectopic beats
Inverted q wave and flattened T wave in III
Poor predictors of tolerating pregnnacy with heart disease
- Pulmonary hypertension
2. High New York Heart Association class I - No breathlessness II - Breathlessness on severe exertion III - Mild exertion IV - At rest
- cyanosis (<80% oxygen saturations)
- Haemodynamic compensation secondary to heart lesion
What is eisenmenger syndrome?
Systemic to pulmonary circulation (e.g. ASD or VSD)
L –> R shunt
increased pulmonary blood flow
pulmonary vascular injury and increased pulmonary resistance
R –> L shunting of blood with hypoxia and erythrocytosis
Pulmonary hypertension mortality rate in pregnancy
10-25%
why do woman die in pregnancy with pulmonary hypertension?
Increased right to left shunt in those with eisenmengers
RHF
Pulmonary hypertensive crises
Management in Pulmonary hypertension and pregnancy
Terminate (still 7% risk mortality)
If continue pregnancy: sildenafil (vasodilator), elective admission for bed rest and oxygen, can have NVB, nothing that decreases afterload - avoid hypovoalemia, beta blockers, careful with regional anaesthesia and oxytocin
How do beta blockers work?
Blocks catecholamine action on beta receptors in heart and peripheral vasculature
- Decreases BP
- Decreases myocardial contractility and therefore oxygen demand on heart
- Decreases CO
- Decreases HR (slows conduction through AV node)
What is severe Aortic stenosis?
<1cm2 across valve. Normally caused by congenital bicuspid aortic valve.
Manage less severe cases with beta blockers if LV not impaired.
What is the genetic of marfans?
Autosomal dominant
What percentage of people with Marfans have cardiac invovlement and what issues do they have ?
80%
Mitral valve prolapse and regurgitation
Arotic root dilatation
> 4.5cm = contraindication to pregnancy. If continues pregnancy ELCS
> 4cm 10% risk of aortic dissection or rupture
Give beta blockers (reduces aortic root dilation)
what is TOF and what risk is it in pregnancy
- Pulmonary stenosis
- VSD R -> L
- Overriding aorta
- RH hypertrophy
Worsened R-> L shunt. Risk CVA.
Fetal ECHO and genetic counselling 2-5% risk (double population)
What disease is mitral stenosis most commonly associated with?
RHD
What symptoms do women with Mitral stenosis get?
Asymptomatic
Dyspnoea
Orthopnoea
PND
Haemoptysis / pink frothy cough
what signs do women with mitral stenosis get?
Mitral facies (flushed cheeks)
Cool peripheries
Tapping undispalced apex
Risk of atrial flutter or fibrillation
pulmonary oedema
Diastolic murmur
What is the major risk in pregnancy for women with mitral stenosis?
Pulmonary oedema
Tachycardia often precipitates this e.g. infection, anxiety, pain, exercise causes a tachycardia, which results in lower filling of left ventricle resulting in lower stroke volume and a build up in pressure
What constitutes severe mitral stenosis?
<1cm2 valve area
How would you treat someone with mitral stenosis in pregnancy?
If severe advise against pregnancy or treat with balloon valvotomy prior to pregnancy
Otherwise
- ECHO
Beta blockers - slow heart so allows time for filling
Treat AF aggressively
Avoid over zealous IVF
Avoid supine and lithotomy
pulmonary oedema: treat with oxygen, diamorphine, diuretics
What is peripartum cardiomyopathy?
Risk factors?
Heart failure that occurs in pregnancy or within 6 months of pregnancy with no other cause known
- Diagnosed based on symptoms, high BNP, ECHO <45% LVEF and dilated heart
Symptoms: CHF symptoms / signs
Risk factors
- HTN
- Multiples
- AMA
- Multiparity
- Afro-carribean
management of peripartum cardiomyopathy
Elective delivery
thromboprohylaxis
Diuretics, vasodilators (hydralazine, nitrates), beta blockers, ACEI following delivery
9% mortality
If persistent issues with LV size or function, 50% will have worsening HF in another pregnancy and 25% will die.
Mechanical heart valves.
What comes into consideration when choosing thromboprophylaxis?
Type of valve: ball and cage (Starr Edwards) more thrombophilic than new bivalve ones (St Judes)
Number of mechanical heart valves
Where the mechanical heart vlave is - MV > AV
Previous thrombolic events or AF
Dose of Warfarin required for therapeutic INR (>5mg = increased risk for fetus)
Patient choice
What do you find with fetal warfarin syndrome?
5-10% affected if exposed at 6-9 weeks
Nasal hypoplasia and absent nasal bridge
Widely spaced eyes
Micropthalmia
Limb hypoplasis, stippled epiphyses
Intellectual abnormality
Can switch to LMWH if you want for first trimester
Stop Warfarin 10-14 days pre delivery
What is the investigation andtreatment for arrhythmias in pregnancy
24h holter sometimes required
ECHO to rule out structural disease
Only treat if life threatening
Digoxin for rate control. OR beta blockers of verapamil (CCB)
Adenosine can be used to terminate SVTs
(Flecainide if tachyarrythmia in fetus)
thromboprophylaxis
What are the cardiac indications for elective CS?
Dilated or expanding aortic root >4.5cm
Severely impaired LVF
PPH management in women with significant heart disease
First line oxytocin
Then misoprostol or carboprost
AVOID ergometrine
(Oxytocin should be given slowly if stenotitc lesions or HCM)
cardiac diseases associated with >15% mortality
- Pulmonary hypertension
- Marfans with aortic root dilation >4.5cm
MS with aortic valve area <1cm2 - Previous peripartum cardiomyopathy with persistent LV abnormalities
LVEF <45% - Unrepaired cyanotic heart disease
How does Warfarin work?
Inhibits hepatic synthesis of vitamin K dependent coagulation factors II VII, IX, X and antithrombotic factors C and S
Respiratory physiological changes
Increased tidal volume
Same RR
Increased inspiratory capacity
Decreased functional residual capacity
Slightly decreased TLC
increased oxygen consumption < increased ventilation = compensated respiratory alkalosis
this increased pO2 to pCO2 facilitates transfer of oxygen to fetus
Anatomical respiratory changes in pregnancy
Engorgment of pharynx, larynx, nasopharynx, trachea
Elevation of diaphragm secondary to uterus
What are the signs of acute severe asthma?
PEFr <33-50% of best
RR >25
HR >110
Unable to complete a full sentence in one breath
Management of acute severe asthma
- SABA inhaled or nebulized, 5mg salbutamol
- ipratropium bromide 0.5m
- IV hydrocortisone 100mg (or oral pred)
- IV rehydration
- CXR if concern re pneumonia or pneumothorax
- admit if PEFR doesn’t improve to >75%
- Life threatenting: IV beta agonists and MgSO4
When should you use IV hydrocortisone in labour?
If using >5mg prednisone for >3/52 prior to labour. Given 100mg IV hydrocortisone TDS / QID
What medicaitons in IOL / PPH management should you avoid in someone who has asthma?
Misoprostol fine (PG E1)
Avoid carboprost (PGF2a - cna cause bronchospasm)
What do you treat Community acquired pneumonia with?
Amoxicillin 500mg - 1g TDS PO + clarithromycin or azithromycin
Severe: 1.5g TDS IV Cefurozime + clarithromyin or azithromycin
Is bacterial or viral pneumonia increased incidence in pregnancy?
Viral: decreased Cell mediated immunity
- VZV
- Influenza
- COVID
Basics of TB in pregnancy
50% more likely to have extrapulmonary manifestation Course of TB unchanged Safer to treat than to not treat Triple / Quadruple therapy (RIPE) Monthly LFts BF is fine
Cystic fibrosis in pregnancy. Genetics and pathogenesis?
Autosomal recessive, 1:25 Caucasians are a carrier
1:2500 incidence in Australia and NZ
Majority of mutations on chromosome 7, CFTR (cystic fibrosis transmembrane chloride channel). Over 1500 different mutations. Most commone delF508
Results in thick mucus in glandular organs and increase sodium in sweat
This causes lung infections, bronchiectasis, respiratory failure, pancreatic insufficiency with malnutrition and diabetes / IGT
Median age for death is 47
Men are sterile
Women are usually fine but sometimes if malnourished or thick cervical mucus - issue with fertility
3 step test for newborn
- Guthrie - measures IRT (indirect measure of pancreatic injury)
- elevated IRT –> test for common DNA mutations
- Sweat test of heterozygous DNA results
Effect of pregnancy on CF
Slightly increased mortality rate
contraindicated if severe lung disease, chronic hypoxia, pulmonary hypertension
Morbidity: worsening lung function (reversible), poor weight gain, infective exacerbation of lung disease
Effect of CF on pregnancy
IUGR - esp if hypoxia
PTB 10-25%
Management of CF in pregnancy
- Pre pregnancy counselling. 1:25 risk of being a carrier. 2% risk of partners risk unknown. Always offer partner carrier testing. If a carrier consider prenatal genetic diagnosis and IVF
- Screen for diabetes
- Education about expectations
- contraindications include Severe pulmonary disease (FEV1 <30-40%), pulmonary hypertension, cor pulmonale (RHF secondary to pulmonary hypertension), recent Burkholderia infection - MDT management
- Adequate maternal nutrition - may need pancreatic enzymes, fat soluble vitamins, dietician invovlement
- Control of pulmonary infections
- Chest physio
- Aggressive treatment with antibiotiics and oxygen, sometimes bronchodilators / steroids - Avoidance of prolonged hypoxia
- May require admission for oxygen - Regular growth assessments
- Delivery plan: aim NVB at term (earlier if deteriorating lung function). Prolonged valsalva can lead to pneumothoraces so offer instrumental
- BF fine
Physiological changes in renal system in pregnancy
Increased renal plasma flow 60-80% increased GFR / creatinine clearance Increased protein excretion Increased Na and H20 reabsoprtion Increased leukocytes and erythrocytes in urine
Dilatation of urinary system (compression and progesterone)
What are the effects of pregnancy on CKD?
Worsening renal function
Worsening proteinuria
Escalating HTN
Effects of kidney disease on pregnancy?
Miscarriage PET FGR PTB Fetal demise (urea >20mmol = risk of fetal death, >10mmol = risk of polyhydramnios)
What stage of kidney disease would you advise against pregnancy?
Stage 4 and 5 (eGFR <30)
Or Cr >250, especially if on dialysis
Management of pregnancies complicated by CKD
- Pre pregnancy counselling - baseline renal function, proteinuria, BP
- MDT
- LDA
- Treat HTN - aim >110/70 and <135/85
- Regular bloods: U+Es, albumin, bicarb, Hb, Plt
- Regular PCR
- consider Vit D
- Growth and LV frequently
- Uterine artery dopplers
- Admit if worsening kidney function, worsening HTN, PET, polyhydramnios
How long should you delay pregnancy following a renal transplant and how successful is a pregnancy past 12/40?
- 1 year
- 95% successful if Cr <125, 75% if >125
Poorer the graft function, poorer the pregnancy outcome
What is the effect of a pregnancy on the renal transplant?
No long term effects
graft rejection 2%
What effect does the renal transplant have on the pregnancy?
HTN / PET 30% FGR 30% PTB 45-60% Infection graft rejection 2% perinatal loss 5%
What is the management of a patient with a renal transplant in pregnancy?
- MDT
- BP monitoring
- Regular renal function tests and PCR
- FBC / LFTs
- Anaemia correction
- Ca ++ (increase or decrease)
- MSU each visit
- USS, regular, uterine artery dopplers
- Maintain level of immunosupressive drugs - prednisone, azathiprine, tacrolimus, cyclosporin fine. Don’t give mycophenolate.
- Admit if deteriorating renal function: ddx. includes renal graft rejection, infection dehydration, obstruction, PET, Calcineurin toxicity (tacrolimus, cyclosporin)
- Aim NVB
- If needs CS for obstetric reason consider midline incision to avoid graft, SMO to do
What are the liver and gastrointestinal physiological changes in pregnancy?
Increased liver metabolism ALP increase to ~400, >1000 = abnormal ALT and AST UL = 30 Bilirubin same Increased fibrinogen, transferrin, thyroid binding globulin
Decreased gastroic motility and peristalsis
decreased lower oesophageal pressure
GI motility slows
What is Wernicke’s encehalopathy?
Thiamine deficiency
Symptoms: blurred vision, unsteadiness, confusion, drowsiness
SignS: nystagmus, ophthalmoplegia, hyporeflexia, abnormal gait, finger ataxia
Associated with a 40% incidence of death!!
Risks of hyperemesis
- Wernicke’s encephalopathy: Thiamine deficiency
- Hyponatraemia (central pontine myelinosis if too rapid correction)
- Vit B6 (pyridoxine) deficiency
- Vit B12 deficiency
- Korsakoff’s psychosis
- Mallory Weiss tears
- Malnutrition
- Psychology
- thrombosis
What is PUQE score?
Score for hyperemesis severity
Scores 0 -5 based on how many hours nausea, vomiting and dry retching. Max score 15
≤6 = mild - community management
7 - 12 = moderate - outpatient management
13 and more = severe - inpatient management
Rates of Hep B transmission to neonate
HbsAg + HbEAg positive = 70-90% risk, 95% at delivery, 5% transplacental
HbsAg +, HbEAg negative = 10-40% risk
CS doesn’t decrease rates of transmission
Given immunoglobulin within and HBV vaccine within 12 hours and vaccine again at 2,4,6 months
Can BF
1% of Australian’s have Hep B
Incidence of intrahepatic cholestasis of pregnancy
0.5-1%
autosomal dominant sex linked genetics
Investigation for intrahepatic cholestasis of pregnancy
LFTs - AST and ALT 3 fold increased, bili sometimes increased, ALP > pregnancy levels, GGT increased, bile acids increased 10-100 times
Liver USS - GS
Hep B and C (+ hep A, E, CMV and EBV if active symptoms of hepatitis)
ONly do smooth muscle antibodies and anti-mitochondrial antibodies if LFT derangement pre-pregnancy or doesn’t normalise post pregnancy
consider drugs
Consider PET and AFLP
what are the risks of intrahepatic cholestasis?
Maternal: Vitamin K deficiency in severe cases, PPH Fetal - 20% intrapartum fetal distress meconium 30% Spotaneous PTB 15% IUFD (0.13% BS <40, 0.28% BS 40-99, 3.44% BS >100) Fetal intracranial haemorrhage
What is the incidence of acute fatty liver of pregnancy?
And maternal and perinatal mortality rate
1/7000 - 1/20,000
10-20% maternal mortality rate previous stydies, UK obstetric surveillance system = 2%
20-30% perinatal mortality rate previously, now 11% likely
Disorder of fatty acid oxidation (mitochondrial disorder)
Risk factors for AFLP?
Male fetus (3:1)
Low BMi
Multiple pregnancy
LCHAD deficiency
What are the symptoms / signs of AFLP?
Starts >30/40 with anorexia, malaise, nausea
Vomiting (60%) severe Abdominal pain (60%)
DIC - 90% postpartum AKI LFTs 3- 10 times Jaundice Lactic acidosis and raised ammonia Risk of fulminant liver failure with hepatic encephalopathy Hypoglycaemia (70%) Symptoms of diabeets insipidus (polyuria, polydyspia) - ADH not cleared
What is the Swansea criteria?
Used to diagnose AFLP
6 or more of Vomiting Abdominal pain Raised transaminases AKI Coagulopathy Encephalopathy Raised uric acid Diabetets insipidus Hypoglycaemia Raised ammonia
How do you manage AFLP
Expedite dleivery
MDT + ICU (65% require ICU, 7% require ventilation)
Coagulopathy: may need FFP and Vit K
hypoglycaemia - treat aggresviely
acidosis and raised lactate: poor outcome
antibiotics: high risk of sepsis - start tazocin
N acetylcysteine - facilitates tissue oxygen delivery
desmopression if high UO
What is the incidence of HELLP?
Maternal and perinatal mortality
5-20% in PET pregnancies
1% maternal mortality
10-60% perinatal mortality rate
How do you differentiate HELLP from TTP and HUS and AFLP?
TTP, HUS and AFLP rarer
Abnormal LFTs and coagulopathy more likely HELLP or AFLP
Profound thrombocytopenia (<10) unusual in HELLP or AFLP
Hyperuricaemia ++ in AFLP compared to HELLP
AFLP
- Higher LFTs, hypoglycaemia, hyperuricaemia, leukocytosis
HELLP complications
Abruption AKI Subcapsular liver haematoma massive hepatic necrosis Liver rupture Death
FGR
PTB
Fetal demise
2-5% risk of recurrence
Incidence of cholecystitis in pregnancy
0.1%
Increased incidence as increased production of gallstones in pregnancy secondary to increased concentration of bile cholesterol, slowed gallbladder motility
Incidence of UC and Crohn’s
5/100,000
Clinical features of ulcerative colitis
Always confined to colon Watery diarrhoea Lower abdominal pain PR mucus and blood Urgency of defecation
Clinical features of Crohn’s disease
Terminal ileum in 30%
Ileum and colon 50%
colon alone 20%
Can affect any part of gGI system from mouth to anus
crampy abdominal pain, weight loss, urgency of defecation, sometimes PR blood and mucus but this is more likely in UC
what are the complications of UC and Crohns?
UC
- Toxic megacolon
- Colon cancer
Crohn’s
- Perforation
- Stricture
- Malabsorption
- fistulae
- Fissures / ulcers
- Abscesses
+ extra intestinal manifestations (arthritis, apthous ulcers (CD), gallstones, cholangitis, conjunctivits, erythema nodosum)
What is the effect of the pregnancy on UC and Crohn’s?
UC: 2 x as likely to flare in pregnancy and 6 x as likely to flare postpartum. Exacerbations are usually mild and occur in first two trimesters
Crohn’s - no more likeyl to flare in pregnancy
Highest risk: active disease at time of conception or new diagnosis in pregnancy (can do colonscopy and biopsy in pregnancy)
What is the effect of IBD on pregnancy?
Active disease: increased rates of miscarriage and PTB
Quiescent disease at time of conception: nil risk
(Risk of immunosupressive drugs if used into third trimester, baby born with higher levels than mother)
Management of IBD in pregnancy
Preconception counselling
- Ensure on correct medications. 5 amino salicylates (sulfasalazine) fine but need 5mg folate as sulfasalazine prevents conversion of folate to its active metabolite, thiopurines (azathioprine) fine, TNFa fine (infliximab, adalimumab) - need to stop by 28/40 as active transport to fetus, higher concentrations in neonate then mother at birth if continued into third trimester, corticosteroids fine.
Can BF with all meds too
- Ensure conceiving when disease quiescent - otherwise increased risk of PTB and miscarriage
- Bloods to assess for malnutrition and active disease
Antenatal management
- If concern re flare: FBC, CRP, LFTs, albumin, stool culture, Faecal calprotection, +/- sigmoidoscopy
- Management of attacks same as prepregnancy
- MDT approach
- Consideration of growth scans especially if active disease
- Management to avoid constipation ?
- Metronidazole if required for pouchitis
Birth plan
- Aim NVB unless active perianal crohns disease resulting in rectal scarring / stiffness / deformity. or a rectovaginal fistulae (can do MRI to assess further
Postnatal
- contact with gastroenterologist if UC as 6 x risk of flare postpartum
- All medications required okay with breastfeeding.
What are the physiological thyroid changes in pregnancy?
Increased thyroid binding globulin synthesis in liver
T4 and T3 increased production to compensate
TSH increases and then decreases in first trimester
Hyperemesis gravidarum can cause a state of biochemical hyperthryoidism - high T4, T3, low TSH
State of relative iodine deficiency because
1. Active transport of iiodine across placenta to fetus
2. Increased excretion through kidney because of increased GFR
3. Increased uptake by thyroid because decreased concentration in plasma
4. Hypertrophy of thyroid can occur to trap iodine in it, if dietary insufficiency
Fetus is fully reliant of transfer to thyroid hormone until 12/40 when it starts making its own
Fetus and breastfed infant is fully dependent on maternal sources of iodine
150mcg / day required in pregnancy and breastfeeding
Thyrotoxicosis and pregnancy
- Implications for thyroid disease
Thyrotoxicosis normally improves in prengnacy becasue of immunosupression (thyroid receptor stimulating antibodies supressed).
- Sometimes have flare in first trimester becasue of HCG and puerperium
- Often have to decreased medications
Thyrotoxicosis and pregnancy
- Effect on pregnancy
Uncontrolled hyperthyroid results in anovulation and infertility
If do get pregnant: increased rates of miscarriage, FGR, PTB, perinatal mortality
Thyroid receptor stimulating ab can cross placenta and cause thyrotoxicosis in fetus or neonate: sinus tachycardia, SVT, AF, thyroid storm and heart failure. Mortality in 25% without treatment
good control: pregnancy unaffected
Both Carbomiazole and PTU cross placenta and can cause hypothyroidism and goitre in fetus. 2-4% risk of congenital abnormalities: Carbimazole > PTU (consider switching to PTU but actually probably better to continue on whatever is working).
Check thyroid stimulating antibodies in first trimester - if high for fetal USS
Check thyroid function in cord blood once born (and in neonate if mother breastfeeding and taking high doses anti thyroid medications)
Look for neonatal thyrotoxicosis: jitteriness, poor weight gain / feeding, hepatosplenomegaly, tachycardia, irritability, goitre, eyelid retraction. Mortality 15% without treatment. Improves after 4 months as antibodies clear.
Hypothyroid and pregnancy
- Causes
- Effect on hypothyroidism
- Effect on pregnancy
1% of pregnancies
Most common cause is autoimmune thyroid disease - atrophic thyroiditis, Hashimotos
25% will need increase in thryoxine throughout pregnancy
Untreated hypothyroidism is assoicated with anovulation and infertility. if do get pregnant assoicated with miscarriage, fetal loss, PTB, PET, anaemia, LBW, perinatal mortality and PPH
Iodine deficiency = hypothyroid in fetus = low IQ / neurodevelopmental delay
Severe maternal iodine deficiency = neurological cretinism (deaf, mute, spastic)
If euthyroid at start of pregnancy maternal and fetal outcome good
Only small amounts of thyroxine cross placenta. Check thyroid function each trimester, 4-6 weeks following any thyroxine dose change
Decrease dose back to pre-pregnancy levels postpartum
Incidental finding of low TSH but no symptoms of hyperthyroidism. Management?
- Check T4, if normal, repeat TSH and fT4 in 4 weeks
- Check HCG
- Check for molar and multiple pregnancy on USS
- Check thyroid receptor antibodies (Thyroid receptor stimulating Ab (GRaves), TPO (risk of postpartum thyroiditis), Hashimotos)
o If positive then this may represent subclinical hypothyroidism of an autoimmune origin and so postpartum thyroiditis risk is increased. No evidence of actually treating subclinical hypothyroidism however. - If persistent derangement involve endocrinologist.
- USS thyroid if elevated t3/t4
What are the physiological changes of related to parathyroid gland in pregnancy?
Increased demand for Ca++ in pregnancy and lactation
Increased urinary excretion of calcium
This means 2 fold increase of calcium absorption from gut is required - vitamin D mediated
Vitamin D requirements are increased by 50-100%
There is a fall in total serum calcium and albumin but same free ionised form of calcium concetrations
risks of hyperparathyroidism in pregnancy?
- To mother
- On pregnancy
Mother: hypercalcaemia actually improves in pregnancy because of increased demand for calcium from fetus
Can get acute pancreatitis + hypercalcaemic crisis, particularly postpartum when fetal demand for calcium is now gone
On pregnancy
- Miscarriage
- IUFD (40% mortality if Ca++ > 3.5)
- PTB
- PET / HTN
- Neonate: tetany, decreased calcium secondary to supressed PTH
Treat with surgery unless mild where it can be managed conservatively.
Drink plenty of fluids
(Hyperplasia or adenoma)
Hypoparathyroid disease in pregnancy
- Risk to mother
- Risk to pregnancy
Increase Vit D by 2 -3 fold to increase calcium absorption
Increased rates of miscarriage, including second trimester miscarriage
Fetal hypocalcaemia, secondary hyperparathyroidism
Bone demineralisation and rickets
neonatal hypocalcaemic seizures
Measure Calcium and albumin monthly
What is the incidence of vitamin D deficiency in Australia and NZ?
5% NZ
23% Aus
Definition of vitamin D deficiency and insufficiency?
Deficiency <50nmol/L
Insufficiency <75nmol/L
risks: Pigmented skin, covered, vegan diet, malnutrition, short interpregnancy interval, obesity, anti epileptic drugs, renal or liver disease, alcoholics
Maternal and fetal clinical features of vitamin D deficiency?
Maternal
- Hypocalcemia
- Poor bone health
- Myopathy
- GDM
- HTN / PET
- SGA
- increased risk CS
Fetal
- Rickets
- Neonatal hypocalcaemia with tetany and seizures
- Asthma / atopy
Management: routine Vitamin D supplementation / day for all pregnant and breastfeeding women (NICE guideline) but RANZCOG: two large quality RCTs hasn’t shown consistently improved outcomes.
RANZCOG recommendations
- Don’t test (CNP recommends testing those at high risk, then giving larger doses of vitamin D if low)
- Recommend 400IU of vitamin D during pregnancy regardless of risk factors
- Advise women about safe sun exposure
- Exclusively BF infants should be given 400IU daily of vitamin D for 6/12
Overview of Renin - angiotensin - aldosterone system
renin is released from juxtaglomerular cells (smooth muscle cells in kidneys vessels) in response to low BP, low Na+ (via macula densa cells in distal tubule sensing hyponatraemia and stimulating JG release of renin via PG) and sympathetic nervous system activation to JG cells.
This renin then converts angiotensinogen (from liver) to angiotensin I which is then converted to angiotensin II in blood vessels to act on 4 target organs
1. Smooth muscle cells in blood vessels –> vasoconstriction
2. Kidney to cause reabsorption of water
3. Posterior pituitary gland to release ADH which then acts on kidney to reabsorb water and blood vessels to vasoconstrict.
4. Adrenal gland to release aldosterone which then acts on kidney to reabsorb water
As a result –> increased BP
Adrenal physiological changes in pregnancy
Increased renin
Increased angiotensin II
Increased cortisol
(Increased cortisol binding globulin)
Pituitary changes in pregnancy
Anteiror pituitary enlarges by 35%
No FSH / LH
Increased Prolactin by 10 times
ADH, GH, ACTH all the same
Hyperprolactinaemia
- Causes
- Pregnancy effect on prolactinoma
- Prolactinoma effect on pregnancy
- Management
Causes
- Pregnancy
- Prolactinoma (macro / micro)
- Hypothalamic stalk lesions (stopping dopamine inhibition)
- Hypothyroidism (TSH stimulates lactotrophs)
- Empty sella syndrome
- Seizures
- some drugs (anti - dopaminergic - antipsychotics, metoclopramide)
- Chronic kidney disease (uraemia–> toxicity to hypothalamus)
Pregnancy effect on prolactinoma
- Sometimes causes it to grow (macro > micro)
- May need to use cabergoline or bromocriptine to prevent further growth
- Usually treated prior to pregnancy however as mostly infertile - amenorrhoea
Prolactinoma effect on pregnancy
- Not usually any issues
- Discontinue dopamine agonists in pregnnacy unless enalrging adenoma or symptomatic.
- both safe in pregnancy and bf
Management
Monthly review
No need for routine PRL testing
No need for routine visual field testing unless symptomatic
MRI if symptomatic
Check PRL level 2/12 post breastfeeding cessation
What is diabetes insipidus?
Deficiency of ADH, causing inability to concentrate urine
Can cause excessive thirst, polyuria, dehydration, seizures
What are the causes of diabetes insipidus?
- Cranial: reduced produciton of ADH e.g. adenomas, destruction of posteiror pituitary, haemorrhage into pituitary, Sheehan’s etc
- Renal: not responding to ADH (CKD, lihtium therapy)
- Transient: increased vasopressinase by placenta breaks down ADH, or decreased breakdown of vasopressinase by liver (HELLP, AFLP, PET)
- Psychogenic: increased drinking resulting in polyuria
How do you treat diabetes insipidus in pregnancy?
Exclude other causes of polyuria (diuretic use, hyperglycaemia, hypokalaemia)
Admit and document urin output and measure urine and plasma osmolality: if urine osmolality <300 and plasma osmolality >295 and/or Na+ >145 = DI
Can give desmopression (doesn’t work if nephrogenic)
Can give Carbamazepine if renal
Advise to drink 20L/day
Regular electrolyte measreuements
Acromegaly
- What is it
- Effects on pregnancy
- How to manage
GH secretion, usually from pituitary adenoma
40% have hyperprolactinaemia secondary to co-secretion or inhibition of dopamine coming down stalk
Minimal effect on pregnancy - increases risk of GDM
Treat outside of pregnancy only
What is Sheehans syndrome?
Infarction of anterior pituitary secondary to massive PPH and hypotension
Anteiror pituitary more vulnerable secondary to increase in size
Presents with
- Failure of lactation
- Amenorrhoea, infertility
- Loss of axillary / pubic hair
- Hypothyroidism
- Adrenocorticotropin deficiency - hypoglycaemia, hypotension, nausea / vomiting
Causes of hypopituitarism
Pituitary surgery Radiation Sheehans pituitary or hypothalamic tumours pituitary haemorrhafe Lymphocytic hypophysitis (chronic inflammatory cell infiltration, symmetrical enlarged putitary gland on MRI)
Low GH, FSH, LH, ACTH, TSH, T4, PRL
Replace hormones based on bloods
To get pregnant need to use FSH / LH and then pregnancy can support itself after that
Otherwise nil effect on pregnancy if appropriately replaced hormones
Otherwise can die form hypoglycaemia or hypotension
What is cushing’s syndrome / effect on pregnancy?
Overproduction of cortisol
<50% from cushing’s disease (ACTH production from pituitary adenoma), most from adrenal adenoma / carcinomas
Very rare as associated with infertility
Dexamethasone suppression test fails to suppress cortisol
Effect on pregnancy
- Fetal loss
- PTB
- Perinatal morbidity and mortality
- Severe PET
- Poor wound healing
- NeonatE: adrenal insufficiency secondary to suppression of fetal corticosteroid secretion
What is Conn’s syndrome and its effect on pregnancy?
Hyperaldosteronism
Adrenal adenoma or carcinoma, bilateral adrenal hyperplasia
Increased aldosterone = hypertension, hypokalameia, high aldosterone, supressed renin activity
Management
- Manage HTN
Replace K+
Surgery PP
What is a phaeochromocytoma?
How does pregnancy affect it?
How does it affect pregnancy?
Adrenal medulla tumour that secretes catecholamines
1/50,000 pregnant women
Hypertensive crises occur in response to various stress: labour, Ga, opioids, metoclopramide, lying supine
Sweaty, nauseated, headahces, palpitations, anxiety, vomiting, HTN, glucose intolerance
Diagnose with 24h urine catecholamines
Then MRI / USS / CT to find tumour (10% bilateral, 10% malignant, 10% extra adrenal)
Effect on pregnany: increased fetal and maternal mortality rate signfiicantly
- Fetal 26% in undiagnosed, 11% diagnosed
- Maternal 17% undiagnosed, 4% diagnosed
Treat with alpha blockade for hypertension and beta blockade for tachycardia for at least 3/7 prior to delivery or surgery (if <23/40) to remove tumour
What is Addisons disease?
- Effect of pregnancy on Addisons
- Effect of Addisons on pregnancy
- Management
Adrenal insufficiency usually secondary to autoimmune process. TB can also cause it
- Low aldosterone (mineralcorticoid)
- Low cortisol (glucocorticoid)
Results in hypotension, hyponatraemia, hyperkalaemia and hypoglycaemia and hyperuricaemia
Symptoms
Weight loss, N, V, Postural hypotension, weakness, lethargy, hyperpigmentation
If diagnosed pre pregnancy not usually an issue, just need to uptitrate steroids sometimes
Previously had high mortality rate
Adrenal Ab can cross placenta but rarely causes neonatal Addisons
Management
- Hydrocortisone (increased at times of stress)
- Fludrocortisone
- IV hydrocortisone in labour and wean back to normal dose over a couple of days PP (otherwise can cause profound hypotension)
What is Congenital adrenal hyperplasia and what enzymes are usually involved?
Excess of androgens, low aldosterone and cortisol
High ACTH / CRH (leads to adrenal hyperplasia)
Low Na+, high K+
21 hydroxylase deficiency –> results in high 17OH progesterone and adrenal androgens (95%)
8-9% 11-beta-hydroxylase (does accumulate some deoxycortisol which has mineralcorticoid activity)
Causes female fetal virilization secondary to high androgens
- Infertile
- Amenorrhoea
- Salt losing crisis in 21 hydroxylase deficiency
- Precocious puberty in a male
How dose having CAH affect pregnancy?
Unlikely to get pregnant
If do, miscarriage, PET, FGR, GDM increased
Ocassionally CS becasue of android shaped pelvis
Increased surveillance becasue of PET risk
Need to continue on glucocorticoids and mineralcorticoids at pre-pregnancy dose, androgen levels will inform if adequate dosing.
Increase corticosteroids if stress including labour
What are the options if concerned about a fetus being at risk of CAH?
Only will know this is a previous fetus has been affected or know father is affected as well as mother
Give dexamethasone from preconception (definitely pre 5/40) to prevent virilization of a female fetus
1/8 fetuses will benefit (autosomal recessive so 1/4 and 1/2 will be female)
CVS or NIPT to confirm female, can do microarray to confirm have disease and therefore continue dexamethasone, otherwise can stop it
Postpartum all female neonates should recieve corticosteroids and all neonates should have their electrolytes tested at about 24 hours becasue of salt losing crisis
Other option: TOP
Insulin and glucose metabolism in pregnancy
- Physiological changees
Pregnancy is an insulin resistant state. Initially in first trimester insulin sensitivity increases and then progressively decreases with increasing gestation
Insulin is 2 fold production by the end of the third trimester
This is partly due to placental production of human placental lactogen, cortisol and glucagon which all promote insulin resistance
glycosuria occurs becasue renal tubule becomes less sensitive to glucose
What proportion of pregnancies are complicated by pre-existing diabetes?
NZ: 1.12% (0.36 = T1D, 0.75% T2D)
Diagnosis of diabetes outside of pregnancy?
Random venous glucose ≥11.1
Fasting ≥7
2h OGTT ≥11.1
HbA1c >48 on 2 occasions (6.5%)
Effect of pregnancy on pre-exisiting diabetes?
Increased insulin resistance in pregnancy resulting in increased insulin requirements in type 1 diabetics (usually 2 fold) and often introduction if insulin in type 2 diabetics.
Diabetic neuropathy gets worse - sometimes irreversible
Diabetic retinopathy risk increases 2 fold
Hypoglycaemia more common (tighter glycaemic control in pregnancy)
diabetic ketoacidosis can occur more easily. 1-3% risk
- BSL >16.3 = risk
- If BSL >15 check ketones (>0.6 in urine or >1 in blood = risk so need to treat)
Can sometimes even occur when euglycaemic. Symptoms: nausea, vomiting, abdominal pain, fruity breath, increased RR, increased HR, decreased UO, dry mouth, confusion.
Maternal ketoacidosis = maternal acidaemia which results in decreased uterine blood flow, decreased placental perfusion, decreased oxygen delivery to fetus - fetal acidosis. Also fetal Hb dissociation curve shifts to right further decreasing oxygen delivery
Treat with insulin, IVf, electrolyte replacement and treat underlying cause
Pre-existing diabetes and maternal considerations in pregnancy
Miscarriage risk 2-3 fold
PET risk 3-4 fold especially if pre-existing hypertension or nephropathy
Diabetic nephroapthy causes severe oedema and normochromic normocytic anaemia
Risk of infection
Shoulder dystocia
Polyhydramnios
CS rate 65%
Fetal and neonatal consequences of diabetes in mother
Increased hyperglycaemia in mother –> fetal hyperglycaemia –> icnreased production of insulin from beta cells in pancreas –> hyperinsulinaemia in fetus
- Macrosomia - increased oxygen requirement - chronic hypoxia / acidosis - catecholamine release - cardiac remodelling and HTN risk later in life, IUFD risk
- Organomegaly
- RDS secondary to PTB / CS rate increase also.
- Polycythaemia - increased jaundice rates
- Neonatal hypoglycaemia - long term neurodevelopmental consequences possible
Shoulder dystocia - brachial plexus injury, hypoxia
Polyhydramnios from polyuria - PPROM, cord prolapse
Increased risk of coengital malformation 4% (2 fold increase)
3 fold increase in NTD and cardiac abnormalities, directly related to HbA!c at the time of conception. Sacral agenesis typically assoicated, also skeletal abnormalities and anecephaly and microcephaly
Recommended weight gain in pregnancy based on BMI
<18.5: 12 - 18
18.5 - 24.9: 12 - 16
25 - 29.9: 7 - 12
≥30: 5-9
Obstetric management in someone with pre-existing diabetes
Pre conception counselling and optimisation of diabetes
- Lower the HbA1c the lower the risk of congenital abnormalities
- 5mg Folic acid
- SCreen for complications: hypertension, nephropahty, retinopathy, coronary artery disease (CARPREG / NYHA), retinal disease, autonomic neuropathy, diabetic foot disease, thryoid disease, coeliac disease, mental health, dental health
- ADIPS targets: <6 pre meal, <8.5 1h post meal, <7.5 2h post meal
- Review meds - ensure safe for pregnancy
- Formally document PCR
- Full bloods
- Contraindications to pregnancy: IHD, untreated proliferative retinopathy, severe gastroparesis, severe renal impairment (Cr>250)
MDT care
Early dating and viability
Low dose aspirin
CAlcium
Individualised weight gain recommendation
CFTS (some factors altered by diabetes). NIPT - fraction of fetal DNA is altered by weight (50% risk of inconclusive result if ≥160kg)
USS 18/40 with fetal ECHO
Regular BP and urinalysis (15% chance PET, 50% if nephropathy)
Retinopathy review once / trimester
28, 32, 36 weeks
Hba1c every trimester
ADIPS recommends weekly CTG from 34/40 because of increased risk of stillbirth (7.2 RR (absolute increased risk 1%)) + AFI and USS
Lactation consultant review from 32/40
If EFW >4500g and diabetes risk of shoulder dystocia is 20% so offer ELCS
Otherwise IOL pre 38+6/40
Pre IOL night before - take normal dose of short or intermediate acting insulin, hald dose of long acting (determir, lantus)
Morning of IOL - 50% of any dose of insulin
CS: same as above but no insulin morning of
Intrapartum: often need sliding scale.
Post partum
T1d: decrease insulin infusion by half after placenta delivered. Then once eating and BSL 8-10mmol/L SC insulin should be restarted at pre-pregnancy dose or 25-50% lower dose if breastfeeding.
T2D: Stop insulin if not on prior to pregnancy. Otherwise drop by 25-40% if itending to breastfeed
LIFESTYLE ADVICE
Encourage breastfeeding: decreased rates of obesity and diabeted in infants who are breastfed
Decreased matenral long term cardiometabolic risks.
Discuss contraception and pre conception care.
What is the HAPO study?
- Published and when
- Aim
- Outcomes
- Results
- Strengths and limitations
New England Journal of Medicine 2009
Hyperglycaemia and adverse pregnancy outcomes
Looked at risks of adverse outcomes associated with various degrees of maternal glucose intolerance less severe than overt diabetes mellitus
23000 women
Bascially just had to do OGTT
Primary outcomes - all increased risk with increasing glucose at testing
1. Macrosomia
2. C peptide in cord blood (measure of insulin production in fetus)
3. Neonatal hypoglycaemia
4. CS rates
Secondary outcomes also altered
1. Shoulder dystocia and birth injury
2. PET
3. PTB
4. Neonatal jaundice
Gave ADIPS cutoffs of fasting 5.1, 1h 10, 2h 8.5
RR 1.75 of adverse outcome
Limitations: observation study, doesn’t report on confounders such as obesity, gestaiotnal weight gain, previous mode of delivery, previous macrosomia, no cost analysis
Strengths: very large study, heterogenous population
What are the cut offs for GDM - RANZCOG
Fasting ≥5,1
1h ≥10
2h ≥8.5
ACHOIS Journal Year Aim Type of study Intervention Outcomes Results Limitations Strengths
NEJM
2005
Does treating GDM improve perinatal outcomes?
RCT
Intervention: dietician, physician, BSL monitoring, +/- insulin vs placebo
blinded if positive for GDM but in placebo arm
Primary outcome
Serious perinatal outcome composite: shoulder dystocia, bone fracture, nerve injury, death, NICU admission, jaundice requiring phototherapy, IOL, CS, maternal anxiety and depression
Secondary outcomes included LGA and macrosomia
Outcome
RR 0.33 primary outcome
Also significant decrease in LGA / macrosomia
Treatment improves outcomes
Strengths: RCT
Limitiation: wide variety of outcomes in perinatal composite outcome
ADIPs indications for early OGTT early in conception and then repeat at 24-28/40 if negative
2 moderate or one high risk factor
High risk
- Previous GDM
- PRevious macrosomic baby
- BMI >35
- AMA
- First degree relative with diabetes or sister with GDM
- Previously elevated BSL
- PCOS
- Corticosteroids or antispychotics
Moderate risk
- Ethnicity other than European or American
- BMI 25-35
Main LGA recommendations - RANZCOG guideline
Increased risk of shoulder dystocia >4000g
No good evidence for IOL - shared decision making principles
>4500g and diabetes or >5000g consider ELCS
What is the incidence of shoulder dystocia and incidence of recurrent shoulder dystocia?
0.65%
Increased significantly with weight
7% >4000g
14% >4500g
21% >4750g
Previous shoulder dystocia 7 - 25%
diabetic mothers: 2-4 fold increased risk. IOL at term reduces risk RR 0.4
Brachial plexus injury incidence
7-20%
Erbs palsy 50% - C5 and 6 - adduction and internal rotation
Erbs palsy PLUS 35% - C5,6,7 (includes wrist and finger flexion and pronation)
Klumpke palsy: C8, T1: Isolated hand paralysis and horners syndrome
Manourves for shoulder dystocia and what their aim is
- Reduce bisacromial diameter
- Increase functional size of bony pelvis
- Change relationship of shoulder to women’s pelvis
H - help
E - evaluate for epis
L - legs - Mcroberts (flexes, abducts, externally rotates) (This plus suparpubic = 50% resolve)
P - pressure on suprapubic region
E - enter
- Rubins II - adduct anterior shoulder
- Woods screw - abduct posterior shoulder as you adduct anterior shoulder
- Reverse Wood screw - adduct posterior shoulder
R - remove posterior arm
R - roll
Try all for 30 seconds, then try again
Then last case scenario
- Symphisiotomy
- Clavicular #
- Zavanelli
- Abdominal surgery, hysterotomy and rotate from above
Recommended weight gain depdening on BMI
<18.5 12 - 18
<25 12 - 16
<30 7 - 11
<35 5 - 9
Maternal medical complications in pregnancy with obesity
Medical complication Risk
Gestational diabetes Increased risk to 7% (from 1% BMI 18.5 – 25)
Hypertension Increased risk to 10 % (from 2 % BMI 18.5 – 25)
Pre-eclampsia Increased risk
VTE Increased risk by 10 times
T1 or T2DM 3 – 4 %
Perinatal death Increased risk to 2% (from 0.5% BMI 18.5 – 25)
Incidence of:
- Hypertension in pregnancy
- PET in pregnancy
- Severe PET in pregnancy
10-15%
3-5% (10% of primips)
1% severe PET
0.03% eclampsia
Risks in pregnancy with chronic hypertension
25% PET 50% CS (70% if PET on top) PTB 28% 17% low birth weight <2500g SGA Abruption Perinatal death 4%
No recommendation given about IOL. Individualised plan
(Always check for other causes of chronic hypertension apart from just “essential”)
Most common causes of death in PET
Cerebral haemorrhage (Secondary to uncontrolled HTN)
Multi-organ failure
Liver rupture
What is the pathogenesis of PET?
- Placental factors
- Failure of spiral arteries to remodel as trophoblast invasion is abnormal. this results in abnormal spiral arteries that do not have high capcitence or low resistance. This can result in uteroplacental ischaemia because there is insufficient blood supply to the placenta. Possibly there is also underperfusion of a large placenta e.g. diabetes, multiple pregnancy, hydrops - all increased risk fo PET - Maternal factors
- PET worsens the pro-inflammatory state of pregnancy
- Metabolic disturbance:
- Pro-inflammatory cytokines increase, TGs increase.
This leads to endothelial dysfunction, increased endothelial cell activation and permeability. Increased cell adhesion molecules on endothelium and prothrombotic factors and platelet activation and vascular tone
(decreased prostacyclin synthesis - usually stops paltelet activation and causes vasodilation)
(increased thromboxane A2 synthesis - causes platelet activation and vasoconstriction
There is widespread microvascular damage which leads to hypertension, proteinuria, hepatic disturbance
Anti-angiogenic factors:
- VEGF and TGFa normally mantain endothelial health. antiangiogenic factors such as soluble Flt and soluble endoglin are secreted by the placenta in PET ni excess which antagonize these factors
What are the risk factors for PET?
General
- Age >40: 2 fold
- BMI >30 : 2 fold
Genetic
- Mother 25%
- Sister 35-40%
Obstetric
- Multiple pregnancy 2 fold
- Previous PET 7 fold
- Primip 2 - 3 fold
- Long pregnancy interval 2-3 fold with 10 years
- IVF, especially with donor egg
- Hydrops with large placenta
- Molar pregnancy
- Triploidy
Medical
- PRe-existing HTN
- CKD
- DM
- BMI
- APS
- CT disease
- Sickle cell
What are the indications for delivery in pre-eclampsia?
- Severe hypertension: Persistent BP >160 despite maximal therapy e.g. 3 agents at maximal doses
- Worsening bloods: Plt <100, coagulopathy, Cr >90, ALT >70, albumin <20
- Eclampsia or other crisis
- Maternal symptoms suggestive of potential crisis: severe headache, epigastric pain, orthopnoea
- Fetal concerns: severe FGR, absent or reversed EDF on UAPI, placental abruption, fetal distress
If the diagnosis of PET is made pre-viability what would you recommend?
Advise tOP
Severe maternal morbidity 70%
Perinatal mortality 80%
What is the mortality rate with HELLP syndrome?
7%
Abruption a risk
What was the hypitat study? Year Journal Aim Type of study Inclusion / exclusion criteria - brief Primary outcomes Results
Comparing IOL vs expectant management in women with mild Gest HTN or PET, did it affect serious maternal outcomes?
Lancet 2009
Multicentre open label RCT
Inclusion: singletons, >36/40, no severe PET or other serious comorbidity
Number 377 and 397
intervention: IOL within 24h vs expectant management with close surveillance
Primary outcome: Composite maternal morbidity
- Mortality
- Development of severe PET: eclampsia, HELLP, abruption, pulmonary oedema, VTE, >170/110 AN or PN, major PPH
Results: significant difference, 29% relative risk reduction, OR 0.58, NNT = 8.
No significant difference in mode of delivery or composite neonatal outcome
Offer IOL to women with PET post 3740
(Cochrane: 2017: lower risk of composite maternal mortality and severe morbidity in those randomsied to early planned birth RR 0.7, HELLP RR 0.4, severe renal impairment RR0.4. No diff CS rates. Increased risk of NICU admission and RDS)
What effect does ACEI have on the pregnancy?
Contraindicated
Teratogenic: cardiac and neurological malformations
Renal disease in fetus, oligohydramnios, hypotension
IUFD
Management of eclampsia
Resuscitation: A, B, C
IV diazepam (2mg/min to max 10mg) or clonazepam may be given while MgSO4 is being prepared if the seizure is prolonged
IV MgSO4 loading dose and infusion for 24-48 hours after delivery or last seizure.
- 4g loading dose then 1-2g/hour diluted in NS
- Side effects: neuromuscular blockade and loss of tendon reflexes, double vision, slurred speech, respiratory depression, cardiac arrest
monitor BP, RR, UO, O2 sats and deep tendon reflexes rregularly
Serum magnsium levels don’t need to be measured routinely unless renal funciton compromised
If AKI - same loading dose, but half the maintenance dose.
Control of hypertension - aim <160/100 - IV Labetalol or IV hydralazine
Delivery once stable!!
CLASP trial -Year Journal Aim Type of study Inclusion / exclusion criteria - brief Primary outcomes Results
1994 Lancet Aim: does low dose aspirin reduce risk of PET and IUGR RCT >9000 women Pregnant with risk factors for PET or IUGR or current concern for PET or IUGR Randomised to aspirin or placebo no significnat change in outcomes - Reduced PEt but not significant Reduced PTB but average of 1 day No signifcant change in birthweight No differnece in SB or NND
Cochrane meta-analysis NNT 160 starting <16/40 with those at high risk PET
Risks in future if have PET in pregnancy
Recurrent PET (15%, 7 fold) Chronic hypertension IHD CVD PPVD DVT CKD Type II diabetes
Indications for low dose aspirin
PET / HTN in previous pregnancy Chronic hypertension CKD Autoimmune disease e.g. APLS, SLE Type 1 or 2 diabetes
OR two of - First pregnancy Age 40 years or older Pregnancy interval more than 10 years BMI >35 FH PET Multiple pregnancy
MAGPIE trial
2002
Lancet
Does MgSO4 prevent adverse outcomes for owmen with PET and their babies
RCT
9996 women
ITT, blinded, multicentre
MgSO4 loading and maintenance vs placebo
Inclusion: pregnant or delivered within 24h, PET, uncertainty whether should have MgSO4
Primary outcomes: eclampsia, death, matneral morbidity
Results: halved chance of eclampsia, reduction in mortality but not signficiant, SS reduced placental abruption
Pre pregnancy counselling main points
- Medical history: optimise medical conditions and medication use
- Genetic / FH: offer prenatal screenning for conditions they are at increased risk of: Fragile X, CF
- Vaccinations
- Lifestyle recommendations: healthy weight, nutrition, exercise, smoking, ETOH, substance use, iodine, folate
- Travel and environmental risks
- Healthy environment
What are the criteria for principles of screening test?
the condition must be
- Common
- Have a latent phase
- Cause significant morbidity and mortality
- Intervention available
- Intervention acceptable
- Cost effective to offer treatment
The test must be
- Voluntary
- Informed consent
- High sensitivity
- Acceptable to the population
- Diagnostic test available
- Strategy for managing incidental findings.
Incidence of CF in Australia
1 in 25 -35 carrier,
1 in 2500 -5000 affected
cost effective to screen for
What is Fragile X?
X linked condition that causes intellectual disability, behavioural and emotional issues, medical conditions such as epilepsy, MVP, recurrent ear infection, eye issues such as strabismus, physical characteristics: large ears, large testes, long face, high broad forehead, high palate, connective tissue problems
FMR1 gene (Fragile X mental retardation protein): trinculeotide repeat increases in copies. >230 = mutation. >55 = premutation. 30 = average unstable, can change in amount of repeats between people
1 in 8000 females
1 in 4000 males
What is combined first trimester screening?
Its sensitivity, specificity and PPV?
PAPPA and BHCG between 10-12 weeks
NT between 11+3 - 13+6 <3.5mm is normal
Also adds in age
Gives risk of T21, T18, T13
(Increased BHCG and low PAPPa - T21, decreased both T18)
Advantages
- early screen and therefore early diagnosis
- highest detection rate
- no added risk of miscarraige
- detection of some fetal abnormalities
- benefits of early scan: accurate dating, diagnosis of multiple pregnancy, diagnosis of early pregnancy failure
Disadvantages
- Will detect some affected pregnancies that may spontaneously miscarry
- Doesn’t provide risk of NTD (but USS will see anencephaly)
- Some women may book later
- USS: accredited operator
- Out of pocket expenses vary
What is NIPT?
Non invasive prenatal testing
Measures fetal fraction of cfDNA and counts chromsomes essentially
if more of chromsome 21, concerning for T21
Still a screening test, do >10/40
Need 2-4% of fetal fraction, average is 10%
Altered by gestational age (10-12 best), maternal weight (BMI >40? = 50% no result), mosaicism, multiple pregnancy, chromosomal abnormality
highly senstivie and specific - both 99%. 45% PPV
For t21, 18, 13 and sex aneuploiides
Still need 12/40 scan
(Can also test for Di-George syndrome and other microdeletion syndromes)
Unreportable: 1-5%. Do diagnostic testing, repeat cfDNA, alternative testing)
Twins need at least 4% FF to have accuracy - better than CFTS
Advantages:
- More sensitive and specific
- Information on sex aneuploidies also
- Don’t need technical skill of ultrasonographer, just a blood test
- Less strict on timing of test
- Can give information on rhesus disease
- Better for twins
- Can use for single gene disorders e.g. achondroplasia
- Overall economic benefit because invasive testing decreased.
Disadvantages
- Cost
- Non reportable result in 5%
- Risk of palcental mocaism
- Can sometimes give information on maternal conditions e.g. cancer
- Still requires invasive testing for confirmation
What is MSS2?
4 blood tests between 15 and 20/40
Best at 17/40
BHCG (increased in T21, decreased in T18)
AFP (decreased in T21, increased in NTD, decreased in T18)
Inhibin A ( increased in T21, decreased in T18)
Oestradiol (decreased in T21 and 18)
picks up 75% of T21 and 85% NTD (when combined with USS 95% NTD)
Good for older women - 95% of affected pregnancies will have a high risk result if affected, 50% of pregnancies overall will have a high risk result if <40yo
75% sensitivty
93% specificity
2-3% PPV
Trisomy 21
- Features
- Medical problems
- Incidence
- Recurrence
- Reason
Autosomal aneuploidy
Non disjunction in meiosis I or II
1:660
- 30: 1:1000, 35 1:300, 40 1:100
(Increases with age, ?because cumulative oxidative stress, depletion in number of normal oocytes available for maturation and shortening of oocyte telomeres
Features: wide nasal bridge, epicanthal folds, bracycephaly, webbed neck, upward slanting of eyes, cardiac and / or GI malformations, developmental delay
Medical problems: intellectual disability, cardiac malformations, GI malformations, hypothyroidism,
epilepsy, respiratory issues, alzheimers, leukaemia, immunodeficiencies
Recurrence rates
1 child previously
1:100
>35y = twice the age related risk
Trisomy 13
1:5000 births
Non translocation trisomy aneuploidy
not compatible with life
Death after 4/7 usually
Issues:
- Craniofacial malformations - cleft lip and palate
- Ocula rmalformations - micropthalmia
- Limb defects e.g. polydactyly
- Kidney problems: cystic kidneys, hydronephrosis
- Cardiac abnormalities
- Neurological abnormalities: holoprosencephaly, NTDs
- Ventral wall defects such as omphlacoele
- Diaphragmatic defects
SEVERE intellectual disability if survive (partial or mosaic types)
Recurrence risk is very low and almost unknown
Trisomy 18 - Edwards syndrome
1:3000 30% die in one month, 90% die within 12 months Severe developmental delay Severe intellectual disability Cardiac defects urinary and renal tract defects Joint contractures LBW Hearing loss Rocker bottom feet
Recurrence rates low and almost unknown
Tuners syndrome
1:2000 45X Webbed neck, cardiac anomalies (coarctation bicuspid AV), renal abnormalities, high arched palate. Primary amenorrhoea Streak ovaries Lack of sexual development at puberty Normal intelligence Short stature Majority mosaic
High FSH, refer to paediatric endocrinologist. Can give oestrogen and GH treatments.
Frequent otitis media
Increased risk of IBD, hypothyroidism, DM
Klinefelters
XXY
1:500-1000
Tall stature Primary hypogonadism Gynaecomastia Small tests Infertile
Delay language
Can give testosterone to promote growht of testes, will still be infertile
CVS
> 11/40
Detects >99% T21
Advantages: can do early so TOP available by curettage, definitive diagnosis
disadvantages: miscarriage risk up to 1%, Detects some pregnancis that may have miscarried anyway, 1% risk of equivocal result (maternal cells, mosaicism), 0.1% risk failure to detect (fetal mocasism, not in placenta)
Amniocentesis
> 15/40 (otherwise risk of talipes)
100% pick up of T21
Advantages: 0.5% misacrriage rate only, definitive test
Disadvantages: in second trimester, if want TOP need IOL, 0.5% miscarriage rate,
Chicken pox / varicella zoster
DNA virus
Infection 1st trimester: 0.55% chance of congential varicella syndrome, 12-28/40 2%, >28/40 - 0%
infectious 48h prior to rash and then until lesions have crusted over
Significant risk: 5 mins face to face, living with someone or ins ame room for >1h
- Define maternal exposure previously - IgG positive = immune. IgG negative = at risk
- risks to mother : pneumonia (5% mortality), neurological manifestations
- Risk to fetus: congenital varicella syndrome or neonatal varicella
- Expsoure <96h –> give ZIG, exposure >96h - no ZIG, Consider aciclovir if high risk
- Chicken pox develops: ≤24h since onset of rash: oral aciclovir, >24h no aciclovir, complications or immunocompromise IV aciclovir
- FM counselling - USS 5/52 post chickenpox - features of varicella zoster syndrome: skins carring 78%, eye (60%), neurological, limb, gut, prematurity / LBW
- Routine scanning following this. No need ofr amniocentesis but can sometimes be useful to know PCR result.
- Only delivery if fetal compromise of unable to ventilate mother because of gravid uterus.
- Chickenpox <7 days before to 2/7 after delivery: ZIG to neonate immediately!
- Chickenpox >2-28 days post deliveyr given infant ZIG if <1000g or <28/40 gestation.
- Breastfeeding encouraged.
CMV
DNa herpes virus
Most common congenital infection
Testing
- IgM + , IgG + (diagnosis of new infection if previously IgG negative)
- IgM - , IgG+ = past infection
- IgM +, IgG - = very recent infection or false positive. repeat 2/52
- IgM +, IgG + low avidity = recent infection - refer FMM, amnio 6/52 post infection and >20/40 (otherwise very poor sensitivity)
- IgM +, IgG + intermediate avidity = probable recent infection = refer
- IgM +, IgG + high avidity, recurrent infection = refer
30-40% risk of transmission in utero
10-20% risk long term sequelae
10-15% symptomatic congenital CMV (50% long term sequelae)
85-90% asymptomatic at birth: 10-15% long term sequelae
Detection of virus is high from aniotic fluid as fetus urinates the virus out
In utero: oligo / poly, cerebral calcifciaitons, microcephaly, hydrocephalus, IUGR, hydrops, heaptopmegaly etc etc etc
Birth: early mortality (3/12), microcephaly, seizures, developmental delay, chorioretinitis, sensoineural hearing loss
Prevfention better than cure!!: high risk parents and people working at daycare.
Listeria
Gram positive rod
Aerobic and facultatively anaerobic. Grows at 4-10 degrees
Predilection for placenta and CNS
pregnant women susceptible because decreased T cell funciton and predilection of placenta
Transmission highest in 3rd trimester, 70-90% of foetuses get infected, 50% mortality
Non specific illness (diarrhoea, fever, flu like illness, meningitis, 1/3 asymptomatic)
Fetus: mec liquor <34/40, PTB, granulomatis infant septica, neonatal late onset disease (sepsis / meningitis
Do blood cultures
If positive: Amoxicillin 2g IV q6h 2/52 AND gentamicin
If allergy: erythromycin and cotrimoxazole (not in first trimester)
AVOID high risk foods and use safe food handling practices
Parvovrius
Single stranded DNA virus
Transmitted by respiratory droplets
Infects erythrocytes precursors and causes fetal death, anaemia and hydrops
- Suppression of bone marrow
40% of women are non immune
50% of those infected will have fetal infection
10% miscarriage <20/40
3% hydrops
- If hydrops 30% resolve, 30% die if no IUT, 30% resolve after IUT, 6% death after IUT
- No need for amnio
- If positive for parvovirus (i.e. IgM and IgG positive), need 2 weekly scans for MCA PSV and hydrops for 12/52, then can stop if normal result.
Rubella
Togavirus
Incidence low secondary to MMR vaccine
Direct droplet spread versus haematogenous spread through placenta
<12/40: 80% risk fetal infection, 85% CRS
13-16: 50% fetal infection, 35% CRS
17- 30: 30% risk fetal infection, CRS rare
30-36: 60% risk fetal infection, CRS rare
>36:40: 100% risk fetal infection, CRS rare
CRS Triad: cataracts, deafness, cardiac defects (PDA, pulmonary artery bracnh stenosis) Microcephaly IUGR, IUFD, PTB Interstital pneumonia Hepatsplenomegaly Blueberry muffin spots Developmental delay etc etc.
IgM and IgG positive, repeat to confirm and then counsel (positive)
First trimester: TOP
Can do CVS and amnio (best if >6/52 post infection and >20/40): PCR, culture, fetal IgM (can get false psoitive with CVS becasue of matenral tissue)
At birth test IgM, PCR and culture for baby
Born with clinical features of Rubella: IgG ≥ maternal IgG, IgM +, PCR +: Ophthalmology and hearing 3-6/12 assessments, infants infectious 12/12.
Toxoplasmosis
Protozoan parasite
From undercooked meat, cat litter, placental transfer, unwashed salads
Lies dormant, never clear it
Problem if immunocompromised or get it for first time in pregnancy
1st trimester: 10% chance of fetal infection, 90% chance of fetal damage
2nd trimester: 45% and 20%
3rd trimester : 90% and 10%
Causes calcifications in liver and brain, ventriculomegaly, non immune hydrops
Exposure: check serology
- 2 blood samples 2 weeks apart
- IgM negative, IgG negative no primary infection
- IgM negative, IgG positive, infection >2 years ago
- IgM + and IgG negative, infection within last 2 weeks
- IgM +, IgG + low avidity: infection within 12 weeks
- IgM +, IgG + high avidity: infection >12 weeks ago
Refer FM uni
Amniocentesis for PCR (must be >18/40 and >4/52 from infection)
Spiramycin if <18 / 40 if mother exposed
If confirm fetal infection or more than 18 weeks given pyrimethamine and sulfadiazine and folinic acid.
Classic triad: chorioretinitis, hydrocephalus, intracranial calcifications. Visual loss if untreated.
Syphilis
Spirochete
Incidence rising, 500 cases last year in Aus
Primary: chancre
Secondary: palms and soles rash, lethargy, fever, malaise, hepatitis, etc.
Early latent <2y: asymptomatic
Late latent: >2 y since acquisition, asymptomatic
Tertiary: cardiovascular, neurological abnormalities, gummas (soft tissue growths)
EIA first, if positiv,e TPPA, if positive RPR to assess disease activity
Other STI checks
Contact tracting: symptom duration + 3/12 if primary, 6/12 if secondary, 1 year if latent, long term partners if teritary
syphilis in pregnancy: miscarriage, stillbirth, SGA, LBW,
Congenital syphilis:
- Primary: up to 100%
- Secondary: up to 100%
- Early latent 40-80%
- Late latent: 10%
- Hepatosplenomegaly, poly, ascites, anaemia, bowel dialtion, long bone abnormalities, IUGR
(Late congneital syphilis - untreated or inadequately treated: teeth abnormalities, bone abnormalities, keratitis, neurosyphilis, hearing loss)
Neonate diagnosis: RPR 4 fold higher than mothers, TPPA positive after 18/12, RPR or VDRL positive after 6 months.
Successful maternal treatment: 4 fold decrease in RPR, check every 4 weeks. Give benzathine benzylpenicillin tetrahydrate 2.4mU IM once if primary ro secondary, 3 x (weekly) if latent or tertiary
Jarisch Herxheimer reaction 45% (admit if viable gestation)
GBS
Streptococcus agalactiae
Colonisation in 10-30% of women
50% of babies will become colonised when born ot these mothers, 1-2% will have EOGBS, fatality rate is 15%, 20 x this in preterm babies
Intrapartum antibiotics decrease EOGBS by 80%, doesn’t change incidence of late onset GBS
EOGBS: pneumonia / resp symptoms
LOGBS: meningitis, septicaemia
NNT 224
0.4 - 4/1000 live births EOGBS without antibitoics
Risk factors
- <37/40
- Previous baby with EO or LOGBS
- GBS in urine earlier in rpegnancy
- GBS on swab in pregnancy
- Prolonged ROM >18h
- Maternal fever ≥38
- Chorio
- Other twin with EOGBS
RANZCOG supports with universal screening at 35-37 weeks or 3-5/52 prior to anticipated delivery with anorectal and vaginal swab, enriched culture media, specify GBS screening, and specify if allergy to pencillin so can do clindamycin resistances (20%) and erythromycin resistances (30%). OR risk factor based screening
Give penicillin in labour
Cefazolin if allergy
Clindamycin or erythromycin if anaphylaxis
Vancomycin if resistance to clinda and erythromycin
PPROM
- IOL form 34/40
ROM at term
- immediate IOL and IAP.
Hep B
Incidence in Australia 1%
Sexual, blood and vertical
Universal testing in pregnancy because 50% of people don’t know they are chronic carriers
HbsAg positive - reflex liver USS, HBsAb, HBeAg, HBeAb, HBcAb, LFTs, prothrombin time
HBsAg + = active infection - acute or chronic
HBsAb +, HBsAg negative: immunity
HBcAb: past or current infection
HBeAg: immune tolerance or immune clearance - high risk of vertical transmission if positive = 70-90% risk vertical transmission
HBeAb + = viral clearance or immune control.
HBV DNA >10to7, give tenofivir from 30/40 and do ALT 4 weekly, if <10-7 don’t
Don’t breastfeed on tenofivir.
HBsAg and HBeAg positive: 70-90% verticla transmission risk. 95% vertical, 5% transplacental. CS doesn’t decrease rates.
If infected at birth 90% risk chronic carrier (high risk cirrhosis and Hepatocellular cancer).
GIVE HBIG and HBV vaccine within 24 horus of birth. HBV vaccine can be given up to 7 days
Give further vaccine at 2,4,6 months.
Serology 9/12 of age
HepB acutely in pregnancy: if HBsAg <10IUml give hep B vaccine and HBIG wihtin 72h. Retest 3/12.
Hep C
RNA virus
Transfusion prior to 1992, IVDU, Sex (uncommon)
RANZCOG: 1% of women in childbearing years
3-5% risk MTCT
Mostly vertical transmission at birth, and confined to those with positive RNA high levels or HIV co-infection (20%)
Measure Hep C Ab in all women, if positive measure HCV RNA and LFts. If HCV RNA negative oculd mean false positive Ab, very low viraemia secondary to treatment or cleared infection, or just very low viraemia
Avoid invasive procedures
CS no benefit
BF okay unless cracked bleeding nipples
Infant born: wash before any injections. Measure HCV RNA at 3/12, if positive another positive test 3/12 later confirms. Otherwise can measure Ab at 18/12 to confirm
Maternal: no treatment during pregnancy or rbeastfeeding. Can treat with Marivet afterwards (DAAT): 95% cure rate.
Influenza
A, B, c (A is the worst)
Orthomyxoviridae family
Pregnant women more at risk becasue of altered lung funciton, increased CO, increased oxygen consumption, alterations in immune function.
Doesn’t cross placenta but can cause congenital abnormalities (cleft palate, NTD, cardiac) or miscarriage, PTB, IUFD from the hyperthermia / maternal unwellness
Influenza vaccine safe in all trimesters (inactivated vaccine)
Maternal benefits: 50-80% reduced risk in influenza, 40% reduction in hospitalisation.
Fetal benefits: 27% reduced risk in stillbirth, 13% reduction in LBW / PTB,
Neonate: 40% reduced risk in infant death and hospitlisation from respiratory infections <3/12 of age
HIV
HIV1/2
Lentivirus
Retrovirus
Low rates in NZ / aus
Antenatal screening universal
- HIV Ab positive (ELISA then Western blot)
- If positive measure HIV RNA< CD4+ count, HIV resistance testing, full STI screen, FBC, U+Es, LFTs
- If positive need physician input, MTCT counselling.
- If negative but high risk recent exposure, remeasure 4/52
MTCT <2% if HIV RNA undetectable, on HAART, appropriate mode of delivery, formula fed baby with PEP
MTCT 20% if optimal measures not in place and 40% if breastfed
HIV+ and conceived on HAART with undetectable viral load at 36/40: vaginal birth fine, no need for IP zidovudine, formula feeding and PEP
HIV+ and naiive to HAART but needed for maternal health start ASAP (Zidovudine and lamivudine are most common combinaiton therapy). If VL <50 copies / mL at 36/40 as above
If VL >50 copies / ml but less than 400 copies / mL: Consider IP Zidovudine and CS at 38-39/40. Formula feeding and PEP
If >400 - IP Zidovudine and CS recommended 38-39/40. Formula and PEP
If naiive to HAARt but doesn’t need for own health still start pre 24/40
IF late presenter with no HAART
- Not in labour >28/40: Give HAART asap, IP Zidovudine, CS, formula, PEP
- If VL really high need extra combination therapy required
- If presents in labour at term: Start combination therapy asap. CS
If pre-term: Start HAART combination asap. Mode of delivery dependent on obstetric factors
Baby: PEP immediately, monotherapy if low risk, combination therapy if high risk. Serology follow up till 18/12. Formula feeding.
Malaria
4 subtypes
Transmitted by anopheles mosquito
1500 cases / year in UK, 0.5 - 1% mortality rate
Replicates in liver then comes out into blood and infects erythrocytes, which then stick to small blood vessels in brain, kindey, lungs etc. Interferes with microcirculation, flow and metabolism. Sequesters in the placenta and evades host defence mechanisms, splenic processing and filtration. This results in poor oxygen transfer and FGR, LBW. Can cross and infect fetus causing fetal anemia
Cyclical fevers, non specific unwellness. Severe malria: cerebral oedema, severe haemolytic anaemia, ARDS, coagulopathy, cardiovascular collapse, kidney failure, metabolic acidosis
Admit
- To ICU if severe
- Treat with quinine and clindamycin if not severe, artesunate if severe.
- Only delivery if fetal distress or failure to treat woman appropriately
- consider thromboprophylaxis if plt >100
risks
- Severe febrile illness: maternal and fetal mortality, SB, premature birth, miscarraige
- Parsitatisation: FGR, LBW, fetal anaemia
Pertussis
Bordetella pertussis
Highly infectious bacteria - gram negative coccbacilli
Babies are vaccinated 6/52, 3/12 and 5/12 of age.
Vaccinate between 20 -32 weeks (or anytime) but transfer of immunity occurs 2/52 form vaccination
Acellular vaccination, safe in pregnancy.
Recommend repeat vaccination in each pregnancy
Infectious until completed 5 days of antibiotics.
Zika
Flavivirus
Transmits via mosquito, or sex, vertical transmission, blood transmission
High endemic areas: south america, central america, africa, indonesia, part of SEA
Fever, arthralgia, headache, conjunctivitis, myalgia, rash etc…
No evidence pregnant women are more susceptible to the virus or seriousness of disease
Ix
<2/52 since exposure: RNA PCR urine and blood
>2/52 or negatibe RNA: test IgM. If positive confirm with PRNT. (+negative PRNT for dengue)
USS: microcephaly, intracranial calcifications, multiple other cranial abnormalities, oligohydramnios, talipes, FGR
~15% transmission of zika transplacentally.
First and second trimester much higher risk of congenital zika syndrome
4/52 USS
Consideraiton MRI
Consideration amnio if >20/40 and more than 5/52 and uncertain if condition secondary to Zika (although doesn’t confirm causality)
Pretravel: avoid travel to high risk areas
Travel: avoid mosquitoes, and UPSI
Post travel
- Avoid UPSI for duration of pregnancy or 6/12 if a male partner has travelled (Zika can live in sperm for up to 6/12)
- Avoid UPSI for 3/12 if both partners travelled
OK to BF
HSV
Risk of neonatal herpes - 3 types
- Eyes, skin, face only. 30% of cases. Good prognosis if treated
- CNS
- Disseminated
CNS and disseminated - 30% mortality with antivirals. 17% long term neurological sequelae
Congenital herpes VERY rare
50% HSV1, 50% HSV2 cause neonatal herpes
HSV in pregnancy
- Recurrent episode: ensure is not a new strain (swab and serology). If not a new strain, give suppressive therapy (e.g. valaciclovir 500mg BD 3/7). Suppressive therapy from 36/40. Time of labour speculum to ensure no active lesions. If active lesions 1-3% risk of transmission (HSV 1 15%, HSV 2 0.01%), individualised discussion. No active lesions NVB fine. Avoid FSE, instrumental, FBS
- New episode 1st and second trimester. Swab and serology. Given 5/7 valaciclovir 500mg BD and then from 36/40 . OK for NVB. As per recurrent episodes.
Screen for STIs
- New episode third trimester. Swab and serology. Give 5/7 valaciclovir and then from 36/40. Check serology 36/40 to ensure seroconverted, if seroconverted then NVB okay as long as no active lesions. If not, CS recommended as risk 25-50% of transmission.
- If primary episode within 6/52 of labour CS recommended
- If SROM with active lesions or primary episode within 6 weeks CS recommended
- If first episode in labour: CS recommended. If declines 20mg/kg aciclovir IV in labour.
- PPROM with first episode: MDT discussion. Given 24-48h aciclovir IV while steroids given
- PPROM recurrent episode: expectant management appropriate - give oral aciclovir 5/7 and then from 36/40
Risk mother getting unwell: disseminated HSV, hepatitis
Neonate:
- Low risk: swabs and PCR at 24h
- High risk (primary genital or systemic herpes close to delivery, or infant born through birth canal with active HSV disease to mother with no history of HSV): full septic screen and give aciclovir immediately from birth
Screening acronym for drinking too much alcohol
T = tolerance A = annoyance at others commenting on your drinking C = cut down - feel like you need to cut down E = eye opener (need a drink to start your day)
Factions of life affected by drug use in pregnancy
Social: homelessness, prostitution, violence, trauma, criminal activity, family disruption
Medical: infections, neurological, CVS, resp, mental health, poor nutrition / dental health / skin
Psychological: 60-80% psychiatric comorbidity, depression, anxiety, mania, drug overdose, abuse, low self worth, self harm, eating disorders, inability to care for children
obstetric risks: miscarriage, neonatal or IUFD, abruption, anaemia, needs for pharmacological alterations in birth and postnatally, congenital abnormalities
Neonatal: LBW, neonatal abstinence syndrome, increased risk of prematurity, increased NICU admission, child protection issues, SIDS
fetal alcohol syndrome
Triad - Facial characteristics - Growth retardation - CNS / brain abnormalities Difficulty transalting sensory modalities into action (e.g. reading into speaking), difficulty generalising information, difficulty perceiving similarities and differences
Also heart, kidney, hearing, eyesight, skeletal, immune system
Part of fetal acohol spectrum disorder (FAS, partial fetal alcohol syndrome, alcohol related birth defects, alcohol related neurodevelopmental disorder)
2/1000
SMoking and pregnancy
11% of Australians smoke
Carbon monoxide binds to Hb and diminshes oxygen carrying ability
Cadmium accumulates in placenta, is a carcinogen, and reduces fetal capillary volume
Nicotine interfers with amino acid transport across the placenta and results in LBW, PTB, IUGR
Also
- spotnaeous abortion
- ectopic
- Placental abruption
- PROM
- Behavioural problems
- Lung issues
- SIDS
- Altered critical autonomic reflexes
Cannabis and pregnancy
THC crosses placenta and is present at 10% higher concentrations in fetus than mother
Neurodevelopmental deficit
No effect on BW
No teratogenicity
Opioid use including heroin
Rapidly crosses placenta
Peaks and troughs in blood
Anaemia, IUGR, Preterm labour, decreased pain threshold, neonatal abstinence syndrome
Buprenorphine benefits and disadvantages. Cat C drug
Benefits
- Partial mu receptor agonist, so less likely to OD or have resp depression
- Neonates recover faster from neonatal abstinence syndrome
- Can BF
- Fewer drug interactions than methadone
Reduces preterm birth and low birth weight. Buprenoprhine better than methadone at this
Risks
- Hepatic dysfunction
lack oflong term data
Methadone
Binds to opioid receptors blocking them so no effect from other opioids
Also binds to NMDA receptors which contributes to pain relief. Stops craving and withdrawal symptoms
Dose needs to be icnreased in pregnancy
Interacts with lots of other drugs including antiretrovirals
Reduced preterm birth and low birth weight
Neonatal abstinence syndrome
High pitched crying, feeding issues, GI disturbance, irritability, yawning, sneezing, increased RR, low grade fevers, seizures, failure to thrive, death
Treat with liquid morphine
Severity doesn’t correlate with dose of Buprenorphine or methadone
Severity is reduced with rooming in, BF, skin to skin
Methamphetamine
increased synaptic dopamine, serotonin and noradrenaline and blocks reuptake Increased risk of psychosis Large cross into breastmilk Neurobehvioural difficulties Probably PTB and LBW rates higher
alertness, elevated mood, increased sustained attention, supressed appetite, increase HR and BP, MI, Arrhythmias, dilated pupils, sweating, hyperthermia, tremor, hyper-reflexic slurred speech, agitation, obsessive behaviour, delirium, psychosis
Cocaine
- Cocaine use can lead to placental abruption and fetal or neonatal cerebrovascular events. Appropriate consultation or referral is recommended o IUGR o Intrauterine hypoxia o Preterm labour o Placental abruption o IVH o Neonatal cerebral infarction o Brain lesions o NEC o Euphoria o Effects on dopamine receptors
Major risk factors for SGA and minor risk factors for SGA
Major
- Medical condition: SLE, APLS, Diabetes with vascular disease, hypertension, renal disease
- Maternal age >40
- Smoker >11 / day
- Bleeding heavy enough to be menses
- PAPP-A <0.4 MOM
- Paternal SGA
- Maternal SGA
- Previous SGA
- Previous stillbirth
- Cocaine
- Daily vigorous exercise
- Fetal echogenic bowel
Minor
- Previous PET
- Low fruit intake pre-pregnancy
- Age >35
- IVF
- Nulliparity
- > 60 months between pregnancies, <6 months between pregnancies
- Smoker 1 - 11
- BMI <20 or >25-35
Delivery rules SGA / FGR
SGA with normal dopplers - by 40/40 (RCOG says 37/40???)
Unless - >34/40 and static growth over 3 weeks.
Abnormal UAPI with positive end diastolic flow or abnormal MCA - 38/40
Abnormal UAPI with absent end diastolic flow and >32/40: by 34/40
Abnormal UAPI with reversed end diastolic flow: 32/40
<32/40 deliver when DV abnormal
(MCA: 55% risk CS)
(Very abnormal uterine artery dopplers, risk of delivery pre 34/40 is 60%)
TRUFFLE
Lancet 2015
Multicentre prospective RCT
500 women
Europe
26-32/40 with FGR (AC <10th with abnormal UAPI), >500g, no delivery plan or fetal anomly, normal DV and normal STV, no karyotype abnormlaity, >18y o
1:1:1 - STV (daily CTG) <3 (26-29), <4 (29-32), Early DV changes (>9th), Lat DV changes (absent or reversed A wave) - twice weekly scans
Safety: STV <2.6 or <3, maternal reason for delivery
Primary outcomes: survival at 2 years without cerebral palsy, neurosensory impairment or Bayley III score <85
Secondary outcomes: death or severe neonatal morbidity
No difference
If take away the deaths in favour of late DV changes
92% survival
2% IUFD
6% NND
Causes of oligohydramnios
Maternal: comorbidities such as PET, ESS HTN, collagen vascualr disease, nephropathy, thombophilia, or medications such as ACEI
Placental: Abruption, TTTS, Placental thrombosis or infarction
Fetal: chromsomal abnormality (T13 and triploidy most common), congenital abnormality (e..g urethral atresia, posterior urethral valves), growth restriction, infections, demise, ROM, Postterm pregnancy
Idiopathic
Management of oligohydramnios
<26/40: poor prognosis. 30% will have severe pulmonary hypoplasia, of which 70-90% will die.
26/40: canalicular stage of lung development, after which lungs are less sensitive to external pertubations
- If die likely from infection, cord compression or uteroplacental insufficiency which is causing the oligo
<20/40
Polyhydramnios causes
Fetal
- Anything that impairs swallowing: brain abnormalities (Dandy Walker, Anencephaly), facial tumours, GI obstruction (duodenal atresia, oesophageal atresia), large pulmonary abnormalities such as diaphragmatic hernia, CPAM
- Multiples: TTTS
- Anaemia: hyperdynamic circulation = increased uriantion
Maternal
- Diabetes
- Lithium use
- Infections: parvo, CMV, Toxo, Syphilis, Rubella
- Hypercalcaemia
Idiopathic: most common
AFI measurements
normal 8-24cm
Mild 25-30
Moderate 30-35
Severe 35
Overall perinatal mortality raised, 2-5 fold compared to normal fluid.
What does the ectoderm, mesoderm and endoderm form?
Ectoderm: skin, nervous system
Mesoderm: connective tissue, bone, muscles, urogenital organs, pleura, peritoneal linings
endoderm: lining of internal organs such as GIT and lungs
Formation of neural tube
Week 3 from conception neuralation starts. Ectoderm starts to form neural crest and neural groove (neurulation - stimulated by notochord). Folds over and forms neural tube by end of weeks 4. Rostral end closed by day 25. Caudal end by day 27.
Risk factors for NTD
Folate deficiency (poor diet, poor absorption, genetic factors that decrease absoprtion / metabolism, Folic acid antagonist (valproate, carbamazepine, methotrexate) Genetics Chromsomal abnormality Syndromes: T12, T18, limb body wall complex, triploidy, Meckel Gruber Fever Amniotic bands pregestational diabetes obesity (2 fold)
USS findings of spina bifida
Lemon sign: abnormal frontal bones Banana sign: hypoplastic cerebellum Ventriculomegaly Splayed lateral pedicles Bulge at lumbar spine- Talipes – movement problems -Scoliosis Direct signs: spine - Looking at vertebral bodies and cystic structure - Gibbus – sharp bend in spine – poor prognosis
Prognostic factors for NTDs
Presence and severity of brain signs Presence of other abnormalities: 20-30% Chromosomal / genetic abnormalities: T18 Gestation at delivery Birth weight Level of lesion In utero limb movements
Consequences of NTDs
Surgical
- Operation within first 24h
- Most need shunt < 1 year of age
Mortality
- 25% SB
- Can die in first year of life secondary to hydrocephalus or infection
- After first year most common cause of death renal failure
Mobility
- Depends on level of lesion
Intelligence
- Most normal or near normal
Continence
- 25% both continent
- 40-85% incontinent of 1
Sexual function can be altered
Psychosocial
- Most report good quality of life
Recurrence risk
<4% unless genetic component
HIGH folate next pregnancy and 12 and 16/40 USS
Affected parent or one siblibng 5%
two affected siblings 10%
NTDs prevalence
5-20/10,0000 births
Anencephaly PRE folate 1/1000
Anencephaly
Failure of rostral pore to close by day 25, results in no cranial ossification
Neural tissue exposed to CSF, necrosis occurs
Face normal
10% chromosomal abnormalities
50% other anomalies
Incompatible with life - IUFD, poly, preterm labour, NND
Recurrence
- 1 affected sibling 5%
- 2 affected siblings 10%
Reduced risk by 75% if folic acid
Echogenic bowel
Echogenic areas in bowel equivalent to bone
1% in second trimester (1st trimester can’t tell, 3rd trimester = not clinically significant)
Non specific USS finding
Can be associated with increased risk of chromosomal and non chromosomal fetal abnormalities (35%)
Possible pathology: inspissated meconium, decreased vascaulrity, bowel hypotonia, swallowed blood
3-25% risk of aneuploidy
CF - 3%
intra-amniotic bleeindg and swallowing of blood
congenital malofrmation of bowel: atresia, proximal obstruction, perforation, hirschprungs, meconium peritonitis
IUGR with increased risk perinatal morbdiity and mortality
congenital infection (CMV), Toxi
Anomaly scan Amnio (karyotype, PCR for virology, DNA analysis for CF) OR cfDNA Maternal virology screen - toxo, CMV prenatal CF screen for carrier status
Management
- if ruled out everything else increased fetal surveillance: monthly growth scans (increased risk of IUGR and IUFD)
choroid plexus cysts
Cysts in lateral ventricles >2mm 90% resolve by 26/40 Present in 2% of fetuses at 20/40 most spontaneously resolve and are benign associated with T18 and T21
When should you change LMP dates for EDD to USS EDD?
When varies by >4/7 from a scan performed 6-13/40 (most accurate time)
If cycle not regular
If LMP not certain
When would you expect to see a GS, YS and embryo? and FH
GS 5/40
GS+YS 5.5/40
GS + YS + emrbyo too small to measure 6/40
FH 6.5 - 7/40
(MSD + 30 = GA is 5-11/40)
(CRL + 42 = GA is 6- 9.5/40)
Fetal pole should grow by 1mm a day at 5 7 weeks
Miscarriage USS criteria
initial scan:
1. No FH when CRL >7mm
- no YS or embryo when MSD ≥25mm
On FU scan
- No FH when previously FH was seen
- MSD ≥12mm with no embryo and a repeat scan shows no embryo or yolk sac after 7 days
- CRL <7mm, no FH after 7 days
- MSD <12mm with no embryo and there is no yolk sac or embryo after 14 days
- If YS seen on initial scan but there is no embryo with a FH after 11 days
Miscarriage criteria
Initial scan
- CRL >7mm no FH
- MSD >25mm no YS
Repeat scan
- FH no longer when present earlier
- CRL <7mm, scan in 7/7 shows no FH
- MSD >12mm, scan in 7/7 shows no YS or embryo
- MSD <12mm, scan in 14/7 shows no YS or embryo
- MSD with YS, scan in 11/7 - no FH
When do you see lambda sign?
9-10/40
HC and BPD: what structures should be present for measurement of this?
CSP Falx Thalami No orbits No posterior fossa
AC: what should be on screen when measuring
Stomach Left and right portal vein continuous (J) one single rib No kidney No lung
FL: what should be on screen to measure?
cartilaginous femoral head and epicondyle
When does Ductus arteriosus close and what casues this to occur?
Day 2 of life
Senstivie to oxygen (low oxygen = PDA), PGs (high PGs = PDA) (PG concentration inversely proportional to O2), and bradykinins (increased as increased blood flow through lungs)
Fetal to adult structures in circulation
Fetus Adult
Ductus vensosus Ligamentum venosum
Foramen ovale Fossa ovalis
Ductus arteriosus Ligamentum arteriosum
Umbilical vein Ligamentum teres
Umbilical artery (2) Medial umbilical ligament (2) + superior vesical artery
Allantois Median umbilical ligament
Clinically significant antibodies in order for haemolytic disease of the newborn
D (15% of people are rhesus negative and 16% will make Ab if make a rhesus +ve fetus, with no intervention)
K
(E +c)
c
(Also duffy, jka, Kidd)
Kell kills becasue
- haemolysis from IgG Ab crossing the placenta
- Fetal bone marrow erythropoiesis suppression leading to aplastic anaemia - severe fetal anaemia can occur at even relatively low titres
Clinically significant Ab test every 4 weeks until 28/40 and then 2 weekly (D, K, c +/- E)
Other Ab retest at 28/40 unless hx HDFN
Referral thresholds to FMM for antibody levels
D: >4IU/mL (Refer at 1:16 to 1:32 depending on local threshold), >15IU/mL = risk fo severe HDFN
K: immediately
c: >7.5IU/mL (>20IU/mL = risk of severe HDFN
E: immediate if c present
Do paternal genotype or NIPT
If paternal genotype negative (i.e. dd or kk) no NIPT / testing required
If paternal genotype heterozygous need NIPt (>16/40 and >20/40 for K)
If paternal genotype homozygous then fetus is at risk of HDFN, refer to FMM for USS, MCA, +/- IUT
DELVIER 37/40 (39/40 if titre remains under critical titire)
Cord blood: Hb, DAT, Bili
Also refer to FMM if unexplained severe neonatal jaundice or anaemia requiring transfusion in last pregnancy
OR a history of HDFN or IUT or any of the Ab >1:32 titre, especially if rising
FMM will do weekly MCA PSV if above titre thresholds or K Ab. If >1.5MoM or other signs of fetal anaemia (poly, cardiomegaly, skin oedema) for invasive treatment - FBS and IUT
MCA PSV is predictive of moderate to severe anaemia with 100% sensitivity and a 12% False positive rate
After 36 weeks not as good.
Risk of fetal loss after FBS is 1-3%, higher if hydrops
If first pregnancy had severe anaemia, then just start doing MCA PSVs from 16-18 weeks as the Ab titres don’t reliably predict the severity of fetal anaemia. (OR 10/52 prior to poor outcome)
Fetal transfusion
- What are the important facts about it?
Give type O or ABO compatible if known Cross match compatible with maternal plasma and negative for relevant antigen. K negative to ensure no future issues <5 days old Citrate phosphate dextrose anticoagulany CMV seronegative Irradiated and transfused within 24h
WE are giving adult Hb which means it doesn’t bind oxygen as well!
Facts about anti D
reduced alloimmunisation by 78%
Give 1 vial for every 6 mL fetal RBC in maternal blood
If more than 2 vials needed disucss with transfusion specialist
Mechanism of action unknown: possible rapid clearance of anti-D coated D positive red cells by macrophages and down regulation of antigen specific B cells
Definition of hydrops
Accumulation of abnormal fluid in at least 2 different fetal compartments
- subcutaneous oedema
- pleural effusion
- pericardial effusion
- ascites
- placental thickening >6cm
- polyhydramnios
3 primary mechanisms
- intrauterine anaemia
- intrauteirne heart failure
- hypoproteinaemia
Poor prognosis, if born with hydrops 50% mortality
Worse prognosis if chromosomal abnormality, cardiac anomaly (100%), other structural anoamlies apart from chylothorax, GA <24/40
Causes of hydrops
90% non-immune
10% immune
C- chromosomal - Turners, T13, 18, 21, tuberous sclerosis, noonans
A - anaemia - FMH, rhesus isoimmunisation, parvovirus, alpha thalassaemia, G6PD, TAPS
U - unexplained - metabolic
S - Structural - Chest: CCAM, CDHB, chylothorax, hydrothorax, masses / skeletal dyplasia / GI and GU anomalies / Placental or fetal tumours
T - Twins - TTTS / TAPS
I - Infection - Parvovrius, coxsackie, adenovirus, STORCH (syphilis, toxo, others incl HIV, Zika, Rubella, CMV, HSV, Varicella
C - Cardiac - tachyarryhtmia, bradyarryhtmia, high output state, cardiac structural anomaly - 1/3 of NIH
Risk factors for placental abruption
Previous abruption - 4% risk if one previous abruption - 25% risk if 2 previous PET Polyhydramnios Multiparty AMA Bleeding first trimester Subchorionic haematoma first trimester IVF Non vertex presentations Low BMI Premature ROM abdo trauma Smoking and cocaine Thrombophilias
Risk factors for placenta praevia
Previous placenta praevia OR 9 Previous CS (background rate of 1%) - 1 = OR2 - 2 = OR4 - 3 : OR 22.4 Previous TOP Multiple pregnancy AMA Assisted conception Deficient endometrium: endometritis, MROP, curretage, submucous fibroid, uterine scar multiparity Smoker
Risks of unexplained APH or placental abruption in ongoing pregnancy
SGA / FGR
oligohydramnios OR 6.2
PROM OR 3.5
PTL / CS OR 4
Recommend serial growth USS and referral to clinic
What does FFP contain?
What does cryoprecipitate contain?
FFP: fresh frozen plasma: coagulation factors apart from platelets. Contains fibrinogen, albumin, protein C, protein S, antithrombin tissue factor pathway inhibitor
Cryoprecipitate: frozen blood product prepared from plasma. Contains fibrinogen, factor VIII, factor XIII, vWF and fibronectin
GIVE
- 4U FFP for every 6U of RBC or if APTT 1.5 control
- platelets if plt count <50
cryoprecipitate if fibrinogen is <1g/L
Goals - Hb >80 Plt >75 PT <1.5 APPT <1.5 fibrinogen >1
What is the incidence of placenta praevia?
Management
1:200 - increasing possibly because of CS rate and ART
TVUSS 93% PPV, 97.6% NPV
90% of LLP will hav resolution by term
cervical length screening can be done to estimate risk of preterm delivery and bleeding at EMCS
More bleeds = more likely to have EMCS
3 or more APH OR 2.53
Management
- Steroids at 34 - 35+6/40 routinely and prior to 34 weeks in cases of higher risk of preterm birth
- No good evidence re outpatient vs inpatient monitoring: multiple APH likely inpatient better. OR of requiring EMCS much higher
- timing of delivery
- 34 - 36+6 if vaginal bleeding or risk factors for PTB- 36 - 37 if uncomplicated placenta praevia
- Risks of bleeding associated with placenta praevia - 5% 35/40, 15% 36/40, 30% 37/40, 60% 38/40
- Cross match blood. RR of PPH is 4. Higher is pre op anaemia, MgSO4 use, diabetes, thrombocytopaenia.
- Weekly G+H
- Regional anaesthesia
- Consider vertical skin and / or uteirne incision when fetus is transverse lie to avoid the placenta, particularly <28/40
Placenta accreta / increta / percreta definition
Mortality rate
Risk factors
Accreta: to endometrium basalis
Increta: through endometrium basalis into myometrium
percreta: through into serosa, sometimes into surrounding pelvic organs
Mortality 7% in 1990s, now less
1/3 to 2/3 of cases not diagnosed pre delivery
Risks
- Previous accreta 4% no CS, 50-67% 3 or more CS
- Previous CS delivery RR 7
first CS 0.24%, second 0.31%, third 0.6&, fourth 2%, fifth 2.3%, sixth 7%
other uterine surgery
repeated endometrial curretage
placenta praevia
- huge increases with each CS. 1 = 3%, 2 = 11%, 3 = 40%, 4 = 61%, 5 = 67%
Maternal age
ART
MROP
PP endometritis
myomectomy
bicronuate uterus, submucous fibroids, adenomyosis
USS findings in accreta
Loss of clear zone abnormal placental lacunae - most common. With large feeding vessels bladder wall interuption myometrial thinning placental bulge - deviation of uterine serosa away from expected plane focal exophytic mass Uterovesical hypervascularity Subplacental hypervascularity Bridging vessels
Delivery for placenta accreta spectrum
no other risk factors for PTB 35 - 36+6
Slightly earlier if think major blood loss suspected
Approach
- CS hysterectomy
- If extent of placenta accreta is limited in depth and surface area and the entire placental implantation area is accesible - can do uterus preserving surgery, including partial myometrial resection. This results in secondary hysteretomy in 30% and 4% deaths. 77% had a further pregnancy
Insufficient data to recommend ureteric stents routinely
Four approaches
1. Primary hysterectomy following delivery of fetus without attempting placental separation
2. Delivery of fetus, avoiding placenta, with repair of incision leaving the placenta in situ
3, Delivery of fetus without disturbing the placenta, followed by partial excision of uterine wall and repair of uterus
4. Delivery of fetus without disturbing the placenta and leaving it in sity, followed by secondary hysterectomy 3-7 days later
if percreta into bladder: ureteric stents recommended.
DONT GIVE ECBOLIC
Risks of expectant management of placenta accreta - i.e. leaving placenta in situ
Risks - 58% will need a hysterectomy haemorrhage infections and sepsis and peritonitis necrosis fistula injury to adjacent structures pulmonary oedema acute renal failure DVt PE DIC
RANZCOG: 2/3 will avoid hysterectomy. 17-29% recurrence of PAS.
Types of vasa praevia
Type 1: associated with velamentous cord insertion. Velamentous cord: umbilical cord inserts into fetal membranes coursing through membranes to the placenta (between amnion and chorion). No Wharton’s jelly. Risk of rupture.
Type 2: vessel connects the placenta with a succenturiate lobe or accessory lobe
USS definition: vessel running in the free placental membranes within 2cm of the cervix
If ruptures fetal mortality is 60% despite urgent CS
1/1200 - 5000 pregnancies
Total blood of fetus is 80mL/kg
Survival rates 97% if diagnosed antenatally and 44% if diagnosed during delivery
<2cm from internal os
Resolves in 20% of cases diagnosed in second trimester
Repeat scan at 32/30
Defintion of marginal cord insertion
Cord inserting within 20mm of placental edge
- 7% of pregnancies
25% of twin pregnancies (MC more likely)
Management of vasa praevia
Admission from 30-32/40 (particularly if high risk factors: multiple pregnancy, antenatal bleeding, TPTL)
Data on TVUSS cervical measurements is limited and role of cervical cerclage is unknown
Delivery: 34-36/40 ELCS
Steroids 32/40
Management of PPROM evidence
3% of pregnancies, associated with 40% of PTB
Causes of death: prematurity, Sepsis, pulmonary hypoplasia, cord prolapse, abruption
Median latency 7/7 to delivery
Observe for signs of clincial chorio
don’t do weekly swabs (25% FP)
Repeat WCC and CRP - WCC will raise 24h post steroid and should be back to normal within 3/7 (twice weekly as OP)
Fetal tachycardia predicts 20-40% of chorio, FP rate of 3%
Erythromycin ethylsuccinate: 400mg QID 10/7. Evidence in cochrane: chorio RR .66, babies born in 48h RR 0.7, babies born within 7/7 RR .8, neonatal infection, surfactant use, oxygen therapy and abnormal cerebral USS reduced. No difference in perinatal mortality. USe penicillin if allergy to erythromycin
Corticosteroids from 24 to 35+6. Meta-analysis: RDS RR 0.8, IVH RR 0.49, no difference in NE, neonatal sepsis, apgar scores.
Tocolysis not recommended - not shown to improve outcomes in cochrane. may worsen outcomes
MgSO4 if <30/40
NICU invovlement
OP care vs IP - cohort studies no difference
Popular to offer weekly AFI and dopplers and growth every two weeks: RCTs don’t show any evidence for this
Emotional support: PTSD more common in women whose pregnancies are complicated by PPROM
Offer IOL at 37/40 (Cochrane review of >3600 women compared planned vs expectant delivery - no difference in neonatal sepsis or infection, increased rates of RDS and CS in planned delivery pre 37. no difference in overall mrotality.
No role for amniocentesis
Amnioinfusion not recommendedyet but is associated with improve fetal artery pH at delivery, death, sepsis, pulmonary hypoplasia and sepsis. Cochrane
If GBS positive offer IOL from 34/40.
See in preterm clinic next pregnancy (RR 0.8 PPROM in next pregnancy)
ORACLE 1 Landmark
Lancet 2001
Kenyon et al
Analysing broad spectrum antibiotic use for women with PPROM <37/40
4800 women
Randomised to erythromycin + placebo vs erythromycin + augmentin vs Augmentin + placebo vs placebo x 2
Primary outcome
- Composite of neonatal death or severe neonatal disease (respiratory or cerebral)
Secondary outcome: lots. Such as number delivered in 48h, number delivered in 7/7, RDS, NEC, birth weight, days in hospital, surfactant use, oxygen use etc. etc.
Results
Both Augmentin and Erythromycin decreased the primary outcome but wasn’t SS
Both Augmentin and Erythromycin significantly decreased number birthed within 48h, and 7/7
Augmentin 4 x risk of NEC
Both decreased chorio, neonatal infection, surfactant use, O2 use, cerebral USS abnormal results
Impression
- Erythromycin decreases composite primary outcome and prolongs gestation
- Avoid Augmentin - NEC x 4 fold.
Limitations
- No data collected on past obstetric history, other fetal or maternal disease
Earliest gestaion not specified
uncertain long term imapcts
Strengths
- LArge multicentre RCT blinded trial
Not many lost to FU
Erythromycin cheap and widely available
ORACLE II
Lancet 2008
Kenyon et al
7y FU from ORACLE trial to assess any long term benefit or adverse outcomes
75% response rate, retrospective cohort trial
Primary outcome: presence of functional impairment from a validated questionaire. Asked questions concerning hospital admissions, respiratory symptoms, neurobehavioural questions, medical conditions, convulsions
No change in primary outcome for any of the groups
No difference in death, neurobehavioural outcomes, CNS / developmental issues, diabetes, bowel issues
Strengths
- Large cohort
- Good response rate
- Validated standardised quesitonairre used
No difference in response rate between groups
Limitations
- Recall questionaire from parents. Relies on parents understanding of childrens medical conditions
- Under-represented were those from lower socioeconomic class
PPROMT
Lancet 2016
Morris
RCT, blinded to assessors, ITT
1800 women
9 year study period
Included if PPROM 34-36+6
(included into study if ROM prior to 34/40 and made it to 34/40_
Randomised 1:1 to immediate management vs expectant and IOL after 37-38/40
Primary outcome: neonatal sepsis: no difference
Secondary outcome
- Neonatal morbidity: increased RDS in immediate, increased NICU stay in immediate, increased CS in immediate
- Maternal morbidity. Decreased fever in immediate, decreased hospital stay in immediate
Interpretation: expectant better to reduce prematurity complications
Limitation: 9 yr study design, women not blinded, hospital polices differed
Strengths: RCT, multi centre, assessors blinded
Mechanisms of preterm labour
- Cervical incompetence
- Decidual haemorrhage e.g. abruption, uterine overdistension such as poly or multiples
- Uterine distortion e.g. mullerian abnormalities, fibroid uterus
- Cervical inflammation e.g. BV, trich etc
- Maternal inflammation / fever e.g. UTI
- Hormonal changes - maternal or fetal stress mediates this
- Uteroplacental insufficiency e.g. HTN, IDDM, drug abuse, smoking, alcohol consumption
- Genetic predisposition 3 genes associated with PTB
- Fetus recognizes a hostile environmental and activates the fetal-placental parturition pathway
Microbial induces intra-amniotic inflammation, decidual haemorrhage or vascular disease, decidual senescence secondary to poor implanation, disruption of maternal fetal tolerance with allograft rejection, decline in progesterone action, etc
Fetal fibronection
- What is it?
Extracellular matrix glycoprotein that sits between chorion and decidua - glue that holds pregnancy to uterus. Present in very low levels in cervicovaginal secretions >22/40, <50ng/mL. Very high levels in amniotic fluid.
- NPV = 99.5%
- Sensitivity 56%
- Specificity 84%
Cervical length and risk PTB - RANZCOG
30mm 10th centile RR 3.8
27mm 5th centile RR 5.4
22mm 2.5th centile RR 6
>25mm = 1% <15mm = 4% <5mm = 78%
Cerclage RANZCOG stats to prevent PTB depending on risk factors
When should we offer one?
RR 0.74 if short cervix
RR 0.64 if short cervix and previous PTB
RR 0.57 in those with short cervix and midtrimester loss
Offer if
- ≥3 previous PTB <33+6/40 and / or second trimester losses
- USS indicated: women with one or more spontaneous PTB (<33+6) or second trimester loss AND cervical length ≤25mm before 24/40
Risks
- Uterine contractions, bleeding, infection, miscarraige, preterm labour, CS
Progesterone MOA
Decreases oxytocin receptors
Decreases sensitivity to oxytocin
Increases prostaglandin dehydrogenase which decreases prostaglandins
Decreases repsonse to prolabour genes such as connexin 43
Evidence for progesterone in various settings throughout pregnancy
Luteal phase progesterone supplementation to promote fertility and prevent miscarriage: heterogeneity in evidence
Unselected population: no evidence
Threatened miscarriage: preliminary evidence RR 0.53
Unexplained recurrent miscarriage: PROMISE trial no difference
Assisted reproductive techniques: yes
Asymptomatic short cervix <25mm in mid trimester: yes
Previous PTB: consider
FONESCA 2003
RCT, placebo controlled, double blinded
Tertiary medical centre in Brazil, high rate of PTB
High risk singletons included if at least one spontaneous PTB, previous prophylactic cerclage and therefore inferred incompetent cervix, uterine malformation
100mg PV suppository between 24-34/40
Swabs at entry and UA monitoring each week
ONLY 157 women
Primary outcome: PTB <37/40 or PTL
Half the rate of PTB - significant
Tocolysis worked better for progesterone group by >twice - delayed PTB rate <37/40
Small sample size
Very high preterm birth rate
Women had extensive follow up
Women had vaginal infections treated
FONESCA 2007
NEJM 2007
Multicentre, double blinded, RCT
Aim: does progesterone pessaries reduce risk of PTB pre 34/40 in asymptomatic women with demonstrated cervical shortening on mid-trimester screening
Singleton or twin pregnancies, with routine anatomy scan TVUSS cervical screening showing length <15mm
Exclusions: major fetal anomaly, painful contractions, SROM, cerclage
Progesterone PV vs placebo 24 - 33+6
Outcome spontaneous PTB <34/40
Secondary outcomes: neontal morbidity and LBW
Screened 25,000 women and entered 250 women
Outcome: OR 0.56 of PTB <34/40, significant
Progesterone protective against neonatal morbidiyt but not statistically significant
no significant difference in twins but only 26 pregnancies included
Limitations: no comment on IOL if SROM, insufficiently powered to detect secondary outcomes, relies on USS assessment
Strengths: blinded, RCT, no loss to follow up, good treatemnt adherence
PROGRESS trial (not landmark)
Progesterone pessaries do not reduced RDS or other respiratory complications in women with a history of previous PTB
787 women
ROMERO et al. Meta-analysis including OPPTIMUM trial
Obstetrics and gynaecology magazine
RCTs comparing progesterone use vs placebo for women with a singleton pregnancy and a mid trimester cervical length <25mm
Primary outcome: PTB <34/40 or fetal death
5 trials
RR 0.66
RANZCOG quotes this study in their cervical length guideline. says progesterone decreases delivery pre 34 weeks and fetal death by 34%
No significant difference in neurodevelopmental outcomes at 2 years of age
RANZCOG recommendations cerclage and progesterone
Progesterone for asymptomatic women with cervix <25mm and consider progesteorne if singeltone pregnancy and history of PTB
OPPTIMUM
Lancet 2016
Does progesterone effect long term neurodevelopmental outcomes for children at 2 years.
Double blinded, multicentre RCT, placebo controlled
progesteorne 200mg daily from 22 - 34/40
Recruited if previous spontaneous PTB <34/40, cervical length <25mm, positive FFN and risk factor
Primary outcomes
- Fetal death or birth pre 34/40, death, brain injury, standardized cognitive score at 2 y
OR was in direction of benefit but wasn’t significant for any of the outcomes
No differences in safety or long term harm
EPPPIC trial 2021 lancet
Meta-analysis of individual participant data from RCTs - evaluating progestogens for preventing ptb
Systematic review of RCTs comparing vaginal progesterone, IM progesterone or oral progesterone with control or with each other in asymptomatic women at risk of PTB
Outcomes evaluated were PTB, early PTB, midtrimester birth,
Adverse neonatal sequelae
31 trials
Vaginal progesterone and IM progesterone both reduced birth before 34 weeks in high risk singeltons
Absolute risk reduction greater in women with a short cervix
Oral progesterone. insufficient evidence to support its use
Pessaries to prevent preterm birth
- MOA
- Trials
MOA: alters axis of cervical canal and displaces the weight from the uterus away from the cervix. Obstructs the cervical os and protects from ascending infection
Goya et al, lancet 2012. <25mm cx RCT. PTV <34/40 OR .18
Nicolaides 2016 NEJM. No difference.
Summary of evidence for cerclage vs pessary
PTB: Not cerclage unless ≥2 (≥3 at CDHB), offer surveillance, No to progesterone
Short cervix, no hx PTB: progesterone, no cerclage unless VERY short
Short cervix, hx PTB: Cerclage especially if cx <15mm, maybe for progesterone
Asymptomatic cervical dilation: cerclage. no progesterone
RANZCOG guideline for measurement of cervical length for prediction of PTB Nov 2021
Challenging
Recommend universal TAUSS for screening of cervical length and if <35mm for TVUSS or for those whose cervix cannot be clearly seen
7% of pregnancies in Australia and NZ occur pre 37/40, 3% pre 34/40
70% of total perinatal mortality from this
2/3 of women have no risk factors
TAUSS with full bladder, use cut off of >35mm because often overestimate length. this has a 96% sensitivity for detecting cx length of 25mm. Specificity low
10th centile = 30mm = RR 4
5th centile = 27mm = RR 5
2.5th centile = 22mm = RR 6
Published data for cost effectiveness in NZ and Australia is lacking but several US studies have shown to be a small increase in overall medical costs
Australia has implemented this universal screening
NZ has not yet offered it - progesterone funded for cervical length <25mm and hx of PTB ≤28/40
CIN is an independent risk factor
- Cone: RR 4.5 <28/40, 3 <32/40, 2.7 <37
- LLETZ RR 3 <28/40, RR 2 <32/40, RR 1.5 <37/40
Cochrane evidence for corticosteroids
Reduces perinatal death , neonatal death, RDS, IVH, developmental delay. No effect on BW
No difference in maternal outcomes
(GIVE <34+6)
Respiratory distress syndrome pathogenesis
Hyaline membrane disease
Prematurity = surfactant deficiency and structurally immature lung.
This results in atelectasis, which results in V/Q mismatch, hypoxia, hypercapnia, hypoventilation.
This results in a respiratory acidosis and hypoperfusion which results in a metabolic acidosis. this results in further reduced surfactant production. Also pulmonary vasoconstriction which increases R heart pressure, pushes r –>L shunt of blood through FO and DA.
Pulmonary vasconstriction as well as barotrauma and high fraction of inspired ocygen also results in capillary leakage, inflammation of alveoli, further decreasing surfactant production and inactivating surfactant from plasma inhibitors.
Proteinaceous exudate ++ in alveoli = RDS.
Lung injury = chronic lung disease
ACTORDS - Landmark
Lancet 2006 RCT
Use of repeated doses of corticosteroids for women at risk of PTB, and neonatal outcomes
NZ and Australia
Crowther et al
1000 women
Placebo or steroids
Women who had received 2 doses of corticosteroids >7/7 prior and are still at risk of PTB, without any contraindication
Rescue dose given weekly until 32/40 or birth if considered still at risk
Primary outcomes: RDS, intubation, oxygen use, weight at hospital discahrge
Secondary outcomes: chorio, neonatal morbidity
Reduction in RDS
Reduction in severe lung disease and no lung disease
No other differences
Safe to give - no short term harm
(FU 2y: NEJM 2007, crowther et al. possible difference in attention problems, otherwise nill differences between groups
