Week 2 Flashcards
Define:
- Gestational Hypertension?
- Chronic Hypertension?
- Hypertensive crisis?
- Preeclampsia?
- HELLP syndrome?
- Eclampsia?
- Postpartum hypertension?
- Gestational hypertension can only be diagnosed if the patient was normotensive prior to 20 weeks’ gestation. Otherwise, high blood pressure during pregnancy is classified as chronic hypertension.
- The three primary features of PREeclampsia are Proteinuria, Rising blood pressure (hypertension), and End-organ dysfunction.
What is the Epidemiology of for gestational hypertension, preeclampsia, and eclampsia?
- 7 General risk factors?
- 6 Pregnancy-related risk factors?
Epidemiology
- Hypertensive pregnancy disorders occur in 6–8% of pregnancies.
- Preeclampsia: 5–7% of pregnancies
- Eclampsia: < 0.1% of all deliveries
- HELLP syndrome: 0.5–0.9% of all pregnancies
Outline the pathophysiology of Hypertensive pregnancy disorders?
- Consequences of vasoconstriction and microthrombosis?
What are the Systemic effects of hypertensive pregnancy disorders?
What are the clinical features of:
- Gestational hypertension? (2)
- Preeclampsia without severe features? (6)
- Preeclampsia with severe features? (7)
Gestational hypertension
1. Asymptomatic hypertension
2. Nonspecific symptoms (e.g., morning headaches, fatigue, dizziness) can occur.
Preeclampsia
- Onset: ∼ 90% occur after 34 weeks’ of gestation.
- In approx. 5% of individuals with preeclampsia, the condition is not diagnosed during pregnancy and symptoms only develop postpartum (postpartum preeclampsia).
What are the clinical features of:
- Eclampsia? (4)
- HELLP syndrome? (5)
Eclampsia
- Onset: The majority of cases occur intrapartum and postpartum.
- Most often associated with severe preeclampsia
- Eclamptic seizures: generalized tonic-clonic seizures (usually self-limited)
- Deterioration with headaches, RUQ pain, hyperreflexia, and visual changes are warning signs of a potential eclamptic seizure.
Outline an approach to the diagnosis of Hypertensive disorders of pregnancy - eg. Pre-eclampsia?
- 7 Initial investigations for pregnant women with Chronic hypertension?
For pregnant women with chronic hypertension, the initial recommended tests are:
1. full blood count
2. urea, creatinine and electrolytes
3. liver function tests
4. uric acid
5. urinalysis and microscopy
6. urine protein:creatinine ratio (to establish a baseline)
7. ECG.
Outline the initial workup for all suspected hypertensive pregnancy disorders. (7)
- Serial blood pressure measurement
- Urine studies - assess for proteinuria
- FBC
- LFTs
- U&Es
- Lactate dehydrogenase
- Other - eg. CT head
What is the diagnostic criteria for:
- Chronic hypertension in pregnancy? (2)
- Gestational hypertension? (4)
What is the diagnostic criteria for:
- Preeclampsia without severe features? (2)
- Preeclampsia with severe features? (5)
What is the diagnostic criteria for:
- HELLP syndrome? (3)
- Chronic hypertension with superimposed preeclampsia? (2)
Preeclampsia should not be diagnosed on the basis of worsening hypertension alone. This is because a reduction in blood pressure occurs naturally in the first and second trimester because of reduced systemic vascular resistance; blood pressure then rises to prepregnancy levels in the third trimester. This may give the appearance of worsening hypertension in a patient diagnosed for the first time in early pregnancy.
In parallel to a maternal workup, what else should be included in the investigation for hypertensive disorders of pregnancy?
= Fetal assessment
Differential diagnoses of Hypertensive pregnancy disorders:
- 4 Differential diagnoses of altered liver chemistries?
- 7 Differential diagnoses of eclampsia?
- 5 Differential diagnoses of HELLP syndrome?
List 3 Antihypertensives for urgent blood pressure control in pregnancy?
List 3 Common oral antihypertensives in pregnancy?
- Which antihypertensives should be avoided in pregnancy?
Antihypertensives for urgent blood pressure control in pregnancy
1. Parenteral labetalol (avoid in patients with contraindications to β-blockers)
2. Nifedipine (immediate release)
3. Parenteral hydralazine
Common oral antihypertensives in pregnancy
1. Labetalol
2. Nifedipine (extended release)
3. Methyldopa
Antihypertensives should be given within 30–60 minutes of diagnosis in urgent hypertensive pregnancy disorders.
What can be used for seizure prophylaxis in hypertensive pregnancy disorders?
- 3 Indications?
- Administration?
- 1 Contraindication?
- Monitoring?
Contraindicated in patients with myasthenia gravis - Magnesium sulfate competes with calcium at presynaptic terminals and, thereby, inhibits calcium-dependent acetylcholine release, which can, in turn, precipitate a severe myasthenic crisis.
Risk factors for preeclampsia
- 6 High risk factors?
- 7 Moderate-risk factors?
- What can be used for preeclampsia prophylaxis? Indications? Regimen?
Aspirin for preeclampsia prophylaxis
- Indications: ≥ 1 high-risk feature or ≥ 2 moderate-risk factors for preeclampsia.
- Regimen: nitiate low-dose aspirin between 12–20 weeks’ gestation (optimally before 16 weeks)
Describe an approach to the Management of urgent hypertensive pregnancy disorders?
- Patients with preeclampsia with severe features, HELLP, or eclampsia require immediate control of hypertension and management of complications (ideally in a tertiary care center) to minimize maternal and fetal mortality and morbidity.
- Administer antihypertensives within 30–60 minutes of diagnosis of an urgent hypertensive pregnancy disorder, if feasible.
- Delivery is the only cure for preeclampsia, eclampsia, and HELLP syndrome.
What are the Indications for expedited delivery in hypertensive pregnancy disorders?
- 7 Immediate delivery?
- 6 Urgent delivery?
Describe the Medical (4) & Obstetric management of Preeclampsia with severe features?
Preeclampsia with severe features - Medical management
1. Start antihypertensives for urgent blood pressure control in pregnancy.
2. Administer magnesium sulfate for seizure prophylaxis.
3. Monitor blood pressure, oxygen saturation, and urine output.
4. Manage complications (e.g., pulmonary edema, headache, renal insufficiency).
Describe the Medical & Obstetric management of Eclampsia?
Describe the Medical & Obstetric management of HELLP syndrome?
Outline the overall Management of nonurgent hypertensive pregnancy disorders?
Outline the Management of chronic hypertension in pregnancy?
- Prophylaxis against superimposed preeclampsia?
- Obstetric management? (2)
Management of hypertension in pregnancy
- All patients: Encourage lifestyle modifications for hypertension.
- Threshold to initiate antihypertensives (in treatment-naive patients):blood pressure ≥ 140/90 mm H
Prophylaxis against superimposed preeclampsia
- Patients with chronic hypertension are at high risk of developing preeclampsia.
- Educate patients on the symptoms of preeclampsia.
- Start aspirin prophylaxis against preeclampsia.
Obstetric management
- Chronic hypertension without superimposed preeclampsia: Deliver between 37 and 39 weeks’ gestation.
- Superimposed preeclampsia without severe features: Consider expectant management till 37 weeks’ gestation with close maternal and fetal surveillance.
Gestational hypertension and preeclampsia without severe features
- Approach to management?
- Hospitalisation and delivery?
- Antihypertensives?
- Outpatient management?
Hospitalization and delivery
- Delivery is recommended at ≥ 37 0/7 weeks’ gestation.
- Expedited delivery is recommended, regardless of gestational age, if there is evidence of maternal or fetal deterioration.
- If feasible, administer corticosteroids for fetal lung maturation if delivery of a viable fetus between 24 and 34 weeks’ gestation is indicated.
Antihypertensives
- Antihypertensives are not routinely recommended in patients with blood pressure < 160/110 mm Hg and no evidence of end-organ damage.
- Severe hypertension (≥ 160/110 mm Hg): Recategorize as preeclampsia with severe features and manage accordingly.
- Nonsevere hypertension ≥ 140/90 mm Hg but < 160/110 mm Hg with evidence of end-organ damage: Start antihypertensives.
Complications of Hypertensive Disorders of Pregnancy
- 4 Fetal complications?
- 12 Maternal complications?
Fetal complications: occur due to insufficient placental perfusion.
1. Fetal growth restriction
2. Preterm birth
3. Seizure-induced fetal hypoxia
4. Fetal death
- Hypertension during pregnancy is the most common cause of placental abruption.
- Ischemic stroke, cerebral hemorrhage, and ARDS are the most common causes of death in patients with preeclampsia.
Prognosis of Hypertensive Disorders of Pregnancy
- Recurrence rate in following pregnancies?
- Maternal mortality?
- Fetal mortality
The prognosis of hypertensive pregnancy disorders depends on the severity of the condition and the complications that occur. In the majority of cases, the conditions resolve within hours or days after delivery.
- A 22 year old primigravida at 38 weeks gestation in a previously normal pregnancy has a blood pressure of 140/90 in the clinic. How would you proceed from there?
- A 25year old primigravida at 33 weeks gestation in a previously normal pregnancy has a blood pressure of 140/90 in the clinic. How would you proceed from there?
How would you treat a pregnant woman who is fitting and has hypertension at 36 weeks of pregnancy? What might happen as a consequence of the fit?
Initial investigations for new onset hypertension after 20 weeks?
Which antihypertensive drugs should be avoided in pregnancy and why?
Which antihypertensive drugs can be safely used in pregnancy? Dose? Adverse effects?
Premature rupture of membranes (PROM)
- Definition?
- Epidemiology?
- 6 Complications?
Premature rupture of membranes (PROM)
- Definition: rupture of membranes occurring before onset of labor at term.
- Epidemiology: between 5 and 10% of all deliveries
- Risk factors
1. Ascending infection (common)
2. Cigarette smoking
3. Multiple pregnancy
4. Previous preterm delivery
5. Previous PROM
Preterm Premature rupture of membranes (PPROM)
- Definition?
- Epidemiology?
- 6 Complications?
Prolonged rupture of membranes
- Definition?
- 4 Risk factors?
- Diagnosis?
Prolonged rupture of membranes
- Definition: Rupture of membranes that occurs > 18 hours before the onset of uterine contractions in term or preterm pregnancies
- Risk factors: young maternal age, smoking, STDs, low socioeconomic status
Prolonged rupture of membranes
- Definition?
- 4 Risk factors?
- Diagnosis?
- Management - Unstable patients?
- Management - Stable patients?
Management: The management of PROM and PPROM depends on the gestational age and the presence of intraamniotic infection or nonreassuring fetal status.
1. Monitor for signs of intraamniotic infection (body temperature, uterine tenderness, WBC count).
2. Perform fetal heart rate monitoring to assess for nonreassuring fetal status.
3. Consider intrapartum risk factors and GBS screening and prophylaxis, depending on whether previous antenatal GBS screening has been performed.
Unstable patients
- Prompt delivery in: Patients with signs of intraamniotic infection, abruptio placentae, cord prolapse & Signs of fetal distress (nonreassuring fetal heart rate)
- Additionally, collect cervical cultures and commence empiric antibiotic therapy ampicillin and gentamicin.
A 27 year old woman in her first pregnancy presents at 30 weeks gestation having lost some fluid from the vagina. What would your management be?
PROM occurs when the amniotic sac surrounding the baby breaks before the onset of labor. The management in this situation would focus on assessing the extent of the amniotic fluid loss, evaluating the well-being of the baby, and deciding on appropriate measures to ensure the best outcome for both the mother and the baby. Here’s how healthcare professionals might proceed with the management:
How would you confirm a diagnosis of ruptured membranes? (4)
Initial assessment of women presenting with term PROM should include
confirmation of the diagnosis, confirmation of gestation, confirmation of presentation and assessment of maternal and fetal wellbeing. Where there is diagnostic uncertainty, a sterile speculum examination should be performed. If uncertainty remains regarding the diagnosis, tests for the presence of amniotic fluid proteins in vaginal fluid (e.g. Amnisure) may be used.
What are the hazards of PROM to mother and baby?
Cervical insufficiency
- Definition?
- Aetiology?
- 10 Risk Factors?
- 3 Clinical features?
- Diagnosis?
Cervical insufficiency
- Definition: painless cervical dilation, in the absence of uterine contractions and/or labor, in the second trimester of pregnancy
- Aetiology: Most cases are idiopathic.
- Risk factors
1. Previous midtrimester pregnancy loss and/or preterm birth
2. Previous obstetric or gynecological trauma (e.g., termination of pregnancy, rapid delivery, multiple gestations, or cervical conization)
3. Short cervical length: transvaginal cervical length < 25 mm on ultrasound before 24 weeks’ gestation
4. Cervical connective tissue weakness (e.g., Ehler-Danlos syndrome)
5. Diethylstilbestrol exposure
Cervical insufficiency - Management: Cervical Clercage
- Definition?
- Methods? (2)
- Timing?
- 4 Indications?
- 5 Contraindications?
- In women with risk factors (i.e. previous preterm birth), serial cervical ultrasound monitoring between 16–24 weeks’ gestation because the lower uterine segment is not well developed before 16th weeks’ gestation, there is no benefit from performing ultrasound before this time.
- A shortened cervical length alone is not sufficient to diagnose cervical insufficiency.
What is Hemolytic disease of the fetus and newborn?
What is Rhesus incompatibility/disease?
- 3 Types of HDFN?
- 3 Risk factors?
Hemolytic disease of the fetus and newborn = HDFN is a condition characterized by blood group incompatibility between the mother and fetus that leads to the destruction of fetal erythrocytes by maternal antibodies.
Rhesus incompatibility = A hemolytic disease in which Rh antibodies from Rh-negative mothers transfer to an Rh-positive fetus or newborn and result in hemolysis; the severity of clinical presentation ranges from isolated mild anemia to marked anemia causing hydrops fetalis and stillbirth.
Describe the pathophysiology of ABO incompatibility in pregnancy?
ABO incompatibility - Pathophysiology
- Highest risk: mother with blood group O; newborn with blood group A or B
- Maternal antibodies (anti-A and/or anti-B) against nonself antigens of the ABO system are present even if sensitization has not occurred , so fetal hemolysis may occur during the first pregnancy.
- The presence of preexisting maternal antibodies anti-A and/or anti-B is possible in maternal blood groups O, A, and B. They are usually immunoglobulin M (IgM) antibodies (unable to cross the placenta) but may also be IgG antibodies (able to cross the placenta), which cause HDFN.
- Combination of predominantly IgM antibodies and late expression of fetal ABO antigens reduces the chances of significant disease.
Describe the pathophysiology of Rhesus incompatibility in pregnancy?
Rh incompatibility - Pathophysiology
- In an Rh-negative mother and Rh-positive newborn: maternal exposure to fetal blood (fetomaternal hemorrhage) → production of maternal IgM antibodies against the Rh antigen → over time, seroconversion to Rh-IgG (able to cross the placenta)
- In a subsequent pregnancy with an Rh-positive newborn: rapid production of maternal IgG anti-D antibodies to fetal RhD antigens → Rh-IgG agglutination of fetal RBCs with hemolytic anemia → risk of HDFN with possible hydrops fetalis
Describe the pathophysiology of Kell blood group system incompatibility in pregnancy?
What are the clinical features of Haemolytic disease of the newborn?
- 1 Prenatal?
- 6 Postnatal?
- ABO incompatibility usually has a significantly milder course of disease than Rh incompatibility.
- Anemia may conceal cyanosis.
Haemolytic Disease of the Fetus & Newborn - Diagnosis
- Prenatal diagnosis?
- Postnatal diagnosis?
The diagnosis of HDFN requires evidence of hemolysis in the presence of fetomaternal blood incompatibility.
Postnatal diagnosis
- If the newborn has signs of hemolysis, conduct a Coombs test (either direct or indirect).
- Rh incompatibility: positive
- ABO incompatibility: weak positive or negative
Rhesus Disease - Outline a pathway of care for a pregnant woman regarding rhesus disease.
About one woman in seven has a Rh(D) negative blood group, and if her baby has a blood group that is
Rh(D) positive there is a small risk that during pregnancy the baby’s blood cells might stimulate an immune
response in the mother’s blood (sensitisation). If this happens and a woman makes antibodies against the
D-positive blood group, there is a risk that a baby could be affected in this or future pregnancy. Giving
anti-D to a woman who has a Rh(D) negative blood group during, or in the days following pregnancy can
reduce the risk of sensitisation, and of adverse consequences in this and future pregnancies.
Outline the pathology testing timeline for Rh disease throughout pregnancy?
Outline the guidelines on the use and timing of Rh D immunoglobulin
for routine immunoprophylaxis in pregnancy for Rh disease?
Outline the use of Rh (D) immunoglobulins?
List 8 Potential sensitising events of Rh disease?
- 4 Contraindications to giving Rh (D) Immunoglobulins?
Potential sensitising events include:
1. Ectopic pregnancy
2. Miscarriage
3. Termination of pregnancy
4. Ultrasound guided procedures including:
− Chorionic villus sampling
− Amniocentesis
− Cordocentesis
− Fetoscopy
5. Abdominal trauma that causes uterine activity and or abdominal pain
6. External cephalic version
7. Antepartum haemorrhage
8. Birth.
A 22 year old woman in her first pregnancy is admitted with minimal antepartum haemorrhage at 28 weeks. She is Rhesus negative. She is given prophylactic anti D gamma globulin. What investigations are needed prior to the administration of anti D? (3) Why is anti D gamma globulin given? In what other circumstances should it be given? (4)
The administration of anti-D gamma globulin is given for Rh isoimmunization, which occurs when an Rh-negative mother is exposed to Rh-positive fetal blood. In this case, if the Direct Coombs test or other indicators show that the mother has developed antibodies against Rh-positive blood (Rh sensitization), anti-D gamma globulin is given to prevent the development of hemolytic disease of the fetus and newborn (HDFN) or erythroblastosis fetalis.
The primary purpose of administering anti-D gamma globulin is to prevent the mother’s immune system from producing Rh antibodies in response to the exposure to Rh-positive blood from the fetus. Anti-D gamma globulin contains Rh antibodies that bind to any Rh-positive fetal red blood cells that may have entered the mother’s circulation. This process helps to clear these cells from the mother’s bloodstream before her immune system can recognize them and mount an immune response.
How is Rhesus iso-immunisation diagnosed?
The diagnosis of Rh isoimmunization is primarily based on the presence of Rh antibodies in the mother’s blood and evidence of fetal anemia or complications on fetal assessment.
What are the effects of iso-immunisation on the fetus? (7)
Rhesus (Rh) isoimmunization, also known as Rh disease or Rh incompatibility, occurs when an Rh-negative mother is exposed to Rh-positive fetal blood during pregnancy or childbirth. This exposure can lead to the development of Rh antibodies in the mother’s blood, which can cross the placenta and attack the red blood cells of an Rh-positive fetus. The effects of isoimmunization on the fetus can be severe and potentially life-threatening.
What are the treatments of iso-immunisation in pregnancy?
To prevent Rh isoimmunization, Rh-negative pregnant women receive anti-D gamma globulin (Rh immune globulin) after specific events that may lead to fetal blood exposure to Rh-positive blood, such as during pregnancy-related bleeding, after delivery of an Rh-positive baby, or after certain invasive prenatal procedures. This preventive measure aims to prevent Rh sensitization and the subsequent development of Rh isoimmunization during subsequent pregnancies.
Is there a need to check for antibodies if a woman is known to be Rh positive? Why or why not?
No, there is no need to check for antibodies if a woman is known to be Rh positive. The reason is that Rh antibodies are only produced in Rh-negative individuals who have been exposed to Rh-positive blood.
When a woman is Rh positive, it means she has the Rh factor (antigen) on the surface of her red blood cells. If an Rh-positive woman becomes pregnant with an Rh-positive baby, there is no risk of Rh isoimmunization or the development of Rh antibodies. This is because there is no antigenic difference between the mother and the baby’s red blood cells, so the mother’s immune system does not recognize the baby’s red blood cells as foreign and does not produce antibodies against them.
A 30 year old Jehovah’s witness attends for antenatal care. She has previously had one uneventful pregnancy and delivery. At her first visit her haemoglobin is noted at 100g/l (Normal range 110-140g/L). What investigation is needed? What advice would you give her regarding nutritional supplementation?
- Anaemia is defined by the WHO as a haemoglobin (Hb) <110 g/L at any stage of pregnancy and <100 g/L postpartum.
- Physiological changes occur in the second trimester, increasing plasma volume alongside a smaller increase in red cell mass resulting in haemodilution – recognised as ‘physiological anaemia’. Therefore, a threshold of Hb <105 g/L in the second trimester is widely used throughout international guidelines in defining and directing management.
At 16 weeks gestation, a 26 year old woman is noted to have a haemoglobin of 98g/l. Her parents were born in Greece. What investigations should be undertaken? What advice should she be given with regards to iron and folate supplementation?
In this scenario, the 26-year-old woman at 16 weeks gestation with a hemoglobin level of 98g/L and a family history of Greek ancestry should undergo further investigations to determine the cause of her low hemoglobin. Certain genetic conditions, such as thalassemia, are more prevalent in individuals with Mediterranean ancestry, including Greek populations. Thalassemia is a group of inherited blood disorders that can lead to anemia.
Maternal complications of gestational and pregestational diabetes mellitus?
In what ways can diabetes mellitus be screened for in a normal obstetric population? (5)
In a normal obstetric population, screening for diabetes mellitus can be performed using various methods to identify women at risk of or already affected by gestational diabetes mellitus (GDM) or pre-existing diabetes.
Criteria for Diagnosis of GDM with a 2-hour Pregnancy Oral GTT?
List 11 clinical risk factors for diabetes mellitus in pregnancy?
The clinical risk factors for diabetes mellitus in pregnancy, particularly gestational diabetes mellitus (GDM), are factors that increase the likelihood of a pregnant woman developing diabetes during her pregnancy. Identifying these risk factors is crucial to implement early screening and appropriate management.
Management of Gestational Diabetes?
- Lifestyle management
- Self-monitoring of blood glucose
- Pharmacological therapies - Metformin or insulin
- Fetal surveillance & delivery planning
- Follow-up post partum
What are the effects of diabetes mellitus on the fetus?
- What is Diabetic embryopathy?
- Onset?
- Pathophysiology?
Pregestational diabetes poses a greater risk of complications than gestational diabetes. Complications during the first trimester are more common in pregestational diabetes, while complications during the second and third trimesters are equally associated with pregestational and gestational diabetes.
List 10 Manifestations of diabetic embryopathy?
List 10 Manifestations of diabetic embryopathy?
What is Diabetic fetopathy?
- Definition?
- Onset?
- Pathophysiology?
- Manifestations? (4)
Diabetic fetopathy
- Definition: any anomaly in a fetus associated with maternal diabetes, caused by fetal hyperinsulinemia during gestation
- Onset: second and third trimesters
- Pathophysiology: maternal hyperglycemia → fetal hyperglycemia → stimulation of fetal pancreas → fetal hyperinsulinemia → ↑ metabolic rate, oxygen consumption, and fetal hypoxemia → metabolic, respiratory, and cardiovascular complications
An asthmatic woman aged 30 seeks your advice before embarking on a pregnancy. What effect will the asthma treatment (Ventolin inhaler, Becotide) have on her pregnancy? Will she have increased frequency of asthmatic episodes?
- About half of Australian women with asthma find their asthma gets a bit worse during pregnancy, often between 17 and 36 weeks gestation.
- The most important thing is that you do not stop taking your asthma medication – especially your preventer.
An asthmatic woman aged 30 seeks your advice before embarking on a pregnancy. What are the possible complications of her pregnancy if she requires systemic steroids?
An 18 year old primigravida presents at 24 weeks gestation with a temperature of 38C. She complains of right loin pain present for 12 hours. What is the likely diagnosis? What is the optimal treatment? How might the pregnancy be affected?
The likely diagnosis for the 18-year-old primigravida presenting at 24 weeks gestation with a temperature of 38°C and right loin pain for 12 hours is acute pyelonephritis. Acute pyelonephritis is a bacterial infection of the kidneys and is more common during pregnancy due to anatomical and hormonal changes that can impair the normal flow of urine and make pregnant women more susceptible to urinary tract infections. Optimal Treatment:
The treatment for acute pyelonephritis in pregnancy typically involves hospital admission and intravenous antibiotics. The choice of antibiotics will depend on local antibiotic sensitivity patterns and should be safe for use during pregnancy. Commonly used antibiotics include penicillins, cephalosporins, or aminoglycosides. The duration of antibiotic therapy will depend on the severity of the infection and the response to treatment. Adequate hydration and pain relief may also be provided to manage symptoms.
What are the management options in pregnancy in a woman who has had a DVT in the past?
Flowchart: Antenatal and postnatal thromboprophylaxis according to risk?
Thromboprophylaxis flowchart for a pregnant woman with Family history of VTE but no personal history VTE?
Flowchart 2: Thromboprophylaxis in women with no prior history of
VTE, but family history of VTE and/or known thrombophilia?
Family history of VTE is significant if it occurs in a first degree relative (ie. parents or siblings).
Outline Antenatal thromboprophylaxis in women with clinical risk factors?
Who gets post-partum thromboprophylaxis? (3)
- Any woman who has been on antenatal anticoagulation (LMWH) for maternal thromboprophylaxis, regardless of mode of delivery: 6-12 weeks.
- Any woman who has a personal history of a thromboembolic event, regardless of mode of delivery or whether they were on antenatal thromboprophylaxis: 6-12 weeks.
- Women with clinical risk factors stratified according to table.
What is a CTG?
- What is it comprised of? (2)
CTG = CardioTocoGraphy
When do we use a CardioTocoGraph (CTG)
- Antepartum? (3)
- Intrapartum: antenatal risk factors? (3)
- Intrapartum factors? (6)
AMA = Advanced Maternal Age
CTG Antepartum Use
1. From 24 weeks onwards
2. High risk pregnancies – routine monitoring. Examples- Diabetes in Pregnancy, Fetal Growth Restriction, Hypertensive Disorders of Pregnancy
3. Emergency admissions: Examples- Reduced fetal movements, Antepartum haemorrhage, Rupture of membranes, trauma, infection
Outline an approach to intepreting CTGs - What are we looking for?
- Dr C BraVADO?
Dr C BraVADO
- Dr : Define risk
- C : Contractions
- Bra : Baseline rate
- V : Variability
- A : Accelerations
- D : Decelerations
- O : Overall impression
CTGs - Dr C BraVADO
- How do we define risk?
CTGs - Dr C BraVADO
- What is a normal number of Contractions?
- What is Hyperstimulation?
- Normally 3-4 contractions in 10 mins each lasting 40-60 seconds every 2-3mins with relaxation of the uterus between contractions to allow for placental blood to be flushed with maternal blood and fetal oxygenation.
- A CTG can only determine the frequency of the contractions but the Strength of contractions is felt clinically or with an intrauterine pressure transducer.
- Hyperstimulation = tachysystole with an abnormal CTG
CTGs - Dr C BraVADO
- What is a normal baseline HR?
- 5 Causes of Fetal Tachycardia?
- 7 Causes of Fetal Bradycardia?
- Baseline rate: Is it normal, or is it bradycardia/tachycardia?
- Is it the same as it was at the start of labour?
- More important to look at the trend
- Normal baseline FHR 110-160bpm
- Bradycardia if FHR < 110 bpm for >5 minutes
- Baseline fetal HR must be determined when there are no uterine contractions!
CTGs - Dr C BraVADO
- What is Variability?
- Variability in HR once baseline has been defined - can vary 5-25 beats above or below baseline
- Variability is the most important aspcet of CTG as it represents the SNS & PSNS balance in the fetal brainstem (Autonomic NS oxygenation)
CTGs - Dr C BraVADO
- What are Accelerations?
- Acceleration = +15 beats above the baseline for >15 seconds more than 2 in a cycle
CTGs - Dr C BraVADO
- What are Decelerations?
- 4 Types?
- What are early decelarations? When are they seen? (2)
Decelerations
- Considered “abnormal”, but may not always be concerning
- Fall in FHR by 15 beats from baseline and lasting 15 seconds
- There are four types and a good recording on the toco is required to differentiate between the four:
1. Early
2. Variable
3. Prolonged
4. Late
CTGs - Dr C BraVADO
- What are 5 instances when decelerations are concerning?
CTGs - Dr C BraVADO
- What are Variable decelerations? What are they generally caused by?
- What 4 things do they vary in?
- What are 5 instances when variable decelerations are concerning?
Some variables are more concerning than others - Consider:
1. A rising baseline or tachycardia?
2. Reducing variability?
3. Persistent deep or long variables?
4. A smooth post deceleration overshoot (NOT shouldering)?
5. Slow recovery?
CTGs - Dr C BraVADO
- What are Prolonged decelerations? What are they a sign of?
- What are Late decelerations? Likely cause?
Late decelarations = fetal hypoxia!
CTGs - Sinusoidal & Pseudosinusoidal patterns
- What do they look like?
- What do they reflect?
SPECIAL PATTERNS on CTG
1. Sinusoidal; reflective of severe anaemia in the fetus, and generally seen with a complaint of RFM (Reduced Fetal Movements)
- THIS IS A COMPROMISED FETUS
- This trace warrants immediate delivery
- Sawtooth appearance
- Pseudosinusoidal; looks sinusoidal, but the trace was normal before/is normal afterwards Often attributed to thumb sucking!
CTG - Case Study
- 27 year old
- 37 weeks and 2 days
- Admitted for induction of labour
- GDM on Insulin poorly controlled
- Renal artery stenosis
- Group B Streptococcus positive
- IOL with Cervidil
- Fetal distress
- Emergency Caesarean section
GBS Positive - means she will need IV antibiotics during labour (either penicillin or clindamycin)
Cervidil = a prostaglandin
CTG at admission
- variability normal
- 2 accelerations in a 10 minute period
- >15beats lasting more than 15 seconds
- Normal CTG
CTG at decision for CS
- prolonged deceleration bordering on bradycardia
- Outcome: Baby cried at birth, Normal cord gases
CTG - Case Study
- G2 P1
- Low risk pregnancy
- Anatomy scan- Placenta covering cervical Os
- Scan 32 weeks- Placenta upper segment
- 40 weeks and 3 days – Stretch and Sweep for IOL
- Presented with bleeding PV 24 hours later
- Scan – Placenta posterior and 5 cm from os
- IOL- fetal distress during IOL
- Emergency CS, Baby 4.5 Kg
- Normal Cord gases
Bleeding = irritable uterus
Mothers HR up and down = pain (pink)
Fetal HR (red) going up during the bleed then it can no longer cope so it drops
2nd CTG - babys HR goes up to compensate but it drops and gets a bradycardia as it cant cope - goes up and down
Outline a clinical approach to Early Pregnancy complications
- Hx, Exam, Ixs, Mx?
Early Pregnancy Complications - Clinical Approach
1. History -dates, pain
2. Examination- abdo, speculum, bi-manual
3. Investigation- hb, group,BHCG, U/S, laparoscopy
4. Management- Anti-D, expectant Mx, evacuation of uterus, treatment of ectopic
When a pregnant patient presents with a high blood pressure, what is the first thing you should do?
= Ensure the Blood pressure measurement is correct
- Seated and relaxed
- Cuff size
- Arm at heart level
- Korotkoff V
- First visit both arms
- Average readings
15 Risk factors of Preeclampsia?
BP ≥ 140/90 (x2) after 20 weeks with normal pre-pregnancy BP and > Pr/Cr ratio >30mg/mmol (≥ 2+ dipstick) or evidence multisystem dysfunction (renal, hepatic, neurological, hematological, IUGR)
List 2 Circulating angiogenic factors which increase in preeclampsia and 1 that descreases?
In the nonpregnant state natural killer cells are a prominent immunological cell in the endometrium. Play a role in eliminating foreign cells, usually malignant cells or infectious agents. the NK cells secrete angiogenic growth factors and are thought to play an important role in implantation and may influence fertility. They surround the spiral arteries and interact with extravillous trophoblast cells to assist their migration into the spiral arteries, in which they cause dilatation by disruption of the elastin in the arterial wall. This process is impaired in the first trimester in pregnancies which go on to manifest with IUGR or preeclampsa.
What are the 3 Preeclampsia subtypes?
- Early onset vs late onset (prior to or after 34 weeks gestation). Ongoing debate re whether different diseases
- Pure maternal (80-90% of cases) vs combined with IUGR (most of these early onset)
- HELLP syndrome
4 Signs/Symptoms of Preeclampsia?
7 Laboratory manifestations?
- Headache
- Visual disturbance
- Epigastric/Right upper quadrant pain
- Rapid weight gain/oedema
Describe what happens to uric acid levels throughout pregnancy? Role in preeclampsia?
- 7 Causes of thrombocytopenia in pregnancy?
- 5 Causes of deranged LFTs in pregnancy?
Preeclampsia & Uric Acid
- Levels fall by 25% early pregnancy then Rise throughout gestation
- Raised in preeclampsia- may be diagnostically useful
- Some correlation of level with eclampsia, severe hypertension, fetal outcome but poor predictor
- Hemolysis, polycythemia and renal disease may also cause elevated levels
Describe what happens to renal function (serum urea/creatinine) during pregnancy?
What is the management for Preeclampsia & Eclampsia? (6)
- Acute antihypertensive treatment?
- Prophylaxis- low dose aspirin & calcium
- Delivery!
- Anti-hypertensive therapy
- Convulsions- primary & secondary
- HELLP syndrome monitoring
- Volume management
10 Life Threatening Manifestations of Eclampsia?
- Seizures
- Cerebral haemorrhage
- Cerebral oedema
- Hepatic failure
- Liver haematoma/ rupture
- Ventricular dysfunction
- Pulmonary oedema
- Placental abruption
- DIC
- Renal failure
