Maternal medicine Flashcards
Types of thrombocytopaenia in pregnancy
75% gestational
-natural fall in pregnancy: dilutional, increased destruction across placenta
- usually >100, can be >70
15-20% PET/ HELLP
<5% AFLP
Differential diagnosis thrombocytopaeni in pregnancy
Gestational - usually >100, normalises post pregnancy
Immune thrombocytopaenic purpura - diagnosis of exclusion. Normal BMAT and absence of other causes. Chronic: sx of menorrhagia/ bleeding episodes/ purpuric rash
HTN related
DIC
Sepsis
Antiphospholipid sx/ SLE
Viral infection
Drug-related (e.g. unfr heparin)
Test panel in thrombocytopaenia
U&E, including urate
LFTs (+ LDH if haemolysis suspected)
Clotting time, FDP and fibrinogen
Antinuclear Ab, anticardiolipin, lupus anticoagulant
Virology screen - TORCH, HIV, malaria
Management of thrombocytopaenia in pregnancy
Monitor plt at least monthly and on admission in labour
- <80: check BP, urine, PET bloods, blood film, refer to haem, anaesthetic r/v
- <50: above but urgently
Antenatal rx:
- steroids: trial if 50-70. Usually work within 7-14/7
- IVIG works within 48hours if not sustained
- cyclosporin
- Check renal fx and monitor fetal growth (FGR with steroids)
- platelet transfusion (may cause antibodies, avoid if possible)
Delivery in thrombocytopaenic pt
XMatch and plts on hold
Aim for plt count >50 for delivery
If for spinal - inform anaesthetics
Avoid kiwi and FBS
Neonate: if maternal plt <80, cord bloods for plt count (D1 & 4), hold IM vit K
Postnatal: check plt at D6 and 6/52 postpartum
Immune/ idiopathic thrombocytopaenic purpura incidence and MOA
Chronic condition
0.1-1/1000 pregnancies
3% of thrombocytopaenia
Ab to platelet surface glycoproteins
Management of ITP
Monitor
1st: prednisolone 20mg dly (low to reduce GDM/ PPP)
2nd: no response to pred –> IVIG
Delivery: plt close to 50, should have plt on standby
- epidural threshold usually 80
Neonatal:
- AN IG can cross placenta, risk of ICH. Cord sampling D1 and D4
- avoid IM vit K
Diagnosing HELLP
Bloods: microangiopathic haemolytic anaemia, thrombocytopaenia, raised LDH, raised bilirubin and abnormal LFTs
Incidence of DIC in HELLP
approx 20%
Management of HELLP
Delivery
If DIC: FFP +/- cryoprecipitate
May worsen in first 24-48 hours then improve
Incidence of thrombotic thrombocytopaenic purpura
1 in 25000
Diagnosis of TTP
Microangiopathic haemolytic anaemia, thrombocytopaenia, neurologic sx
Aetiology of TTP
Severe vWF cleaving protein ADAMTS 13
Acquired with autoantibodies or congenital deficiency (microthrombosis)
Management of TTP
Plasma exchange to remove antibodies
1-1.5l FFP
Incidence of obs chole
0.7% gen population
1.2-1.5% asian population
Typical timing of onset obs chole
Third trimester
Which patients have a higher incidence of Obs Chole
Prev hx
CLD
Hep C
AMA
Fam hx
Symptoms of obs chole
Itch
Dark urine
Steatorrhoea/ pale stools
Jaundice
Atypical features of obs chole
Elevated ALT/ AST
Early onset- T1/T2
Rapidly progressive
Liver failure
Delayed resolution
Diagnosis and grades of obs chole
Diagnosed on hx of gestational pruritis, abnormal LFTs and BAs >19
Gestational pruritis: itching + peak BA concentration<19
Mild ICP: itching+ BA 19-39micromol/L
Mod ICP: itching + BA 40-99 micromol/L
Severe ICP: itching + BA >100
Maternal risks assoc w obs chole
Higher risk PET (3.4 - 12.2%)
Higher risk of GDM (5.9 - 13.%)
Increase in hepatobiliary disease later
Fetal effects related to obs chole
Increased risk SB
- Only in population w BA>100
- Risk of SB when BA 19-39: same as general population
- Risk of SB when BA 40-99: same risk until 38-39/40
- presence of other RF (PET/ GDM) increase r/o SB
- higher risk of SB if twin + ICP
Preterm delivery - iatrogenic d/t IOL
Inc risk of mec and fetal distress, NICU
Management of obs chole
Monitoring:
- bloods every 1-2/52
— mild: weekly approaching 38/40
— mod: weekly approaching 35/40
— severe: further testing +/- hepatology r/v
- Monitor FM
Topical emollients
Antihistamines - chlorphenamine
Ursofalk- no evidence of benefit
Delivery timing in obs chole
Mild: delivery at term
Mod: IOL 38-39/40
Severe: 35-36/40 w CEFM
Postnatal follow up in obs chole
Bloods 4-6/52
Hepatology if non-resolving or symptomatic
Inc chance of recurrence in future pregnancy
- LFTs and BAs at booking
Classification of liver disease in pregnancy
Pregnancy-related:
- Hyperemesis gravidarum
- PET
- ICP
- HELLP
- AFLP
Non pregnancy-related:
- Pre-existing liver disease
— cirrhosis + portal hypotension
— Hep B, C, E
— NAFLD
— Wilson’s disease
— AI liver disease
- Co-incident with pregnancy:
— Viral hepatitis
— Biliary disease (cholelithiasis, PSC)
— vascular alterations (eg Budd-Chiari syndrome)
— DILI
— liver transplant
Deranged LFTs in HG- incidence, onset, ix, rx, cx
0.3 - 3.6%
Onset T1/2
Ix: normal bloods & USS
Rx: supportive, anti-emetics, vit supplements
Cx: hyponatraemia, encephalopathy
Deranged LFTs in ICP: incidence, onset, ix, rx, cx
0.1 - 5%
Onset: T2/3
Ix: bloods- clotting prolonged, USS- exclude cholelithiasis
Rx: antihistamines, emollients, monitoring
Cx: PTL, SB
Deranged LFTs in PET. - incidence, onset, ix, rx, cx
5-10%
Onset> 20/40
Ix: proteinuria, bloods: haemolysis, thrombocytopaenia, inc LDH, r/o DIC, aki. USS: hepatic rupture, haematoma, infarcts
Rx: anti-HTN, MgSO4, delivery
Cx: eclampsia, mortality
Deranged LFTs in HELLP - incidence, onset, ix, rx, cx
0.2-0.6%
Onset: T2/3, postnatal
Ix: proteinuria, bloods: haemolysis, thrombocytopaenia, inc LDH>600, risk of DIC, AKI. USS: hepatic rupture, haematoma, infarcts
Rx: anti-HTN, MgSO4, delivery
Cx: liver rupture, mortality
Deranged LFTs in AFLP- incidence, onset, ix, rx, cx
0.01%
Onset T2/3, postnatal
Ix: proteinuria, bloods: thrombocytopaenia, inc LDH, prolonged PT/APTT, hypoglycaemia, AKI. USS: normal, looks brighter
Rx: correct coag, rx hypoglycaemia, delivery
Cx: fulminant liver failure, mortality
Swansea criteria for dx AFLP
6+ of the following in the absence of another explanation:
- vomiting
- abdo pain
- polydipsia/ polyuria
- encephalopathy
- high bilirubin. (>14)
- hypoglycaemia (<4)
- high uric acid (>340)
- Leucocytosis (>11)
- ascites or bright liver on ultrasound
- high AST/ ALT (>42)
- high ammonia (>47)
- renal impairment, creat > 150
- coagulopathy (PT> 14 sec, APTT> 34 sec)
- microvesicular steatosis on liver biopsy
Incidence of liver disease in pregnancy
3-5%
Rx Wilsons disease in pregnancy
Penicillamine, zinc
Rx biliary disease in pregnancy
ERCP if severe - biliary pancreatitis, symp choledocholithiasis, cholangitis
- endoscopy safe but defer to T2
Lap chole if severe sx cholecystitis
Rx AI hepatitis in pregnancy
Steroids
AZA
Mx liver masses in pregnancy
Asymptomatic haemangioma: no monitoring
Adenomas: monitor and if >5cm, refer for resection
Reduction in transmission of hep B with appropriate intervention
90-95%
Modifications in intrapartum monitoring with hep B
Minimise direct exposure
Avoid invasive monitoring
Neonatal hep B immunisations
Mother HbsAg +ve: hepB immunoglobulin and hep B vaccine ASAP, w/in 12 hours of delivery
Hep B results interpretation
HBsAG -ve, anti-HBc -ve, anti-HBs -ve = susceptible
HBsAG -ve, anti-HBc +ve, anti-HBs +ve = immune due to natural infection
HBsAG -ve, anti-HBc -ve, anti-HBs +ve = immune d/t vaccination
HBsAG +ve, anti-HBc +ve, IgM anti-HBc +ve, anti-HBs -ve = acutely infected
HBsAG +ve, anti-HBc +ve, IgM anti-HBc -ve, anti-HBs -ve = chronically infected
When to test for Hep C
HIV+
Hep B +ve
Risk factors: recreational drugs, tattoos, partner w Hep C
Risk of HIV transmission when on ART and VL suppressed
1 in 1000
Antenatal monitoring in HIV +ve
MDT
Refer to HIV service ASAP, full STI screen
Assess for co-infection
Late bookers: urgent HIV test, start ART immediately
Start ART immediately after T1
Combined screening/NIPT, avoid/ minimise invasive testing
If invasive testing required - ideally VL<50
Blood monitoring antepartum in HIV
If conceived on ART:
- min CD4 count at baseline and delivery
If started in pregnancy:
- CD4 count at start
- every 2-4/52 post starting
- Every trimester, 36/40 and delivery
VL monitoring:
- if <50, check adherence, test for resistance, optimise regimen +/- therapeutic level monitoring
Modifications in intrapartum management of HIV+ve mother
Avoid ARM, FBS
Limit ROM - w/in 24 hours
Oral ART during labour
Zidovudine no longer necessary if VL suppressed
IV zidovudine:
- PTL/ PROM < 37/40
- receiving ZDV monotherapy
- 36/40 and VL>40
- <4/52 ART
- Non-adherent to rx
- ELCS
MOD in HIV +ve mother
Determined by 36/40 VL
<40 - SVD
40-400 - guided by RFs. Duration of AN ART, VL response to ART, maternal adherence
>400 - ELCS at 38-39/40
Neonatal ART prophylaxis
4/52 ZDV if virally suppressed
Otherwise:
Triple therapy (4/52 zidovudine + lamivudine, + 2 doses NVP w/in 48-72 hours)
Breast feeding advise HIV +ve mothers
Avoid, recommendation is formula feeding
Risk on ART: 1% at 6/12, as low as 0.3-0.6% at 1 year if continue ART
Increased r/o transmission if detectable VL, advanced disease, longer duration of feeding, breast/ nipple infection, infant mouth/ gum infection
Can offer cabergoline to suppress lactation
Monitoring HIV +ve mums & babies if BF
Monthly maternal VL
Infant monthly testing for duration of BF and 2/12 post cessation
Postpartum cardiomyopathy defn
dilated cardiomyopathy of unknown origin
Occurs in final month to 5 months PP
Absence of any other identifiable cause of HF
LV systolic dysfunction w LVEF <40% with or without LV dilatation
** leading cause of direct and overall maternal death
Morbidity assoc w PPCMO
5-7%
Incidence of PPCMO
1 in 1000-4000
Highest incidence in Nigeria and Haiti
<0.1% patients
Risk factors for PPCMO
Multiparity >4
Multiple pregnancy
Obesity
Chronic HTN/ PET
Cocaine abuse
PET (22% women w PPCMO)
AMA>30
Pathogenesis PPCMO - 3 theories
2hit hypothesis
- genetic predisposition + vascular hormonal insult
- a vascular input secondary to hormonal effects of advanced pregnancy
Theories
- excessive prolactin excretion, viral myocarditis, abnormal immune response to pregnancy, stress-activated cytokines, maladaptive response to haemodynamic changes in pregnancy, prolonged tocolysis
Vasc hormonal models:
- STAT3; prolactin secretion
Symptoms of PPCMO
Dyspnoea
Orthopnoea
Unexplained cough
Palpitations
Dizziness
Leg swelling
Weight gain
Abdo discomfort - hepatic congestion, praecordial pain
Clinical findings in PPCMO
Sinus tachy
Raised JVP
Hypoxia
Lung creps
Third HS
Displaced apex
Arrhythmias - AF, flutter, VT
Differential diagnosis PPCMO
VHD
ACS
CAD
PE
AFE
Onset of PPCMO
78% 4 months after birth
9% last 2/12 of pregnancy
13% prior to a month before or 4 months after delivery
Less common <36/40
Ix and findings in PPCMO
ECG: non-specific, sinus tachy, LVH
Labs: BNF, FBC, troponin
CXR: alveolar shadowing, septal lines, cardiomegaly, pulm oedema, pleural effusion
ECHO:LVEF<45%, LVED diameter >6cm, global dilation, hypokenises, valvular dysfunction
Cardiac MRI: cardiac tissue injury
Endomyocardial biopsy: rare
ECHO findings in PPCMO
Severely impaired LV systolic function
LVEF = 20% at most
LV wall motion is globally hypokinetic
LV severely dilated at 6cm
Severe, wide, turbulent jets of mitral and tricuspid regurg
Marked bi-atrial enlargement
Management PPCMO
As for CHF:
- diuretics, B-blockers, hydralazine and nitrates, dig, anti-coags
- avoid ACEI/ARBs in pregnancy
O2
Optimise preload
Haemodynamic support w inotropes and vasopressors
Relief of symptoms
Institute therapies for LT outcomes
ECHO every 6/12
CVS changes in pregnancy
Increase in blood volume
Increase HR
Increase CO
Changes peak at 28-32/40
Implications and causes of mitral stenosis
Causes: rheumatic fever
Obstructs LV inflow
Severe MS–> decreased CO, increased LA volume, LA pressure, pulm congestions and HTN, R-sided dilatations
CVS changes with MS
Mild- normally tolerate pregnancy well
Can cause decompensation of previously asymptomatic MS
Prepregnancy counselling in pts w MS
Optimise MS
Correction- surgery or percutaneous intervention (intervention after 4th month if not optimised before)
Cardiology input+ ECHO
Control tachycardia - increased HR increases pressure on valve. Rx w beta-blockers but ARDS= fetal brady and IUGR
Antepartum monitoring in pt w MS
MDT
Cardiology
Anaesthetics
Cardiac exam: MS murmur diminishes in pregnancy (decrease in regurg volume caused by reduction of SVR)
Serial USS: inc risk of IUGR
Fluid monitoring
Red flags- HF symptoms
Intrapartum monitoring/ management of pt w MS
Mortality greatest intrapartum and PP - sudden increase in preload –> pulm oedema
Symptomatic severe MS= high risk of pulm oedema during SVD. Advise planned elective CS
Mild MS: SVD w epidural appropriate
Augment 2nd stage
Impact of thyrotoxicosis on pregnancy
Miscarriage
PTL
FGR
SB
Perinatal mortality
Sinus tachy/ SVT/ AF –>. thyroid storm. around timeof delivery
R/O heart failure
Retrosternal extension of goitre
Impact of pregnancy on thyrotoxicosis
Often improves
May exacerbate T1due to presence of HCG and in puerperium
No effect on opthalmology
Incidence of thyrotoxicosis in pregnancy
1 in 2000
Causes of thyrotoxicosis in pregnancy
Graves - most common, affects 1% of pregnancies
Toxic nodules
Toxic multinodular goitre
Subacute thyroiditis
Trophoblastic disease
Definition and management of gestational hyperthyroidism
1-3% pregnancies.
Due. to stimulation of TSH receptors by b-hcg
bhcg normalises in T2
Supportive mx
Maternal concerns if hyperthyroidism present
Heart failure- myocardial effects of T4 worsened by PET, anaemia, infection
Thyroid storm
PET
Fetal effects of hyperthyroidism
PTL
IUGR
Fetal/ neonatal thyrotoxicosis - crossing of AB and T4
- affects 10% babies of mothers with graves
- TSH and T3 don’t cross placenta
- NB to take cord blood and neonatal TFTs
In utero: fetal tachy/ FGR/ goitre
Rx w antithyroid meds as they cross placenta
No rx: mortality 25%
Medications. to rx hyperthyroidism
PTU- blocks thyroixine synthesis and converts. T4–>T3
Carbimazole - blocks thyroxine synthesis
ADRs to hyperthryoid meds
PTU: maternal hepatotoxicity
Carbimazole: possible teratogen, not used in T1
Combo of both:
- rash
- agranulocytosis 0.2%
- fever
- crosses placenta
- small risk of aplasia cutis (absent skin on scalp)
Why is PTU preferred rx in hyperthyroidism
Reduced level teratogenicity
Signs and symptoms of thyroid storm
Fever
Tachycardia
Cardiac failure
Restlessness
Coma
Seizures
GI
* medical emergency
Target T4 level
1.2 - 1.8
Management of thyroid storm
TFTs
Endo review
Large dose PTU/ carbimazole
K iodide
Dexamethasone
Propanolol
Supportive: IV fluids, O2, antipyretic
Incidence of hypothyroidism in pregnancy
1-3 per 1000
Implication of overt hypothyroidism
0.5% fertility reduction
Increase in T1 miscarriage
Causes of hypothyroidism
Hasimotos- thyroid peroxidase AB and antithyroglobulin AB
Post-surgery
Post-iodine
Maternal concerns in light of hypothyroidism
PET
PTL
Fetal concerns in light of hypothyroidism
Fetal requirement of T4 until 12/40 for neurodevelopment
Rare: neonatal hypothyroidism due to TSH receptor blocking antibodies crossing placenta
Target TSH in hypothyroidism
<2 iu/l
Complications of hypothyroidism - maternal
Anaemia
PPH
Cardiac dysfunction
PET
Placental abruption
Complications of hypotyroidism - fetal
FD in labour
Prematurity/ LBW
Congenital malformations
Perinatal death
SB
Neurodevelopmental delay
Congenital hypothyroidism (if autoimmune)
Risks assoc w sickle cell disease in pregnancy
Increased miscarriage
Painful crises
Worsening anaemia
Increased infections
FGR
PTL
CS
VTE
NB hx to note in sickle cell disease
Crises - frequency and severity
Bone problems
Chest problems
Pulm HTN
Retinal disease
Incidence/ prevalence of sickle cell disease
Higher in African, Caribbean and middle eastern descent
MC inherited condition WW
UK: 12000-15000 affected
Affects 100-200 pregnancies per year
Preconception advise and workup- sickle cell
Education
Contraception
Partner haemoglobinopathy. - screen partner or CVS in pregnancy to determine fetal status
Updated vaccination status
Folic acid 5mg
Penicillin prophylaxis
Meds review: stop ACEI, stop hydroxycarbamide (hydroxyurea) 3/12 before conception
Bloods: LFTs, U&E, cardiac fx, Hb, iron studies +/- need for chelation
RC AB reg transfusions
Mx acute painful crisis (Sickle cell)
MDT
No pethidine - increased seizure risk, diamorphine
IV fluids
O2
VTE prophylaxis
Awareness of other complications - ACS, stroke, acute anaemia
LMWH
Antenatal care of pt w sickle cell disease
MDT
Medical review by haematology to assess end organ review
Avoid precipitating factors
Persistent vomiting –>deydration and SC crisis
Monthly MSU
Meds: FA, Fe, Px AB, aspirin, LMWH as inpatient, influenza vaccine
Crises: pain relief, hydration, use of antibiotics
US: viability at7-9/40, routine T1 and anomaly, 4 weekly growth scan from 24/40
Intrapartum mx of SCD
Normal growth, no complications –> delivery after 38/40
No CI to SVD
Crossmatch if atypical AB
Position discussion if hip replacements (AVN)
Keep warm and hydrated
CEFM
Analgesia- anaesthetic RV in T3, regional for CS, no pethidine
Postpartum mx SCD
Early neonatal testing if high risk
Maintain O2 sats >94%
Adequate hydration
LMWH: SVD x 7/7, CSx 6/52
Contraception: progesterone only first line, E second line
CuIUD= r/o anaemia
Depo reduces SC crises
Preconceptual counselling in T1DM
Education
FA 5mg 3/12 preconception
Glycaemic control:
- fasting: 3.5-5; 1 hr postprandial <7
Aim for HbA1c <48
Do not conceive w HbA1c >86
Screening for DM complications: renal, retinopathy, neuropathy, CVS, thyroid
Med review: stop ACE, statins
Contraception until optimised
Optimise weight
Benefits of glycaemic control in DM
Reduces risk of:
Miscarriage
Congenital malformations
SB
NND
Complications of DM neuropathy antenatally
UTIs from bladder atony
N&V
Uterine atony. - PPH
Autonomic dysfunction –> lack of FM detection
Complications of T1DM
PET : 4x more common
PTL : may require AN steroids (*compromised HGT control)
Macrosomia+/-shoulder dystocia
Delivery timing and monitoring T1DM
37-38+6 if no complications
37 if complications
CEFM
1 hourly BSL
Risk factors for GDM
PCOS
BMI >30
Prev macrosomic baby >4.5kg
Prev GDM
Fam hx DM
Ethnicity
Diagnosing GDM
Screening: glycosuria 2+ on 1 occasion, 1+ on 2 occasions –> test
OGTT 24-28/40
OGTT: 75g 2 hrs
-fasting 5.6
- 2 hour 7.8
USS: poly/LGA
When to assess for retinopathy in. T1DM
T1
16-20/40
28/40
* allow SVD
When to get nephrology r/v
Creat=/> 120
uACR >30
Protein >0.5g/day
Risk factors for LGA
Male
Multiparity
White
DM
GA > 41/40
Complications of LGA
CS
Shoulder dystocia
Chorioamnionitis
4th degree tear
PPH
Long stay
Longterm health risks LGA
Asthma
Life time risk of breast Ca
Incr BMI
Incidence of LGA
15-25%
Contributing factors to increased incidence LGA
Increase in:
maternal height
BMI
gestational weight gain
DM
reduced smoking
change in economy
Definition of LGA
weight > 90th centile or 2SD from mean
Definition of thalassaemia
Inherited disorder of globin chain synthesis
- alpha: 1-4 chains of alpha genes deleted
- beta: 1-2 of the genes defective
Implications of alpha thalassaemia major
No functional alpha genes –> incompatible with life
Management of patients with beta thal trait
Asymptomatic
Folic acid 5mg
Iron supplement if ferritin low
Implications and mx beta thal major
Defective B gene from both parents
Require regular transfusions
Counselling NB:
- iron overload d/t rpt transfusions
- hepatic, endocrine, cardiac & bone deformities
- endo deformities: DM, hypogonadism, hypothyroid
Pre-pregnancy end organ assessment in thalassaemia
Pancreas:
- diabetes screening
- serum fructosamine <300nmol/l for 3/12 preconception (= HbA1c 43)
Cardiac:
- cardio r/v w ECG, ECHO
Thyroid:
- TFTs
Liver:
- LFTs, ferriscan <7mg/g
- US to o/r cholelithiasis, cirrhosis from overload, transfusion-related hepatitis
Bone density scan
Changes in mx if prev. splenectomy/ at risk transfusion viral hepatitis
Penicillin prophylaxis
Vaccination- HiB, pneumococcus, hep B
Antenatal care thalassaemia
Monthly r/v until 28/40, then 2 weekly
Monthly fructosamine if diabetic
Thal major: cardiac assessment at 28/40
Monthly TFTs if hypothyroid
USS: 7-9/40, routine T1, anomaly, growth scan every 4 weeks from 28/40
Transfusions: thal major reg transfusions; aim for pre-TF Hb>10
VTE prophylaxis: abN red cell fragments and high plt count
Aspirin if plt >600, LMWH if splenectomy
Monitor for cardiac decompensation
Mx of delivery in thalassaemia
MDT opinion
Check Hb prior - Xmatch 2u
Thal Maj- IV desferrioxamine 2g over 24 hours
Cont CTG
Active mx 3rd stage
LMWH post delivery
Timing of use of desferrioxamine
Stop 3/12 preconception
Start after 20/40
When to give prophylactic progesterone
Hx of spontaneous PTL <34/40
Pregnancy loss from 16/40
Cx length </= 25mm on TVUS from 16-24/40
American College of Rheumatology classification criteria for SLE
MD SOAP BRAIN
M- Malar rash
D- discoid rash
S- Serositis
O- Oral ulcers
A- arthritis
P- photosensitivity
B- blood: all low, anaemia, leukopaenia, thrombocytopaenia
R- renal, proteinuria
A- ANA +ve
I- immunologic, anti-DNA
N0 neurologic; seizures, psych
Implications of antiphospholipid ab
Assoc w art/venous thrombosis
recurrent miscarriage
FGR
fetal loss
PTL d/t placental insufficiency
Neonatal implications anti-Ro/La and antiphospholipid abs
Congenital heart block
Neonatal cutaneous lupus syndrome
SLE meds and fertility
Cyclophosphamide –> ovarian failure
NSAIDs –> inhibit COX, which controls ovulation –> infertility
TOP offered/ PTL in SLE if
Uncontrolled HTN
- with optimal pharmacology
Active nephritis with HTN and proteinuria
Use of cyclophosphamide and mycophenolate mofetil
- teratogenic in T1
Features of high risk SLE patient
History of nephritis
HTN
APS
Active SLE
Anti-Ro/La
Meds in APLS
Aspirin 75mg preconception
LMWH when PT+ve
Definition and mx lupus nephritis
Autoantibody complexes deposited in kidneys –> activate compliment cascade –> inflammatory response
Haematuria and rise in dsDNA titre= lupus nephritis
Usually have hx of LN
Definitive diagnosis = renal biopsy; only done in pregnancy if it would change management
Typical management: steroids, azathioprine
Investigations for assessment of SLE disease activity pre-pregnancy
Cardiac:
- complications: pulm HTN, VHD, cardiomyopathy
- ECHO
Respiratory:
- cx: pulm fibrosis
- CXR, CT chest, PFTs
Renal:
- nephritis, pre-existing renal dysfx
- urine dipstick, uPCR
Haem/ immunology:
- cx thrombosis - assess risk and need for anticoag
- FBC to determine anaemia, neutropaenia, thrombocytopaenia
- autoantibody profile: aPL, anticardiolipin, anti lupus coagulant, anti-dsDNA, anti-Ro/ anti-La, complement C3/C4 levels
Incidence of FGR with SLE
1 in 40
Cause, incidence, diagnosis, prognosis congenital heart block
Anti-Ro/La AB cross placenta and destroy Purkinje fibres
Usually presents with fixed fetal brady 60-80bpm
Affects 2-3% pregnancy, recurrence of 16% in future pregnancies
Develops from 18-28/40, noted on fetal ECHO
Significant endomyocardial fibrosis and myocarditis –> hydrops
Maternal ARDS antenatal low dose steroids
weight gain
immunosuppression
acne
GI irritation
glucose intolerance
GDM
When to withdraw anti-epileptic drugs
seizure free x 2 years
minimal doses of AEDs
Negative EEG
6/12 before pregnancy
Seizure trigger risks
Sleep deprivation
Stress
AED adherence
Seizure type and frequency
Best contraceptives in epilepsy
CuICD, mirena, depot
Meds to avoid in epilepsy
Avoid stemetil
No pethidine 0 use diamorhpine instead
Associations with weight loss
Reduce incidence of:
stillbirth
HTN
macrosomia
Inc rate of VBAC
Risks assoc. w increased BMI
PET
VTE
mental health
SB
difficult US
sleep apnoea
macrosomia
Considerations in pt with bariatric surgery
Recommend delaying conception for 12-18/12
High risk pregnancies in consultant led care
Dietician input
Thromboprophylaxis regimen in pregnancy in women with mechanical heart valves
Therapeutic LMWH in BD doses from 13/40- late third trimester
If on warfarin, change to LMWH at 34-36/40
IV unfractionated heparin before planned induction and stop once labour commences or 4-6 hours prior to planned LSCS
Recommence unfractionated herparin or prophylactic LMWH 4-6 hours post delivery
Warfarin may be recommenced after 48 hours - therapeutic LMWH should be continued until INR in therapeutic range
Risk of VTE in pregnancy
6x increase
More common in left than right
More ileofemoral in pregnancy
Interpretation of compression duplex USS for DVT
Negative - discontinue LMWH
Negative but high suspicion - discontinue LMWH, but repeat USS D3 and D7
Positive: LMWH x 3/12 or 6/52 postpartum (whichever first) + TEDS x 12/12
Diagnosing PE
ECG: sinus tachy, right axis deviation, RBBB, peaked P waves (classical S1Q3T3 nor reliable)
CXR: atelectasis, wedge infarct, pleural effusion
ABD: hypoxia and hypocapnia
CTPA: slight increase risk of childhood Ca and low risk maternal breast Ca. Absolute risk very small
Treatment PE
IV unfractionated heparin
Vena cava filter for recurrent despite full anticoagulation
Effects of pregnancy on IBD
Disease in remission at time of conception = low risk for flares
2/3 pt with active disease at conception have persistant flares
Longer disease duration and use of immunosuppressives increases risk of relapse
Effects of IBD on pregnancy
Similar fertility rates except if active disease or undergone major surgery
High rates of miscarriage, PTL, LBW
Diagnosis of active IBD in pregnancy
CRP
Faecal calprotectin (indication of amount of neutrophil breakdown)
MRI if complex
Medical management of IBD in pregnancy
No MTX or mycophenolate mofetil
Smallest dose to treat
Amniosalicylates, sulfasalazine, thiopurines = safe
High dose FA
Metronidazole for perianal CD
Corticosteroids: increase in cleft lip/ palate, maternal HTN, GDM, SGA, PROM, PTL. If on for >4/52, will need IV in labour
Biologics: stop by 30-32/40. Cause immunosuppression in neonate
Considerations for labour and delivery in IBD
Episiotomy may trigger perianal disease
Active perianal disease –> LSCS
If prev on regulat po steroids, will need IV hydrocort in labour to reduce risk of adrenal crisis
Signs and symptoms of methadone overdose
Resp depression
Pinpoint pupils
Hypotension
Circulatory failure
Pulmonary oedema
Coma
Death
Benefits of methadone vs heroin
Improved perinatal outcomes
Higher birth weight
Fewer obstetric complications
Less PTB
Reduced neonatal morbidity
Methadone dose
10mg every 4 hours as needed for withdrawal
To remain on ward 60-120 min after dose for observation
T1/2 24 hours
Highest risk of overdose mortality in first two weeks on methadone
What is MBRACE-UK
Annual investigation into the deaths of women during pregnancy, childbirth and the year after birth
At risk groups as highlighted in MBRACE
4 x black
3x mixed
2 x asian
AMA:
4 x >40
2 x 35-39
Contribution of indirect causes of maternal morbidity in MBRACE
58%
Cardiac and neurological
Direct causes of morbidity
VTE
Suicide
