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RANZCOG 2024 - maternal medical conditions > Haematology > Flashcards

Haematology Flashcards

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USMLE® Step 1 flashcards
1
Q

Discuss anaemia in pregnancy
-Definition (2)
-Causes (4)
-Fe requirements in pregnant women
-Folic acid requirements in pregnant women
-B12 requirements in pregnant women

A
  1. Definition
    -Hb <110 in first and second trimester
    -Hb <105 in third trimester
  2. 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)
  3. Fe requirement - 9mg / day
  4. Folic acid requirement 20-30x non pregnant woman
  5. B12 requirement 2x non-pregnant woman
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2
Q

Describe iron deficient anaemia in pregnancy
-Incidence
-Risk factors (5)
-Effects on pregnancy
-Diagnosis
-Management

A
  1. Incidence - most common cause of anaemia
  2. Risk factors
    -Menorrhagia
    -Poor Fe diet
    -Interpregnancy interval <1yr
    -Breastfeeding
    -Low Fe at start of pregnancy (Rapid worsening)
  3. Effect on pregnancy
    -PTL, LBW, Increased blood loss at delivery
  4. Diagnosis
    -Low MCH/Low MCV
    -Serum iron <12, Serum ferritin <12
  5. Management
    -Treat if ferritin <50
    -PO Fe ferrous fumerate 200mg or Ferrous sulphate 325mg
    -Consider IV Fe if intolerant to PO
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3
Q

Discuss folate deficiency in pregnancy
-Incidence
-Risk factors
-Diagnosis
-Management

A
  1. Incidence: Second commonest cause of anaemia
  2. Risk factors
    -Anti epileptic drugs
    -Folate antagonists
  3. Diagnosis
    -High MCV
    -Low serum and red cell folate
    -Hypersegmented neutrophils
  4. Management
    -PO replacement 800mcg in NZ 5mg Aus.
    -3 months preconception and till 12 weeks
    -High dose in certain groups
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4
Q

What women should receive high dose folic acid supplementation in pregnancy (6)

A

-Have spina bifida
-Previous fetus with NT defect
-Taking folic acid antagonist
-Diabetes
-Obesity
-Malabsorption
-Family Hx of NT defect

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5
Q

Discuss B12 deficiency in pregnancy
-Incidence
-Causes
-Impact on fetus
-Diagnosis
-Management

A
  1. Incidence: Less common
  2. Causes
    -IBD
    -Pernicious anaemia
  3. Impact to fetus
    -Neurological sequalae in exclusively breast fed women
  4. Diagnosis
    -High MCV
    -Reduced B12 levels
    -Hypersegmented neutrophils
  5. Treatment
    -Supplement women with vegan or vegetarian diets in pregnancy and breastfeeding
    RDI 2.6mcg/day
    -B12 injections
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6
Q

Discuss transfusion reactions
-Delayed (4)
-Common acute reactions (2)
-Relatively common acute reactions
-Relatively rare acute reactions

A
  1. Delayed reactions
    -Can occur days to weeks post transfusion
    -Haemolysis, thrombocytopenia, graft vs host disease
  2. Common acute reactions
    -Urticaria 1-3%
    -Febrile non-haemolytic transfusion reaction 1%
  3. Relatively common acute reactions
    -Transfusion associated circulatory overload (<1%)
    -Transfusion related acute lung injury (<0.01%)
  4. Relatively rare acute reactions
    -Anaphylaxis 1:20,000
    -Acute haemolytic transfusion reaction 1:76,000
    -Sepsis 1:50,000
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7
Q

Discuss disseminated intravascular anticoagulation in relation to pregnancy
-Pathophysiology (3)
-Diagnosis (4)
-Obstetric causes (5)
-Management

A
  1. 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
  2. Diagnosis
    -Low fibrinogen <2 in pregnancy is significant
    -Elevated fibrin degradation products
    -Prolonged APTT and PT
    -Low platelets
  3. Obstetric causes
    -Massive haemorrhage / placenta abruption
    -PET/HELLP
    -AFE
    -Massive infection
  4. 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
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8
Q

Discuss sickle cells disease in pregnancy
-Epidemiology (1)
-Risk factors (3)
-Types(4)
-Inheritance (2 points)
-Pathophysiology (3 points)
-Clinical manifestation (5)

A
  1. Epidemiology
    -Most common inherited condition world wide
  2. Risk factors
    -African, Central/South American decent
  3. 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
  4. Inheritance
    -Autosomal recessive. Single point mutation in B globin gene
  5. 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
  6. 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
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9
Q

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)

A
  1. 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)
  2. Impact of SCD on pregnancy (maternal)
    -Infection
    -PET/gHTN
    -Placental abruption
    -Maternal mortality 2.5%
    -PTL
  3. Impact of SCD on pregnancy (fetus)
    -Spontaneous miscarriage 9-25%
    -IUGR from chronic hypoperfusion
    -Still birth 4-6fold higher
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10
Q

Discuss the management of women with SCD in pregnancy
-Preconception (6)
-Antenatal (10)
-Intrapartum (6)
-Postpartum (6)

A
  1. 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
  2. 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
  3. Intrapartum
    -Aim delivery 38-40/40
    -Keep warm, hydrated and oxygenated
    -Continue prophylactic antibiotics
    -Recommend epidural
    -Avoid pethidine - increase seizure risk
    -Can aim VB.
  4. Postpartum
    -Ensure warm, hydrated, oxygenated
    -Early mobilisation
    -VB clexane 7/7
    -CS clexane 6/52
    -Low threshold for broad-spectum antibiotics
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11
Q

Discuss thalamssaemia in pregnancy
-Epidemiology
-Types
-Risk factors
-Inheritance pattern

A
  1. Epidemiology
    -Common inherited disorder
  2. Types
    -Alpha Thalassemia -defect in the alpha subunit of the globin
    -Beta thalassemia - defect in the beta subunit of globin
  3. Risk factors
    -Alpha Thal: SEA, India, Africa
    -Beta Thal: Middle East, China, Mediterranean, SEA
  4. Inheritance
    -Autosomal recessive
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12
Q

Discuss the genetics of Alpha thalassemia
-Four types
-Symptoms experienced
-Impact to fetus
-Impact to mother

A
  1. 4 genes on chromosome 16 code for alpha subunit
  2. 1 defective gene = alpha-thal trait (A+). Asx
  3. 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
  4. 3 defective genes = HbH disease
    -mild to moderate haemolytic anemia.
    -Doesn’t require blood transfusions
  5. 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.
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13
Q

Discuss the genetics of Beta thalassemia
-Types
-Symptoms experienced

A

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

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14
Q

Discuss management of women with Beta thalassemia major or intermedia in during pregnancy
-Preconception
-Antenatally
-Intrapartum
-Postpartum

A
  1. 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
  2. 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
  3. Intrapartum care
    -No need for IOL
    -Aim VB
    -Continuous monitoring
    -Active management of third stage and cross matched blood available
  4. Postnatal
    -Thromboprophylaxis LMWH regardless of mode of delivery
    -No contra-indications to any contraception
    -Breastfeeding OK with Fe chelating agents
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15
Q

Discuss Von Willerbrand disease in pregnancy
-Incidence
-Types and prevalence
-Pathophysiology
-Clinical features

A
  1. Incidence
    -Most common bleeding disorder - 1/10 000
  2. 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%
  3. Pathophysiology
    vWF helps platelets adhere to injured endothelium and stop VIII from degradation
  4. Clinical features: menorrhagia, mucosal bleeding, prolonged bleeding, easy bruising
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15
Q

Discuss Von Willerbrand disease in pregnancy
-Incidence
-Types and prevalence
-Pathophysiology
-Clinical features

A
  1. Incidence
    -Most common bleeding disorder - 1%
  2. 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%
  3. Pathophysiology
    vWF helps platelets adhere to injured endothelium and stop VIII from degradation
  4. Clinical features: menorrhagia, mucosal bleeding, prolonged bleeding (APTT), easy bruising
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16
Q

How does vWF deficiency affect pregnancy

A
  1. Levels of vWF and VIII increase d3-4 fold in pregnancy and so most women are not effected
  2. Can experience increased bleeding with ectopic, miscarriage, CVS when levels have not peaked
  3. Levels drop rapidly postnatally and women are at risk of perineal and vulval haematomas and secondary PPH
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17
Q

How should vWF deficiency be managed in pregnancy
-Antenatal care
-Intrapartum care
-Postpartum care

A
  1. 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
  2. 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
  3. 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
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18
Q

Discuss haemophilia in pregnancy
-Incidence
-Inheritance pattern
-Types
-Impact on female carriers
-Management

A
  1. Incidence
    -Rare Haem A> Haem B.
    -Prevalence of female carriers is unknown
  2. Inheritance - X-Linked recessive
  3. Types
    -Haemophilia A - reduced factor VIII
    -Haemophilia B - reduced factor IX
    -Haemophillia C - reduced factor XI
  4. Impact on female carriers
    -Clotting factor 20-50% of normal
    -Increased risk of bleeding with invasive procedures/ TOP etc
  5. Management
    -Haem A - Desmopressin and factor VIII
    -Haem B - TXA and factor IX
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19
Q

Discuss haemophillia in pregnancy
-Effect on pregnancy Mother (3)
-Fetus (1)

A

-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)

20
Q

Discuss management of women affected by haemophilia in pregnancy
-Antenatal (5)
-Intrapartum (6)
-Postpartum (6)

A
  1. 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
  2. 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
  3. 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
21
Q

Discuss essential thrombocythemia
-Definition
-Diagnosis
-Impact on pregnancy
-Management

A
  1. Definition
    -Myeloproliferative disorder with increased platelets
  2. Diagnosis
    -Platelet count over >600 with reactive causes ruled out
  3. Impact on pregnancy
    -Increased miscarriages
    -Only 60% of pregnancies result in live birth
    -PET, IUGR, Placental abruption, PPH, VTE
  4. 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
22
Q

Discuss gestational thrombocytopenia
-Definition
-Incidence
-Diagnosis
-Impact to fetus
-Impact to mother
-Management

A
  1. Definition
    -Platelets <150
  2. Incidence
    -5-10% of pregnancies
    -75% of women with thrombocytopenia in pregnancy will have gestational thrombocytopenia
  3. 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
  4. Impact on fetus - nil
  5. Impact on mother - nil.
  6. 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
23
Q

Discuss immune thrombocytopenic purpura
-Pathophysiology
-Incidence
-Diagnosis

A
  1. Pathophysiology
    -Maternal antibodies against maternal platelet surface glycoproteins resulting in increased platelet destruction
  2. Incidence
    -100 times less common than gestation thrombocytopenia
    -Affects 1:1000 pregnancies
    -Makes up 3-5% of cases of thrombocytopenia in pregnancy
  3. 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)
24
Q

Discuss immune thrombocytopenic purpura
-Impact of pregnancy on IPT (1)
-Impact of IPT on pregnancy (mother (1) and fetus (2))

A
  1. Impact of pregnancy on IPT
    -No impact
  2. 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)
25
Q

Discuss management of immune thrombocytopenic purpura in pregnancy
-Antenatal (5)
-Intrapartum
-Postnatal

A
  1. 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)
  2. Intrapartum
    -Avoid FSE, Ventouse, FBS, difficult forceps
    -Active third stage
  3. Postpartum
    -Repair trauma promptly
    -Avoid NSAIDS
    -LMWH if platelets >50
26
Q

Discuss the management of the fetus in immune thrombocytopenic purpura (6)

A
  1. Avoid FBS
  2. Test cord blood at birth and regularly thereafter
  3. Platelet count reaches nadir at day 3-5
  4. Treat with IVIG if bleeding or severe thrombocytopenia
  5. USS of brain if concern for intracranial haemorrhage
  6. No advantage to CS over VB for fetal wellbeing
27
Q

Discuss thrombotic thrombocytopenic purpura/Haemolytic uraemic syndrome.
-Pathophysiology
-Clinical features TTP
-Clinical features HUS
-Difference between HUS/TTP and HELLP

A
  1. 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.
  2. Incidence
    -Rare
    -More common in women
    -Up to a 33% of case in women a=occur during pregnancy
  3. Clinical features TTP
    -Classic pentad: thrombocytopenia, haemolytic anaemia, fever, AKI, CNS involvement
    -More extensive disease than HIS
  4. Clinical features HUS
    -Classic triad: thrombocytopenia, haemolytic anaemia, renal episode. Commonly presents with AKI.
    -Can evolve from HELLP
  5. Difference between TTP/HUS and HELLP
    -HELLP - more common. Low grade haemolytic anaemia. Abnormal LFTs
    -HUS/TTP - profound haemolysis and thrombocytopenia
28
Q

Discuss thrombotic thrombocytopenic purpura/haemolytic syndrome
-Management

A
  1. Involve haematologist, ICU, senior obstetrician
  2. Delivery doesn’t alter course
  3. Consider plasma exchange
  4. Give blood products (FFP) but NOT platelets
  5. Folate supplementation
  6. Low dose aspirin if platelets >50
  7. High dose steriods
  8. Manage AKI
29
Q

Discuss fetal alloimmune thrombocytopenia
-Incidence
-Pathophysiology
-Diagnosis
-Impact to fetus
-Impact to mother

A
  1. Incidence
    -1:1000 pregnancies
  2. 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
  3. 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
  4. Impact to fetus
    -High risk ICH
    -High mortality 7-15%
    -High neurological morbidity: CP, ICH, blindness
30
Q

Discuss management of fetal alloimmune thrombocytopenia
-Prenatal
-Antenatal
-Intrapartum

A
  1. Prenatal
    -Test mother for platelet specific antibodies if previously affected child
    -Platelet type both parents
    -70-90% risk of recurrence
  2. 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
  3. Intrapartum
    -Delivery by CS preferred
    -Aim delivery 36-37 weeks
31
Q

discuss inherited thrombophilias
-Types (5)
-Incidence (2)
-Complications to pregnancy (4)

A
  1. Types
    -Factor V Leiden
    -Protein C and Protein S deficiency
    -Antithrombin deficiency
    -Prothrombin gene mutation
  2. Incidence
    -Affect 15% of western population
    -Responsible for 20-50% of VTE in pregnancy
  3. Complication to pregnancy
    -Severe early onset PET
    -Recurrent miscarriage
    -Abruption
    -Severe IUGR
32
Q

Who should be screened for inherited thrombophillias?

A
  1. 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.
33
Q

Discuss risk stratification for thrombotic disorders and corresponding management. (RCOG guideline)
-Very high risk (2)
-High risk (1)
-Intermediate risk (5)
-Low risk (1)

A
  1. Very high risk
    -Previous VTE on long term anticoagulation
    -Antithrombin or APLS with previous VTE
    Management: High dose LMWH through pregnancy and PP
  2. High risk
    -Previous VTE
    Management: Prophylactic LMWH pre + PP
  3. 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
  4. Low risk
    -Asx low risk thrombophillias - prothrombin or FVL
    Management: Consider as a RF for scoring for PP anticoagulation
34
Q

Discuss thromboembolic disease in pregnancy
-Incidence
-Increased risk compared to nonpregnant women
-Incidence of mortality
-Impact of thromboprophylaxis

A
  1. Incidence
    -1-2:1000 pregnancies
  2. 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
  3. 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
  4. Impact of thromboprophylaxis
    -Thromboprophylaxis decreases risk by 60-70%
35
Q

Discuss the risk factors for Thromboembolic disease in pregnancy
-Pre-existing factors (7)
-Obstetric risk factors (6)
-Transient reversible risk factors (5)

A
  1. Pre-existing risk factors
    -Smoking
    -Obesity >30BMI
    -Age >35yrs
    -Multiparity >3 deliveries
    -Heritable thrombophillias
    -Acquired thrombophillias
    -Medical comorbidities
  2. Obstetric risk factors
    -Long labour
    -Mid cavity/rotational forceps
    -CS
    -Multiple pregnancy
    -PET
    -PPH >1L requiring transfusion
  3. Transient risk factors
    -Surgical procedures in pregnancy
    -Hyperemesis/dehydration
    -OHSS
    -IVF
    -Immobility >3 days
    -Systemic infection requiring admission to hospital
36
Q

Discuss deep vein thrombosis in pregnancy
-Presentation
-Diagnosis
-Management

A
  1. Presentation
    -L leg&raquo_space; R leg secondary to L Illiofemoral vein compression
    -Illiofemoral&raquo_space;poplitofemoral
    -Oedema, swelling, pain, redness
    -Can have lower abdo pain from extension into pelvic vessels
  2. Diagnosis
    -NO D-dimer. False negs possible and negative result not reassuring
    -Duplex compression USS if negative but high suspicion repeat day 3-7.
  3. 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
37
Q

Discuss PE in pregnancy
-Presentation
-Diagnosis
-Management

A
  1. Presentation
    -SOB, Pleuritic CP, cough, haemoptysis, collapse, sinus tachycardia >115
    -No signs or symptoms adequately predict PE diagnosis in pregnancy
  2. 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
  3. 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
38
Q

Discuss CTPA vs VQ scan in pregnancy
Pros and Cons

A
  1. 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
  2. CTPA cons
    -Higher radiation to breast tissue
    -Higher % of non-diagnostic scans
    -Requires contrast
  3. 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
  4. VQ scan cons
    -More radiation to fetus and increase in childhood cancers
    -Not available in all centers
    -Have to pump and dump
39
Q

Discuss cerebral vein thrombosis
-Incidence
-Mortality rate
-Risk factors (5)
-Presentation
-Diagnosis

A
  1. Incidence
    -2% of pregnancy related strokes
    -1:10,000 pregnancies
  2. Mortality rate
    -4-36%
  3. Risk factors:
    -AMA
    -HTN
    -CS
    -Infection
    -Dehydration
  4. Presentation
    -Headaches
    -Seizures
    -Signs of ICP
    -Focal and global neurological sx
  5. Diagnosis
    -CT venogram or MRI
40
Q

Discuss management of thromboembolic disease
-Anticoagulation
-Around timing of labour
-Postpartum considerations

A
  1. 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
  2. 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
41
Q

How should thromboprophylaxis be managed in pregnancy (4 points)

A
  1. All pregnant women should be reviewed for risks of VTE
  2. If VTE prophylaxis is recommended it should be commenced as soon as possible in pregnancy
  3. Screening for thrombophillia should not be routinely undertaken without discussion with haematologist and appropriate counselling
  4. Protein S&C can’t be investigated for in pregnancy
42
Q

Which women should be offered therapeutic anticoagulation in pregnancy (3)

A
  1. Needs long term anticoagulation for another reason
  2. ALPS + prev VTE Hx
  3. Antithrombin + VTE Hx
43
Q

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

A
  1. Stop if any vaginal bleeding
  2. Avoid regional techniques
    -until 12 hrs after prophylactic LMWH
    -until 24 hrs after treatment LMWH
    -until 6hrs after UFH dose
  3. 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
  4. When to give anticoagulants after removal of epidural
    -4 hrs but not within 12 hrs of last injection
  5. When should UFH be used
    -Use if risk factors for thombosis
  6. Surgical techniques to consider if anticoagulated
    -Abdominal sheath drains
    -Close skin with interrupted sutures to allow for any haematoma drainage
44
Q

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)

A
  1. 6 weeks of 52 thromboprophylaxis
    -Any previous VTE
    -Anyone requiring antenatal LMWH
    -High risk thrombophillia
    -Low risk thrombophillia + FHx
  2. At least 10 days thromboprophylaxis
    -CS in labour
    -BMI >40
    -Readmission with immobilisation >3 days
    -Medical co-morbidites
    -Anyone with >=2 major RF
  3. Early mobilisation
    -Less than 2 risk factors
  4. 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
45
Q

Discuss beta thalassemia in pregnancy
-Impact to mother (4)
-Impact to fetus (2)

A
  1. Impact to mother
    -Increased risk of cardiomyopathy
    Inability to undergo Fe chelation in pregnancy = endocrinopathies
    -Increased hypothyroidism
    -Increase in diabetes
    -Increase in hypoparathyroidism
  2. Impact to fetus
    -IUGR
    -Genetic inheritance of haemoglobinopathies
46
Q

Discuss management of Thalassemia trait and HbH in pregnancy
-Impact of pregnancy (1)
-Management (3)

A
  1. Impact of pregnancy
    -May increase anaemia
  2. 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
47
Q
A

RANZCOG 2024 - maternal medical conditions (14 decks)

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