Week 4 part 2 Flashcards
Women are routinely screened for anaemia twice during pregnancy:
- Booking clinic
* 28 weeks gestation
The normal ranges for haemoglobin during pregnancy are:
Booking bloods > 110 g/l
28 weeks gestation > 105 g/l
Post partum > 100 g/l
The mean cell volume (MCV) can indicate the cause of the anaemia:
- Low MCV may indicate iron deficiency
- Normal MCV may indicate a physiological anaemia due to the increased plasma volume of pregnancy
- Raised MCV may indicate B12 or folate deficiency
Iron requirements for anemic pregnant women
Iron replacement (e.g. ferrous sulphate 200mg three times daily). When women are not anaemic, but have a low ferritin (indicating low iron stores), they may be started on supplementary iron.
If Vitamin B12 deficiency is suspected in pregnancy, what disease needs to be investigated as a cause?
Women with low B12 should be tested for pernicious anaemia (checking for intrinsic factor antibodies).
Management of Vitamin B12 deficiency in pregnant women.
- Intramuscular hydroxocobalamin injections
* Oral cyanocobalamin tablets
Risk factors for VTE in pregnancy:
- Smoking
- Parity ≥ 3
- Age > 35 years
- BMI > 30
- Reduced mobility
- Multiple pregnancy
- Pre-eclampsia
- Gross varicose veins
- Immobility
- Family history of VTE
- Thrombophilia
- IVF pregnancy
The RCOG guidelines (2015) advise starting prophylaxis for VTE
28 weeks if there are three risk factors
First trimester if there are four or more of these risk factors
Management of pregnant women at risk of VTE
Women at increased risk of VTE should receive prophylaxis with low molecular weight heparin (LMWH) unless contraindicated. Examples of LMWH are enoxaparin, dalteparin and tinzaparin.
Prophylaxis is started as soon as possible in very high risk patients and at 28 weeks in those at high risk. It is continued throughout the antenatal period and for six weeks postnatally.
Prophylaxis is temporarily stopped when the woman goes into labour, and can be started immediately after delivery (except with postpartum haemorrhage, spinal anaesthesia and epidurals).
Deep vein thrombosis FEATURES
- Calf or leg swelling
- Dilated superficial veins
- Tenderness to the calf
- Oedema
- Colour changes to the leg
Investigations for DVT in pregnancy
Doppler ultrasound is the investigation of choice for patients with suspected deep vein thrombosis. The RCOG guideline (2015) recommends repeating negative ultrasound scans on day 3 and 7 in patients with a high index of suspicion for DVT.
Investigations for PE in pregnancy
• Chest xray
• ECG
CT pulmonary angiogram (CTPA) or ventilation-perfusion (VQ) scan.
When considering the choice between CTPA and VQ scan:
• CTPA is the test for choice for patients with an abnormal chest xray
• CTPA carries a higher risk of breast cancer for the mother (minimal absolute risk)
• VQ scan carriers a higher risk of childhood cancer for the fetus (minimal absolute risk)
Diagnosis of DVT and PE in pregnancy
Patients with a suspected deep vein thrombosis and pulmonary embolism should have a Doppler ultrasound initially, and if a DVT is present, they do not require a VQ scan or CTPA to confirm a PE. The treatment for DVT and PE are the same.
Women with a massive PE and haemodynamic compromise need immediate management. This is a life-threatening scenario. Treatment options are:
- Unfractionated heparin
- Thrombolysis
- Surgical embolectomy
Pre-eclampsia
Pre-eclampsia refers to new high blood pressure (hypertension) in pregnancy with end-organ dysfunction, notably with proteinuria (protein in the urine). It occurs after 20 weeks gestation, when the spiral arteries of the placenta form abnormally, leading to a high vascular resistance in these vessels.
Pre-eclampsia features a triad of:
- Hypertension
- Proteinuria
- Oedema
Pre-eclampsia complications
Significant cause of maternal and fetal morbidity and mortality. Without treatment, it can lead to maternal organ damage, fetal growth restriction, seizures, early labour and in a small proportion, death.
Chronic hypertension in pregnancy
Chronic hypertension is high blood pressure that exists before 20 weeks gestation and is longstanding. This is not caused by dysfunction in the placenta and is not classed as pre-eclampsia
Pregnancy-induced hypertension or gestational hypertension
Pregnancy-induced hypertension or gestational hypertension is hypertension occurring after 20 weeks gestation, without proteinuria.
Eclampsia
Eclampsia is when seizures occur as a result of pre-eclampsia.
High-risk factors for pre-eclampsia
- Pre-existing hypertension
- Previous hypertension in pregnancy
- Existing autoimmune conditions (e.g. systemic lupus erythematosus)
- Diabetes
- Chronic kidney disease
Moderate-risk factors for pre-eclampsia
- Older than 40
- BMI > 35
- More than 10 years since previous pregnancy
- Multiple pregnancy
- First pregnancy
- Family history of pre-eclampsia
Pre-eclampsia has symptoms of the complications:
- Headache
- Visual disturbance or blurriness
- Nausea and vomiting
- Upper abdominal or epigastric pain (this is due to liver swelling)
- Oedema
- Reduced urine output
- Brisk reflexes
Diagnosis of Pre-eclampsia
- Systolic blood pressure above 140 mmHg
- Diastolic blood pressure above 90 mmHg
PLUS any of:
> Proteinuria (1+ or more on urine dipstick)
> Organ dysfunction (e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia or haemolytic anaemia)
> Placental dysfunction (e.g. fetal growth restriction or abnormal Doppler studies)
Proteinuria can be quantified using:
- Urine protein:creatinine ratio (above 30mg/mmol is significant)
- Urine albumin:creatinine ratio (above 8mg/mmol is significant)
Management of pre-eclampsia risk factors
Aspirin is used for prophylaxis against the development of pre-eclampsia. It is given from 12 weeks gestation until birth to women with:
• A single high-risk factor
• Two or more moderate-risk factors
When pre-eclampsia is diagnosed, the general management is similar to gestational hypertension, except:
- Scoring systems are used to determine whether to admit the woman (fullPIERS or PREP S)
- Blood pressure is monitored closely (at least every 48 hours)
- Ultrasound monitoring of the fetus, amniotic fluid and dopplers is performed two weekly
Medical management of pre-eclampsia is with:
- Labetolol is first-line as an antihypertensive
- Nifedipine (modified-release) is commonly used second-line
- Methyldopa is used third-line (needs to be stopped within two days of birth)
- Intravenous hydralazine may be used as an antihypertensive in critical care in severe pre-eclampsia or eclampsia
- IV magnesium sulphate is given during labour and in the 24 hours afterwards to prevent seizures
- Fluid restriction is used during labour in severe pre-eclampsia or eclampsia, to avoid fluid overload
Management of eclampsia
Eclampsia refers to the seizures associated with pre-eclampsia. IV magnesium sulphate is used to manage seizures associated with pre-eclampsia.
HELLP syndrome
HELLP syndrome is a combination of features that occurs as a complication of pre-eclampsia and eclampsia. It is an acronym for the key characteristics:
• Haemolysis
• Elevated Liver enzymes
• Low Platelets
Significant immediate complications of gestational diabetes
is a large for dates fetus and macrosomia. This has implications for birth, mainly posing a risk of shoulder dystocia. Longer-term, women are at higher risk of developing type 2 diabetes after pregnancy.
Risk factors for gestational diabetes
- Previous gestational diabetes
- Previous macrosomic baby (≥ 4.5kg)
- BMI > 30
- Ethnic origin (black Caribbean, Middle Eastern and South Asian)
- Family history of diabetes (first-degree relative)
Diagnostic tool for gestational diabetes
The screening test of choice for gestational diabetes is an oral glucose tolerance test (OGTT). An OGTT is used in patients with risk factors for gestational diabetes, and also when there are features that suggest gestational diabetes:
• Large for dates fetus
• Polyhydramnios (increased amniotic fluid)
• Glucose on urine dipstick
Oral glucose tolerance test results for gestational diabetes
Normal results are:
• Fasting: < 5.6 mmol/l
• At 2 hours: < 7.8 mmol/l
Results higher than these values are used to diagnose gestational diabetes.
The initial management suggested by NICE for gestational diabetes
- Fasting glucose less than 7 mmol/l: trial of diet and exercise for 1-2 weeks, followed by metformin, then insulin
- Fasting glucose above 7 mmol/l: start insulin ± metformin
- Fasting glucose above 6 mmol/l plus macrosomia (or other complications): start insulin ± metformin
What drug is given in gestational diabetes when the pregnant women declines insulin or is intolerant of metformin?
Glibenclamide (a sulfonylurea) is suggested as an option for women who decline insulin or cannot tolerate metformin.
Gestational Diabetes blood sugar targets in pregnancy
- Fasting: 5.3 mmol/l
- 1 hour post-meal: 7.8 mmol/l
- 2 hours post-meal: 6.4 mmol/l
- Avoiding levels of 4 mmol/l or below
Delivery in gestational diabetes
NICE (2015) advise a planned delivery between 37 and 38 + 6 weeks for women with pre-existing diabetes. (Women with gestational diabetes can give birth up to 40 + 6).
A sliding-scale insulin regime is considered during labour for women with type 1 diabetes. A dextrose and insulin infusion is titrated to blood sugar levels, according to the local protocol. This is also considered for women with poorly controlled blood sugars with gestational or type 2 diabetes.
What is a screened for in gestational diabetes?
Retinopathy screening should be performed shortly after booking and at 28 weeks gestation. This involves referral to an ophthalmologist to check for diabetic retinopathy. Diabetes carries a risk of rapid progression of retinopathy, and interventions may be required.
Babies of mothers with diabetes are at risk of:
- Neonatal hypoglycaemia
- Polycythaemia (raised haemoglobin)
- Jaundice (raised bilirubin)
- Congenital heart disease
- Cardiomyopathy
Neonatal hypoglycemia management after birth
Babies need close monitoring for neonatal hypoglycaemia, with regular blood glucose checks and frequent feeds. The aim is to maintain their blood sugar above 2 mmol/l, and if it falls below this, they may need IV dextrose of nasogastric feeding.
Obstetric cholestasis
Obstetric cholestasis is characterised by the reduced outflow of bile acids from the liver. The condition resolves after delivery of the baby.
Relatively common complication of pregnancy, occurring in around 1% of pregnant women. It usually develops later in pregnancy (i.e. after 28 weeks), and is thought to be the result of increased oestrogen and progesterone levels.
Presentation of Obstetric cholestasis
Present later in pregnancy, particularly in the third trimester.
Itching (pruritis) is the main symptom, particularly affecting the palms of the hands and soles of the feet.
Other symptoms are related to cholestasis and outflow obstruction in the bile ducts:
• Fatigue
• Dark urine
• Pale, greasy stools
• Jaundice
Investigations in Obstetric cholestasis
Women presenting with pruritus should have liver function tests and bile acids checked.
Obstetric cholestasis will cause:
• Abnormal liver function tests (LFTs), mainly ALT, AST and GGT
• Raised bile acids
Raised ALP in pregnancy
It is normal for alkaline phosphatase (ALP) to increase in pregnancy. This is because the placenta produces ALP. A rise in ALP without other abnormal LFT results is usually due to placental production of ALP, rather than liver pathology.
Management of Obstetric cholestasis
Ursodeoxycholic acid is the primary treatment for obstetric cholestasis.
Symptoms of itching can be managed with:
• Emollients (i.e. calamine lotion) to soothe the skin
• Antihistamines (e.g. chlorphenamine) can help sleeping (but does not improve itching)
Water-soluble vitamin K can be given if clotting (prothrombin time) is deranged
Acute fatty liver of pregnancy
A rare condition that occurs in the third trimester of pregnancy. There is a rapid accumulation of fat within the liver cells (hepatocytes), causing acute hepatitis. There is a high risk of liver failure and mortality, for both the mother and fetus.
Acute fatty liver of pregnancy pathophysiology
Results from impaired processing of fatty acids in the placenta. This is the result of a genetic condition in the fetus that impairs fatty acid metabolism. The most common cause is long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency in the fetus, which is an autosomal recessive condition.
Th LCHAD enzyme is important in fatty acid oxidation, breaking down fatty acids to be used as fuel. The fetus and placenta are unable to break down fatty acids. These fatty acids enter the maternal circulation, and accumulate in the liver. The mother’s defective copy of the gene may also contribute to the accumulation of fatty acids. The accumulation of fatty acids in the mother’s liver leads to inflammation and liver failure.
Presentation of Acute fatty liver of pregnancy
- General malaise and fatigue
- Nausea and vomiting
- Jaundice
- Abdominal pain
- Anorexia (lack of appetite)
- Ascites
Investigations in Acute fatty liver of pregnancy
Liver function tests will show elevated liver enzymes (ALT and AST).
Other bloods may be deranged, with:
• Raised bilirubin
• Raised WBC count
• Deranged clotting (raised prothrombin time and INR)
• Low platelets
Elevated liver enzymes and low platelets
In your exams, elevated liver enzymes and low platelets should make you think of HELLP syndrome rather than acute fatty liver of pregnancy. HELLP syndrome is much more common, but keep acute fatty liver of pregnancy in mind as a differential.
Management of Acute fatty liver of pregnancy
Acute fatty liver of pregnancy is an obstetric emergency and requires prompt admission and delivery of the baby. Most patients will recover after delivery.
Management also involves treatment of acute liver failure if it occurs, including consideration of liver transplant.
Polymorphic eruption of pregnancy
It is an itchy rash that tends to start in the third trimester. It usually begins on the abdomen, particularly associated with stretch marks (striae).
It is characterised by:
• Urticarial papules (raised itchy lumps)
• Wheals (raised itchy areas of skin)
• Plaques (larger inflamed areas of skin)
Atopic eruption of pregnancy
Refers to eczema that flares up during pregnancy. This includes both women that have never suffered with eczema and those with pre-existing eczema. Atopic eruption of pregnancy presents in the first and second trimester of pregnancy.
Melasma
Characterised by increased pigmentation to patches of the skin on the face. This is usually symmetrical and flat, affecting sun-exposed areas.
Melasma is thought to be partly related to the increased female sex hormones associated with pregnancy. It can also occur with the combined contraceptive pill and hormone replacement therapy. It is also associated with sun exposure, thyroid disease and family history.
Pyogenic Granuloma
Benign, rapidly growing tumour of capillaries. It present as a discrete lump with a red or dark appearance. They occur more often in pregnancy, and can also be associated with hormonal contraceptives. They can also be triggered by minor trauma or infection.
Pyogenic granuloma present with a rapidly growing lump that develops over days up to 1-2 cm in size, (but can be larger). They often occur on fingers, or on the upper chest, back, neck or head. They may cause profuse bleeding and ulceration if injured
Pemphigoid gestationis
Autoimmune skin condition that occurs in pregnancy. Autoantibodies are created that damage the connection between the epidermis and the dermis. This causes the epidermis and dermis to separate, creating a space that can fill with fluid, resulting in large fluid-filled blisters (bullae).
Usually occurs in the second or third trimester. The typical presentation is initially with an itchy red papular or blistering rash around the umbilicus, that then spreads to other parts of the body. Over several weeks, large fluid-filled blisters form.
Placenta praevia
Placenta praevia is where the placenta is attached in the lower portion of the uterus, lower than the presenting part of the fetus. Praevia directly translates from Latin as “going before”.
Placenta praevia happens when your placenta (afterbirth) attaches in the lower part of your uterus (womb), sometimes completely covering the cervix (neck of the womb).
What is placenta praevia a risk factor for?
antepartum haemorrhage
The three causes of antepartum haemorrhage
Placenta praevia, placental abruption and vasa praevia. These are serious causes with high morbidity and mortality. Causes of spotting or minor bleeding in pregnancy include cervical ectropion, infection and vaginal abrasions from intercourse or procedures
Placenta praevia is associated with increased morbidity and mortality for the mother and fetus. The risks include:
- Antepartum haemorrhage
- Emergency caesarean section
- Emergency hysterectomy
- Maternal anaemia and transfusions
- Preterm birth and low birth weight
- Stillbirth
The risk factors for placenta praevia are:
- Previous caesarean sections
- Previous placenta praevia
- Older maternal age
- Maternal smoking
- Structural uterine abnormalities (e.g. fibroids)
- Assisted reproduction (e.g. IVF)
Diagnosis of placenta praevia
The 20-week anomaly scan is used to assess the position of the placenta and diagnose placenta praevia.
Presentation of placenta praevia
Many women with placenta praevia are asymptomatic. It may present with painless vaginal bleeding in pregnancy (antepartum haemorrhage). Bleeding usually occurs later in pregnancy (around or after 36 weeks).
Management of placenta praevia
Repeat transvaginal ultrasound scan at:
• 32 weeks gestation
• 36 weeks gestation
Corticosteroids are given between 34 and 35 + 6 weeks gestation to mature the fetal lungs, given the risk of preterm delivery.
Planned delivery is considered between 36 and 37 weeks gestation. It is planned early to reduce the risk of spontaneous labour and bleeding.
Emergency caesarean section may be required with premature labour or antenatal bleeding
Vasa praevia
Where the fetal vessels are within the fetal membranes (chorioamniotic membranes) and travel across the internal cervical os. The fetal membranes surround the amniotic cavity and developing fetus. The fetal vessels consist of the two umbilical arteries and single umbilical vein.
Pathophysiology of vasa praevia
Under normal circumstances, the umbilical cord containing the fetal vessels (umbilical arteries and vein) inserts directly into the placenta. The fetal vessels are always protected, either by the umbilical cord or by the placenta. The umbilical cord contains Wharton’s jelly. Wharton’s jelly is a layer of soft connective tissue that surrounds the blood vessels in the umbilical cord, offering protection.
In vasa praevia, the fetal vessels are exposed, outside the protection of the umbilical cord or the placenta. The fetal vessels travel through the chorioamniotic membranes, and pass across the internal cervical os (the inner opening of the cervix). These exposed vessels are prone to bleeding, particularly when the membranes are ruptured during labour and at birth. This can lead to dramatic fetal blood loss and death.
There are two types of vasa praevia:
- Type I vasa praevia – the fetal vessels are exposed as a velamentous umbilical cord
- Type II vasa praevia – the fetal vessels are exposed as they travel to an accessory placental lobe
Risk factors for vasa praevia
- Low lying placenta
- IVF pregnancy
- Multiple pregnancy
Presentation of vasa praevia
Diagnosed by ultrasound during pregnancy. This is the ideal scenario, as it allows a planned caesarean section to reduce the risk of haemorrhage.
It may present with antepartum haemorrhage, with bleeding during the second or third trimester of pregnancy.
It may be detected by vaginal examination during labour, when pulsating fetal vessels are seen in the membranes through the dilated cervix.
Finally, it may be detected during labour when fetal distress and dark-red bleeding occur following rupture of the membranes. This carries a very high fetal mortality, even with emergency caesarean section.
Management of vasa praevia
• Corticosteroids, given from 32 weeks gestation to mature the fetal lungs
• Elective caesarean section, planned for 34 – 36 weeks gestation
Where antepartum haemorrhage occurs, emergency caesarean section is required to deliver the fetus before death occurs.
Placental abruption
Refers to when the placenta separates from the wall of the uterus during pregnancy. The site of attachment can bleed extensively after the placenta separates. Placental abruption is a significant cause of antepartum haemorrhage.
Risk factors for placental abruption
- Previous placental abruption
- Pre-eclampsia
- Bleeding early in pregnancy
- Trauma (consider domestic violence)
- Multiple pregnancy
- Fetal growth restriction
- Multigravida
- Increased maternal age
- Smoking
- Cocaine or amphetamine use
Presentation of placental abruption
- Sudden onset severe abdominal pain that is continuous
- Vaginal bleeding (antepartum haemorrhage)
- Shock (hypotension and tachycardia)
- Abnormalities on the CTG indicating fetal distress
- Characteristic “woody” abdomen on palpation, suggesting a large haemorrhage
Concealed placental abruption
Where the cervical os remains closed, and any bleeding that occurs remains within the uterine cavity. The severity of bleeding can be significantly underestimated with concealed haemorrhage.
Concealed abruption is opposed to revealed abruption, where the blood loss is observed via the vagina.
Management of massive hemorrhage in placental abruption
The initial steps with major or massive haemorrhage are:
• Urgent involvement of a senior obstetrician, midwife and anaesthetist
• Bloods include FBC, UE, LFT and coagulation studies
• Crossmatch 4 units of blood
• Fluid and blood resuscitation as required
• CTG monitoring of the fetus
• Close monitoring of the mother
The risk of what complication is increased after placental abruption?
There is an increased risk of postpartum haemorrhage after delivery in women with placental abruption. Active management of the third stage is recommended.
Placenta accreta
Refers to when the placenta implants deeper, through and past the endometrium, making it difficult to separate the placenta after delivery of the baby. It is referred to as placenta accreta spectrum, as there is a spectrum of severity in how deep and broad the abnormal implantation extends.
Pathophysiology of placenta accreta
Usually the placenta attaches to the endometrium. This allows the placenta to separate cleanly during the third stage of labour, after delivery of the baby.
With placenta accreta, the placenta embeds past the endometrium, into the myometrium and beyond. This may happen due to a defect in the endometrium. Imperfections may occur due to previous uterine surgery, such as a caesarean section or curettage procedure.
The deep implantation makes it very difficult for the placenta to separate during delivery, leading to extensive bleeding (postpartum haemorrhage).
Superficial placenta accreta
is where the placenta implants in the surface of the myometrium, but not beyond
Placenta increta
is where the placenta attaches deeply into the myometrium
Placenta percreta
is where the placenta invades past the myometrium and perimetrium, potentially reaching other organs such as the bladder
Risk factors for placenta accreta
- Previous placenta accreta
- Previous endometrial curettage procedures (e.g. for miscarriage or abortion)
- Previous caesarean section
- Multigravida
- Increased maternal age
- Low-lying placenta or placenta praevia
Placenta accreta presentation
Does not typically cause any symptoms during pregnancy. It can present with bleeding (antepartum haemorrhage) in the third trimester.
It may be diagnosed on antenatal ultrasound scans, and particular attention is given to women with a previous placenta accreta or caesarean during scanning.
It may be diagnosed at birth, when it becomes difficult to deliver the placenta. It is a cause of significant postpartum haemorrhage.
Management of placenta accreta
Ideally, placenta accreta is diagnosed antenatally by ultrasound. This allows planning for birth.
MRI scans may be used to assess the depth and width of the invasion.
A specialist MDT should manage women with placenta accreta. This may include:
• Complex uterine surgery
• Blood transfusions
• Intensive care for the mother
• Neonatal intensive care
Delivery is planned between 35 to 36 + 6 weeks gestation to reduce the risk of spontaneous labour and delivery. Antenatal steroids are given to mature the fetal lungs before delivery.
Breech presentation
Refers to when the presenting part of the fetus (the lowest part) is the legs and bottom. This is opposed to cephalic presentation, where the head is the presenting part. Breech presentation occurs in less than 5% of pregnancies by 37 weeks gestation.
Management of breech presentation
Babies that are breech before 36 weeks often turn spontaneously, so no intervention is advised. External cephalic version (ECV) can be used at term (37 weeks) to attempt to turn the fetus.
Where ECV fails, women are given a choice between vaginal delivery and elective caesarean section. Vaginal delivery needs to involve experienced midwives and obstetricians, with access to emergency theatre if required.
External Cephalic Version
External cephalic version (ECV) is a technique used to attempt to turn a fetus from the breech position to a cephalic position using pressure on the pregnant abdomen. It is about 50% successful.
Women are given tocolysis to relax the uterus before the procedure. Tocolysis is with subcutaneous terbutaline. Terbutaline is a beta-agonist similar to salbutamol. It reduces the contractility of the myometrium, making it easier for the baby to turn.
Stillbirth
Stillbirth is defined as the birth of a dead fetus after 24 weeks gestation. Stillbirth is the result of intrauterine fetal death (IUFD). It occurs in approximately 1 in 200 pregnancies.
Stillbirth diagnosis
Ultrasound scan is the investigation of choice for diagnosing intrauterine fetal death (IUFD). It is used to visualise the fetal heartbeat to confirm the fetus is still alive.
Management of IUFD and stillbirth
Vaginal birth is first-line for most women after IUFD, unless there are other reasons for caesarean section.
Expectant management involves awaiting natural labour and delivery. Women with expectant management need close monitoring. The condition of the fetus will deteriorate with time.
What drugs can suppress lactation after delivery of a stillbirth baby?
Dopamine agonists (e.g. cabergoline) can be used to suppress lactation after stillbirth.
