Haematology Flashcards
Discuss anaemia in pregnancy
-Definition (2)
-Causes (4)
-Fe requirements in pregnant women
-Folic acid requirements in pregnant women
-B12 requirements in pregnant women
- Definition
-Hb <110 in first and second trimester
-Hb <105 in third trimester - Causes
-Nutritional deficiency (Fe, B12, Folic acid)
-Haemolytic anaemia (HELLP, PET, HUS, TTP)
-Acute anaemia from haemorrhage
-Hereditary anaemia (Thalassemia and sickle cell)
-Anaemia of chronic disease (Chronic renal disease) - Fe requirement - 9mg / day
- Folic acid requirement 20-30x non pregnant woman
- B12 requirement 2x non-pregnant woman
Describe iron deficient anaemia in pregnancy
-Incidence
-Risk factors (5)
-Effects on pregnancy
-Diagnosis
-Management
- Incidence - most common cause of anaemia
- Risk factors
-Menorrhagia
-Poor Fe diet
-Interpregnancy interval <1yr
-Breastfeeding
-Low Fe at start of pregnancy (Rapid worsening) - Effect on pregnancy
-PTL, LBW, Increased blood loss at delivery - Diagnosis
-Low MCH/Low MCV
-Serum iron <12, Serum ferritin <12 - Management
-Treat if ferritin <50
-PO Fe ferrous fumerate 200mg or Ferrous sulphate 325mg
-Consider IV Fe if intolerant to PO
Discuss folate deficiency in pregnancy
-Incidence
-Risk factors
-Diagnosis
-Management
- Incidence: Second commonest cause of anaemia
- Risk factors
-Anti epileptic drugs
-Folate antagonists - Diagnosis
-High MCV
-Low serum and red cell folate
-Hypersegmented neutrophils - Management
-PO replacement 800mcg in NZ 5mg Aus.
-3 months preconception and till 12 weeks
-High dose in certain groups
What women should receive high dose folic acid supplementation in pregnancy (6)
-Have spina bifida
-Previous fetus with NT defect
-Taking folic acid antagonist
-Diabetes
-Obesity
-Malabsorption
-Family Hx of NT defect
Discuss B12 deficiency in pregnancy
-Incidence
-Causes
-Impact on fetus
-Diagnosis
-Management
- Incidence: Less common
- Causes
-IBD
-Pernicious anaemia - Impact to fetus
-Neurological sequalae in exclusively breast fed women - Diagnosis
-High MCV
-Reduced B12 levels
-Hypersegmented neutrophils - Treatment
-Supplement women with vegan or vegetarian diets in pregnancy and breastfeeding
RDI 2.6mcg/day
-B12 injections
Discuss transfusion reactions
-Delayed (4)
-Common acute reactions (2)
-Relatively common acute reactions
-Relatively rare acute reactions
- Delayed reactions
-Can occur days to weeks post transfusion
-Haemolysis, thrombocytopenia, graft vs host disease - Common acute reactions
-Urticaria 1-3%
-Febrile non-haemolytic transfusion reaction 1% - Relatively common acute reactions
-Transfusion associated circulatory overload (<1%)
-Transfusion related acute lung injury (<0.01%) - Relatively rare acute reactions
-Anaphylaxis 1:20,000
-Acute haemolytic transfusion reaction 1:76,000
-Sepsis 1:50,000
Discuss disseminated intravascular anticoagulation in relation to pregnancy
-Pathophysiology (3)
-Diagnosis (4)
-Obstetric causes (5)
-Management
- Pathophysiology
-Endothelial injury - release of procoagulation substances
-Rapid consumption of coagulation factors leads to uncontrolled bleeding
-Stimulation of fibrinolysis causes further bleeding as products are powerful anticoagulants - Diagnosis
-Low fibrinogen <2 in pregnancy is significant
-Elevated fibrin degradation products
-Prolonged APTT and PT
-Low platelets - Obstetric causes
-Massive haemorrhage / placenta abruption
-PET/HELLP
-AFE
-Massive infection - Management
-Treat underlying cause
-Replace factors for coagulopathy with help from haematology
-FFP for coag factors
-RBC for losses
-Platelets if <50
-Cryo for fibrinogen
-Recombinant fibrinogen if fibrinogen <1
-Recombinant factor VIIa for life threatening haemorrhage
Discuss sickle cells disease in pregnancy
-Epidemiology (1)
-Risk factors (3)
-Types(4)
-Inheritance (2 points)
-Pathophysiology (3 points)
-Clinical manifestation (5)
- Epidemiology
-Most common inherited condition world wide - Risk factors
-African, Central/South American decent - Types
-Many types depending on type of haemaglobin.
-HbAS is sickle cell combined with normal Hb - aSx - sickle cell trait.
-HbSS is homozygous for sickle cell
-Types give similar phenotype of varying severity - Inheritance
-Autosomal recessive. Single point mutation in B globin gene - Pathophysiology
-HbS aggregates when deoxygenated causing cell ridigitiy and sickling of the cell
-Leads to occlusions of the microvasculature
-Premature removal of sickled cells from circulation leads to haemolytic anaemia - Clinical presentation
Sickle cell crisis is bought on by exertion, infection, dehydration
-Acute chest symptoms
-Pain from microinfarctions
-Pulmonary HTN
-Renal disease
-Retinal disease
-Stroke
Discuss sickle cell disease in pregnancy
-Impact of pregnancy on sickle cell disease
-Impact of sickle cell on pregnancy (maternal)
-Impact of sickle cell on pregnancy (fetus)
- Impact of pregnancy on sickle cell disease
-25% increase in SCD complications during pregnancy
-Increased VTE, stroke, PE
-Increase in SCD crisis 27-50%
-Increase in infections (UTI, pneumonia) - Impact of SCD on pregnancy (maternal)
-Infection
-PET/gHTN
-Placental abruption
-Maternal mortality 2.5%
-PTL - Impact of SCD on pregnancy (fetus)
-Spontaneous miscarriage 9-25%
-IUGR from chronic hypoperfusion
-Still birth 4-6fold higher
Discuss the management of women with SCD in pregnancy
-Preconception (6)
-Antenatal (10)
-Intrapartum (6)
-Postpartum (6)
- Preconception
-Genetic counselling and assessment of partners genotype
-Screening for end organ damage
-Echo (Pulmonary HTN), retinal screening, renal and liver function
-High dose folic acid 5mg continue throughout pregnancy
-Stop hydroxcarbamide (Hydroxyurea) - teratogenic 3 months pre conception.
-Discuss vaccination given hyposplenia/dysfunction
-Document baseline O2 and BP - Antenatal
-Manage in MDT clinic
-Prophylactic penicillin
-Aspirin for PET prevention
-Regular Hb, Urinalysis and BP checks. Monthly urine cultures
-Fetal serial growth scans
-Tertiary anatomy scan if exposed to hydroxcarbamide looking at spine (16/40) and fetal echo (24/40)
-Switch ACEi or ARBs to lab or methyldopa if necessary
-TEDs and mobilisation. LMWH if admitted
-Avoid routine blood transfusions
-Baseline renal and liver function and PCR - Intrapartum
-Aim delivery 38-40/40
-Keep warm, hydrated and oxygenated
-Continue prophylactic antibiotics
-Recommend epidural
-Avoid pethidine - increase seizure risk
-Can aim VB. - Postpartum
-Ensure warm, hydrated, oxygenated
-Early mobilisation
-VB clexane 7/7
-CS clexane 6/52
-Low threshold for broad-spectum antibiotics
Discuss thalamssaemia in pregnancy
-Epidemiology
-Types
-Risk factors
-Inheritance pattern
- Epidemiology
-Common inherited disorder - Types
-Alpha Thalassemia -defect in the alpha subunit of the globin
-Beta thalassemia - defect in the beta subunit of globin - Risk factors
-Alpha Thal: SEA, India, Africa
-Beta Thal: Middle East, China, Mediterranean, SEA - Inheritance
-Autosomal recessive
Discuss the genetics of Alpha thalassemia
-Four types
-Symptoms experienced
-Impact to fetus
-Impact to mother
- 4 genes on chromosome 16 code for alpha subunit
- 1 defective gene = alpha-thal trait (A+). Asx
- 2 defective genes = alpha-thal trait (A0).
-Can be a loss of both from one parent or one from each parent.
-Asx but can become anaemic in pregnancy - 3 defective genes = HbH disease
-mild to moderate haemolytic anemia.
-Doesn’t require blood transfusions - 4 defective genes = Homozygous alpha thalassemia
-Incompatible with life. Die in utero in 2-3rd trimester of immediately after delivery.
-Have anaemia, develop heart failure and hydrops = Hb Barts Hydrops.
-Mother at risk of severe polyhydramnios, severe PET, PPH.
Discuss the genetics of Beta thalassemia
-Types
-Symptoms experienced
2 genes on chromosome 11 make up beta subunit
1. Types
1defective gene = beta thal minor/trait
- mild anaemia or asx,
-Anaemia and symptoms can be unmasked in pregnancy
-2 defective genes = thal major/transfusion dependant
-Thal intermedia, Homozygous but milder form - spectrum of symptoms
2. Symptoms experienced
-Marked haemolytic anemia, splenomegaly, bone deformities, Fe overload.
-Life expectancy 5-10yrs without treatment
- Transfusion dependent and Fe chelation required
-Associated with endocrine abnormalities (subfertility)
-Thal trait - mild anaemia with decreased MCV
-Thal intermedia - spectrum of symtoms from transfusion requiring to aSx
Discuss management of women with Beta thalassemia major or intermedia in during pregnancy
-Preconception
-Antenatally
-Intrapartum
-Postpartum
- Preconception care
-Screen all women for haemoglobinopathies
-If positive screen partners
-Offer genetic counselling and prenatal Dx (CVS)
-With women who have Fe overload check for end organ damage (Heart, liver, joints, thyroid, pancrease)
-With women who are transfusion dependent check for RBC antibodies and Hep C virus
-Give 5mg folic acid pre and during pregnancy
-Stop Fe chelation prior to pregnancy as Teratogenic
-Aggressively chelate prior to pregnancy to optimally reduce Fe overload
-Check for thyroid and diabetes as increased risk
-Vit D levels optimised - Antenatal care
-Low dose aspirin if plts >600 or splenectomy
-Manage with MDT
-Continue folic acid 5mg
-Treat anaemia with transfusion not Fe. Aim Hb >100
-Monitor fetal growth (risk IUGR, PTB, fetal hypoxia)
-High suspicion for development of HDN
-LMWH if thal major or intermidia - Intrapartum care
-No need for IOL
-Aim VB
-Continuous monitoring
-Active management of third stage and cross matched blood available - Postnatal
-Thromboprophylaxis LMWH regardless of mode of delivery
-No contra-indications to any contraception
-Breastfeeding OK with Fe chelating agents
Discuss Von Willerbrand disease in pregnancy
-Incidence
-Types and prevalence
-Pathophysiology
-Clinical features
- Incidence
-Most common bleeding disorder - 1% - Types and prevalence
-Type 1 mild, Autosomal dominant, 80%
-Type 2, Autosomal dominant, associated with thrombocytopenia
-Type 3, Severe, not vWF, autosomal recessive
-Type 2 and 3 make up other 20% - Pathophysiology
vWF helps platelets adhere to injured endothelium and stop VIII from degradation - Clinical features: menorrhagia, mucosal bleeding, prolonged bleeding (APTT), easy bruising
How does vWF deficiency affect pregnancy
- Levels of vWF and VIII increase d3-4 fold in pregnancy and so most women are not effected
- Can experience increased bleeding with ectopic, miscarriage, CVS when levels have not peaked
- Levels drop rapidly postnatally and women are at risk of perineal and vulval haematomas and secondary PPH
How should vWF deficiency be managed in pregnancy
-Antenatal care
-Intrapartum care
-Postpartum care
- Antenatal care
-Include haematologist in care
-Offer genetic counseling and testing if at risk of type 3
-Avoid NSAIDS and aspirin
-Refer to anaesthetics - avoid neuraxial block in type 3 and caution with type 2
-Check baseline levels of vWF and FVIII checked - Intrapartum care
-If neonate at risk avoid instrumental delivery, ECV FBS and FSE
-If Type one can consider Desmopressin to increase vWF prior to delivery or epidural
-If type 2 or 3 have to give FFP to increase platelets and VIII
-Active third stage - Postpartum care
-Monitor VIII levels daily to to ensure levels remain satisfactory 3 days for NVB, 5 days for CS or instrumental
-Monitor for secondary PPH and haematomas
-Check baby cord blood
-Avoid IM injections until bleeding disorder is excluded
-Consider a course of TXA
Discuss haemophilia in pregnancy
-Incidence
-Inheritance pattern
-Types
-Impact on female carriers
-Management
- Incidence
-Rare Haem A> Haem B.
-Prevalence of female carriers is unknown - Inheritance - X-Linked recessive
- Types
-Haemophilia A - reduced factor VIII
-Haemophilia B - reduced factor IX
-Haemophillia C - reduced factor XI - Impact on female carriers
-Clotting factor 20-50% of normal
-Increased risk of bleeding with invasive procedures/ TOP etc - Management
-Haem A - Desmopressin and factor VIII
-Haem B - TXA and factor IX
Discuss haemophillia in pregnancy
-Effect on pregnancy Mother (3)
-Fetus (1)
-Factor VIII increases in pregnancy no change in factor IX
-Increased risk of excessive bleeding in early pregnancy (CVS, ectopic, miscarriage)
-Increased risk of PPH (Primary and secondary)
-Increased risk of intracranial haemorrhage in VB (OR 44)
Discuss management of women affected by haemophilia in pregnancy
-Antenatal (5)
-Intrapartum (6)
-Postpartum (6)
- Antenatal
-MCT approach
-Offer genetic counselling - ideally preconception
-Determine sex of fetus to determine risk NIPT or USS
-Offer CVS at 11-13 weeks to confirm diagnosis (do factor level first and treat prior to procedure if <50)
-Offer termination if affected fetus
-Measure factor levels in early pregnancy and before delivery (28-34 weeks) or any invasive procedure.
-Anaesthetic review
-Can uses DDAVP (Desmopressin antenatally to raise VIII)
-Avoid ECV - Intrapartum
-CS not routinely recommended but consider if neonate at high risk of severe haemophillia.
-ELCS safest delivery method.
-Ventouse contra-indicated
-Avoid prolonged second stage
-Have G&H, FBC, IV access
-Consider treatment if factor levels <50 prior to invasive procedures
-Avoid FSB, FSE, high forceps
-Epidural/Spinal OK if factor levels are >0.5IU/mL - Postpartum
-Active third stage
-Monitor for secondary PPH
-Prompt repair of any trauma
-Maintain factor levels >0.5IU/mL for 3-4days post VB and 4-5 days post CS/ instrumental delivery
-Avoid IM injections in neonate until bleeding disorder status known
-Send cord bloods for analysis of bleeding disorder status
-Give PO Vit K to neonate
-Use TXA for at least 7/7 PP following CS
Discuss essential thrombocythemia
-Definition
-Diagnosis
-Impact on pregnancy
-Management
- Definition
-Myeloproliferative disorder with increased platelets - Diagnosis
-Platelet count over >600 with reactive causes ruled out - Impact on pregnancy
-Increased miscarriages
-Only 60% of pregnancies result in live birth
-PET, IUGR, Placental abruption, PPH, VTE - Management
-Ref to haematologist
-Aspirin (Doesn’t change pregnancy outcomes)
-LMWH if previous VTE through pregnancy and PP
-Avoid cytoreductive drugs - all contraindicated. Can used IFN-alpha
Discuss gestational thrombocytopenia
-Definition
-Incidence
-Diagnosis
-Impact to fetus
-Impact to mother
-Management
- Definition
-Platelets <150 - Incidence
-5-10% of pregnancies
-75% of women with thrombocytopenia in pregnancy will have gestational thrombocytopenia - Diagnosis
-Rule out other causes of low platelets (HELLP, PET, HIV)
-Diagnosis of exclusion. Made once platelets return to normal PP
-Less likely if low platelets develop in early pregnancy - Impact on fetus - nil
- Impact on mother - nil.
- Management
-Monitor platelets monthly till 36/49 then weekly
-If >80 can have regional anaesthesia
-Check cord blood at birth
-Avoid unnecessary interventions in labour
-Check platelet levels at 1- 3 months for resolution
Discuss immune thrombocytopenic purpura
-Pathophysiology
-Incidence
-Diagnosis
- Pathophysiology
-Maternal antibodies against maternal platelet surface glycoproteins resulting in increased platelet destruction - Incidence
-100 times less common than gestation thrombocytopenia
-Affects 1:1000 pregnancies
-Makes up 3-5% of cases of thrombocytopenia in pregnancy - Diagnosis
-Diagnosis of exclusion
-Onset usually before pregnancy so differentiates from gestational thrombocytopenia but can be difficult to tell
-Rule out other causes of thrombocytopenia (HIV/Meds/APLS/SLE/HELLP/PET)
Discuss immune thrombocytopenic purpura
-Impact of pregnancy on IPT (1)
-Impact of IPT on pregnancy (mother (1) and fetus (2))
- Impact of pregnancy on IPT
-No impact - Impact of IPT on pregnancy
-Very small bleeding risk if platelets >50
-Antiplatelet IgG can cross the placenta and affect the fetus causing thrombocytopenia and neonatal intracranial haemorrhage (0-1.5% risk)
Discuss management of immune thrombocytopenic purpura in pregnancy
-Antenatal (5)
-Intrapartum
-Postnatal
- Antenatal
-Monitor platelet count monthly till 28/40, fortnightly until 36/40 then weekly thereafter
-Consider treatment if symptomatic or platelets <20, or needing invasive procedures (CVS) in 1st and 2nd trimester
-Consider treatment in third trimester if:
-Platelets <50
-If platelets 50-80 and wanting regional anaesthetic
-Treat with prednisolone 20-30mg / day the wean to maintain platelets >50
-Treat with IVIG if intolerant to prednisolone or need urgent increase in platelet numbers
-Delivery is safe with platelets >50 (CS or VB) - Intrapartum
-Avoid FSE, Ventouse, FBS, difficult forceps
-Active third stage - Postpartum
-Repair trauma promptly
-Avoid NSAIDS
-LMWH if platelets >50
Discuss the management of the fetus in immune thrombocytopenic purpura (6)
- Avoid FBS
- Test cord blood at birth and regularly thereafter
- Platelet count reaches nadir at day 3-5
- Treat with IVIG if bleeding or severe thrombocytopenia
- USS of brain if concern for intracranial haemorrhage
- No advantage to CS over VB for fetal wellbeing
Discuss thrombotic thrombocytopenic purpura/Haemolytic uraemic syndrome.
-Pathophysiology
-Clinical features TTP
-Clinical features HUS
-Difference between HUS/TTP and HELLP
- Pathophysiology
-Damaged epithelial cells release ultra-large form of vWF causing microvascular aggregation of platelets and obstruction of arterioles and capillaries resulting in organ damage.
-Can be idiopathic or precipitated by infection, pregnancy etc. - Incidence
-Rare
-More common in women
-Up to a 33% of case in women a=occur during pregnancy - Clinical features TTP
-Classic pentad: thrombocytopenia, haemolytic anaemia, fever, AKI, CNS involvement
-More extensive disease than HIS - Clinical features HUS
-Classic triad: thrombocytopenia, haemolytic anaemia, renal episode. Commonly presents with AKI.
-Can evolve from HELLP - Difference between TTP/HUS and HELLP
-HELLP - more common. Low grade haemolytic anaemia. Abnormal LFTs
-HUS/TTP - profound haemolysis and thrombocytopenia
Discuss thrombotic thrombocytopenic purpura/haemolytic syndrome
-Management
- Involve haematologist, ICU, senior obstetrician
- Delivery doesn’t alter course
- Consider plasma exchange
- Give blood products (FFP) but NOT platelets
- Folate supplementation
- Low dose aspirin if platelets >50
- High dose steriods
- Manage AKI
Discuss fetal alloimmune thrombocytopenia
-Incidence
-Pathophysiology
-Diagnosis
-Impact to fetus
-Impact to mother
- Incidence
-1:1000 pregnancies - Pathophysiology
-Due to Maternal antibodies specific to fetal platelet antigens.
-Antigens on the fetal platelets are inherited from the father
-80% due to anti-HPA1 antibodies
-Results in profound fetal thrombocytopenia - Diagnosis
-Ventriculomegaly, cerebral cysts, hydrocephaly on antenatal scan
-Picked up at birth generally from bruising and internal bleeding.
-Screening not recommended
-If previous babies have have had a dx or ICH - Impact to fetus
-High risk ICH
-High mortality 7-15%
-High neurological morbidity: CP, ICH, blindness
Discuss management of fetal alloimmune thrombocytopenia
-Prenatal
-Antenatal
-Intrapartum
- Prenatal
-Test mother for platelet specific antibodies if previously affected child
-Platelet type both parents
-70-90% risk of recurrence - Antenatal
-Offer intrauterine FBS to check fetus
-Treat if fetus not compatible with mother
-Immunoglobulin infusion to mother to reduce antibodies - weekly
-Corticosteroids if no response to immunoglobulin infusion
-Intra uterine platelet transfusion - Intrapartum
-Delivery by CS preferred
-Aim delivery 36-37 weeks
discuss inherited thrombophilias
-Types (5)
-Incidence (2)
-Complications to pregnancy (4)
- Types
-Factor V Leiden
-Protein C and Protein S deficiency
-Antithrombin deficiency
-Prothrombin gene mutation - Incidence
-Affect 15% of western population
-Responsible for 20-50% of VTE in pregnancy - Complication to pregnancy
-Severe early onset PET
-Recurrent miscarriage
-Abruption
-Severe IUGR
Who should be screened for inherited thrombophillias?
- Test only if it will change management
-Test if family hx in first degree relative with VTE <50yrs
-Test if have had a VTE
-Screening for protein S&C def in pregnancy pointless
-Screening for FV Leiden or prothrombin gene mutation OK if deemed necessary.
Discuss risk stratification for thrombotic disorders and corresponding management. (RCOG guideline)
-Very high risk (2)
-High risk (1)
-Intermediate risk (5)
-Low risk (1)
- Very high risk
-Previous VTE on long term anticoagulation
-Antithrombin or APLS with previous VTE
Management: High dose LMWH through pregnancy and PP - High risk
-Previous VTE
Management: Prophylactic LMWH pre + PP - Intermediate risk
-Asx high risk thrombophillia (Antithrombin + APLS)
-Homozygous FVL
-Compound FVL/prothrombin x
-Protein C&S deficiency
Management: Consider prophylactic LMWH early antenatally.
Recommended from 28/40 to PP - Low risk
-Asx low risk thrombophillias - prothrombin or FVL
Management: Consider as a RF for scoring for PP anticoagulation
Discuss thromboembolic disease in pregnancy
-Incidence
-Increased risk compared to nonpregnant women
-Incidence of mortality
-Impact of thromboprophylaxis
- Incidence
-1-2:1000 pregnancies - Increased risk compared to nonpregnant women
-4-5 x increased risk in pregnancy
-12 x increased risk if ELCS
-24 x increased risk if EMCS
-20 x increased risk in Postpartum - Incidence of mortality
-1:40 PEs are fatal
-Amoungst the top 5 causes of maternal mortality
-Third most common cause of maternal death in NZ and Aus - Impact of thromboprophylaxis
-Thromboprophylaxis decreases risk by 60-70%
Discuss the risk factors for Thromboembolic disease in pregnancy
-Pre-existing factors (7)
-Obstetric risk factors (6)
-Transient reversible risk factors (5)
- Pre-existing risk factors
-Smoking
-Obesity >30BMI
-Age >35yrs
-Multiparity >3 deliveries
-Heritable thrombophillias
-Acquired thrombophillias
-Medical comorbidities - Obstetric risk factors
-Long labour
-Mid cavity/rotational forceps
-CS
-Multiple pregnancy
-PET
-PPH >1L requiring transfusion - Transient risk factors
-Surgical procedures in pregnancy
-Hyperemesis/dehydration
-OHSS
-IVF
-Immobility >3 days
-Systemic infection requiring admission to hospital
Discuss deep vein thrombosis in pregnancy
-Presentation
-Diagnosis
-Management
- Presentation
-L leg»_space; R leg secondary to L Illiofemoral vein compression
-Illiofemoral»_space;poplitofemoral
-Oedema, swelling, pain, redness
-Can have lower abdo pain from extension into pelvic vessels - Diagnosis
-NO D-dimer. False negs possible and negative result not reassuring
-Duplex compression USS if negative but high suspicion repeat day 3-7. - Management
-Elevate leg/ TEDS
-Anticoagulation with LMWH 1mg/kg BD based on booking weight.
-Treatment dose for remainder of pregnancy and until 6/52 PP
Discuss PE in pregnancy
-Presentation
-Diagnosis
-Management
- Presentation
-SOB, Pleuritic CP, cough, haemoptysis, collapse, sinus tachycardia >115
-No signs or symptoms adequately predict PE diagnosis in pregnancy - Diagnosis
-CXR - helps rule out other causes of sx and signs
-ECG - usually sinus tachy. Classic signs of PE can be normal in pregnancy so not useful
-Duplex USS only if suspicion for DVT
-ABG - Normal doesn’t exclude PE. Limited value
-CTPA or VQ scan. Both have pros and cons. choice based on local expertise and availability
-Echo if large PE suspected. RV overload or dysfunction
-Do not use d-dimer to exclude PE
-Only 2-6% of women with suspected PE have PE - Management
-MDT approach
-BD weight adjusted LMWH 1mg/kg
-No need to monitor anti-Xa levels unless extremes of weigh, antithrombin deficiency, or renal dysfunction
-Treat 3-6months and at least 6weeks PP
-Initially should be managed as inpatient for monitoring
-Thrombolysis and thrombectomy are not contra-indicated in pregnancy
-No need to do a thrombophilia screen
-Plan around delivery - stop 24hrs before delivery or epidural/spinal
-Anaesthetic review
Discuss CTPA vs VQ scan in pregnancy
Pros and Cons
- CTPA pros
-Less radiation to fetus
-Quicker and more widely available
-Better for proximal PEs
-Modality of choice if CXR abnormal - can see other possible causes for presentation
-Can identify other lung pathology - CTPA cons
-Higher radiation to breast tissue
-Higher % of non-diagnostic scans
-Requires contrast - VQ scan pros
-Better for distal PEs
-Less radiation to maternal breast tissue
-Higher negative predictive value
-Choice of modality in normal CXR
-More accurate for diagnosis in 3rd trimester - VQ scan cons
-More radiation to fetus and increase in childhood cancers
-Not available in all centers
-Have to pump and dump
Discuss cerebral vein thrombosis
-Incidence
-Mortality rate
-Risk factors (5)
-Presentation
-Diagnosis
- Incidence
-2% of pregnancy related strokes
-1:10,000 pregnancies - Mortality rate
-4-36% - Risk factors:
-AMA
-HTN
-CS
-Infection
-Dehydration - Presentation
-Headaches
-Seizures
-Signs of ICP
-Focal and global neurological sx - Diagnosis
-CT venogram or MRI
Discuss management of thromboembolic disease
-Anticoagulation
-Around timing of labour
-Postpartum considerations
- Anticoagulation
-1mg/kg BD LMWH as per booking weight
-Referral to Anaesthetics
-Advice to stop if any PVB and present
-Give therapeutic LMWH for all of pregnancy and until 6 weeks PP or until at least 3 months of treatment taken
-Can switch to Warfarin PP but increases PPH so wait 5-7 days - Timing around delivery
-Can time delivery so can manage anticoagulation
-Day 2 prior to delivery last dose LMWH
-Day 1 Start UFH bolus and infusion maintain APTT 2-3 above baseline
-Day 0 Stop 6 hours prior to spinal/epidural. Can restart UFH 1 hr after epidural sited if needed
-6-12 hrs PP restart UFH
-Consider warfarin PN
How should thromboprophylaxis be managed in pregnancy (4 points)
- All pregnant women should be reviewed for risks of VTE
- If VTE prophylaxis is recommended it should be commenced as soon as possible in pregnancy
- Screening for thrombophillia should not be routinely undertaken without discussion with haematologist and appropriate counselling
- Protein S&C can’t be investigated for in pregnancy
Which women should be offered therapeutic anticoagulation in pregnancy (3)
- Needs long term anticoagulation for another reason
- ALPS + prev VTE Hx
- Antithrombin + VTE Hx
Discuss intrapartum management for women on thromboprophylaxis
-When to stop
-When to stop for regional techniques (3)
-When to stop for ELCS
-When to start after removal of epidural
-When should UFH be used
-What surgical techniques should be considered for anticoagulated patients
- Stop if any vaginal bleeding
- Avoid regional techniques
-until 12 hrs after prophylactic LMWH
-until 24 hrs after treatment LMWH
-until 6hrs after UFH dose - Stopping for ELCS
-Stop treatment dose and switch to prophylactic dose day before.
-Avoid dose on day of surgery
-Do surgery in am if possible - When to give anticoagulants after removal of epidural
-4 hrs but not within 12 hrs of last injection - When should UFH be used
-Use if risk factors for thombosis - Surgical techniques to consider if anticoagulated
-Abdominal sheath drains
-Close skin with interrupted sutures to allow for any haematoma drainage
Who and how should women be manged for thromboprophylxis post partum. (RCOG)
1. 6/52 thromboprophylaxis (4)
2. At least 10 days thromboprophylaxis (5)
3. Early mobilisation (1)
4. Risk factors (17)
- 6 weeks of 52 thromboprophylaxis
-Any previous VTE
-Anyone requiring antenatal LMWH
-High risk thrombophillia
-Low risk thrombophillia + FHx - At least 10 days thromboprophylaxis
-CS in labour
-BMI >40
-Readmission with immobilisation >3 days
-Medical co-morbidites
-Anyone with >=2 major RF - Early mobilisation
-Less than 2 risk factors - Risk factors
-ELCS
-Instrumental delivery
-BMI >30
-Systemic infection
-Immobility
-PET
-Multiple pregnancy
-PTB
-SB in current pregnancy
-Gross varicose veins
-Prolonged labour >24hrs
-Age >35
-PPH >1000mL
-Extensive perineal trauma with prolonged repair
-Smoker
-FHx of VTE
-Low risk thrombophillias
Discuss beta thalassemia in pregnancy
-Impact to mother (4)
-Impact to fetus (2)
- Impact to mother
-Increased risk of cardiomyopathy
Inability to undergo Fe chelation in pregnancy = endocrinopathies
-Increased hypothyroidism
-Increase in diabetes
-Increase in hypoparathyroidism - Impact to fetus
-IUGR
-Genetic inheritance of haemoglobinopathies
Discuss management of Thalassemia trait and HbH in pregnancy
-Impact of pregnancy (1)
-Management (3)
- Impact of pregnancy
-May increase anaemia - Management
-HbH women (alpha thal 3) have chronic haemolytic anaemia - need 5mg folic acid through pregnancy
-Check Fe levels if Fe deficient can have PO but not IV Fe
-Hardly ever need transfusion
Discuss Von Willerbrand disease in pregnancy
-Incidence
-Types and prevalence
-Pathophysiology
-Clinical features
- Incidence
-Most common bleeding disorder - 1/10 000 - Types and prevalence
-Type 1 mild, Autosomal dominant but complicated, 80%
-Type 2, Autosomal dominant, associated with thrombocytopenia
-Type 3, Severe, no vWF, autosomal recessive
-Type 2 and 3 make up other 20% - Pathophysiology
vWF helps platelets adhere to injured endothelium and stop VIII from degradation - Clinical features: menorrhagia, mucosal bleeding, prolonged bleeding, easy bruising
