Rapid Obstetrics and Gynaecology

Obstetrics

Acute fatty liver of pregnancy

DEFINITION

Rare pregnancy-associated disorder characterised by fatty infiltration of the liver.

AETIOLOGY

Likely to be due to a mitochondrial disorder affecting fatty acid oxidation.

ASSOCIATIONS/RISK FACTORS

Nulliparity, multiple pregnancy, obesity, male fetus, pre-eclampsia.

EPIDEMIOLOGY

UK prevalence estimated at 5 per 100 000.

HISTORY

Often non-specific, normally in third trimester: nausea, vomiting, abdominal pain, jaundice, bleeding.

EXAMINATION

Liver tenderness, jaundice, ascites, manifestations of coagulopathy. Fifty percent of women will have proteinuric hypertension.

PATHOLOGY/PATHOGENESIS

Accumulation of microvesicular fat in haepatocytes, periportal sparing, small yellow liver on gross examination.

INVESTIGATIONS

Bloods: FBC (assess Hb, haemoconcentration, thrombocytopenia), clotting (↓ synthesis + consumption of clotting factors), LFT (↑ transaminases, mild hyperbilirubinaemia), U&E, glucose (hypoglycaemia common).

MANAGEMENT

Delivery is necessary to halt deterioration. Treatment is supportive: fluid management; correction of hypoglycaemia; blood transfusion as appropriate; correction of coagulopathy with platelets/FFP/cryoprecipitate. Liver transplantation is rarely necessary.

COMPLICATIONS

Maternal: Death, haemorrhage (secondary to DIC), renal failure, hepatic encephalopathy, sepsis, pancreatitis.

Fetal: Death.

PROGNOSIS

Maternal mortality 10–20%; perinatal mortality 20–30%.

Amniotic fluid embolism

DEFINITION

Obstetric emergency in which amniotic fluid and fetal cells enter the maternal circulation causing cardiorespiratory collapse.

AETIOLOGY

Unclear. Entry of amniotic fluid or fetal debris to the maternal circulation provokes either an anaphylactoid reaction or activation of the complement cascade.

ASSOCIATIONS/RISK FACTORS

Often occurs in the absence of identifiable risk factors. Multiparity, ↑ maternal age, Caesarean section, uterine hyperstimulation, use of uterotonics, placental abruption, trauma, termination of pregnancy.

EPIDEMIOLOGY

UK prevalence is 1.8 per 100 000 maternities.

HISTORY

Sudden-onset dyspnoea ± chest pain, ?collapse.

EXAMINATION

Tachypneoa, cyanosis, hypotension, tachycardia, evidence of coagulopathy.

PATHOLOGY/PATHOGENESIS

The precipitating reaction causes pulmonary artery spasm, ↑ pulmonary arterial pressure and ↑ right ventricular pressure, resulting in hypoxia. Hypoxia leads to myocardial and pulmonary capillary damage and LVF. Post mortem reveals fetal squames and debris in the maternal pulmonary circulation.

INVESTIGATIONS

Bloods: ABG, FBC, clotting, U&E, X-match.

Imaging: CXR.

Other: ECG.

MANAGEMENT

Largely supportive; manage in ITU.

Airway: Maintain patency.

Breathing: High-flow oxygen ± intubation.

Circulation: Two large-bore IV cannulae, fluid resuscitation, consider pulmonary artery catheter and ionotropic support, correct coagulopathy with FFP/cryoprecipitate/platelets, blood transfusion if necessary.

Consider delivery.

COMPLICATIONS

Cardiac arrest, death, DIC, seizures, uterine atony and haemorrhage, pulmonary oedema, ARDS, renal failure.

PROGNOSIS

In the UK: 37% mortality, of which 25% occurs within the first hour.

Cardiac disease in pregnancy

DEFINITION

Cardiac disease in a pregnant woman.

AETIOLOGY

Congenital heart disease: PDA, ASD, VSD, coarctation of the aorta, Marfan’s, Fallot’s tetralogy, Eisenmenger’s syndrome.

Acquired heart disease: Valvular defects, ischaemic heart disease.

Cardomyopathies: Including peripartum cardiomyopathy (new-onset cardiomyopathy and heart failure usually within time period of last month of pregnancy and 5 months post-partum).

ASSOCIATIONS/RISK FACTORS

As for cardiac disease in general: family history, obesity, hypertension, smoking, ↑ age, diabetes.

EPIDEMIOLOGY

Increasing prevalence due to ↑ maternal age, ↑ life expectancy for patients with congenital heart disease, ↑ immigrant populations.

HISTORY

Assess new/deterioration of symptoms: SOB, palpitations, orthopnoea, paroxysmal nocturnal dyspnoea, decreased exercise tolerance, chest pain.

EXAMINATION

General: Pulse, BP, JVP, ?oedema, ?cyanosis.

Chest: Heart sounds, murmurs (note: ejection systolic common in pregnancy), basal crepitations.

Abdomen: Fundal height (associated with IUGR).

PATHOLOGY/PATHOGENESIS

Dependent on aetiologies noted above. There is 40% increase in blood volume during pregnancy, hence cardiac strain. Women with cardiac disease are unable to increase cardiac output (uterine hypoperfusion, ↑ risk of pulmonary oedema).

INVESTIGATIONS

Bloods: FBC, U&E, LFT.

Cardiac: ECG, echo.

Fetus: Serial USS for fetal growth, cardiac anomaly scan if there is maternal congenital heart disease.

MANAGEMENT

Dependent on the aetiology.

General: Combined obstetric/cardiology care (tertiary referral centre).

Preconceptual: Assess cardiac status, address risks and absolute contraindications to pregnancy.

Antenatal: Optimise treatment, monitor fetal wellbeing, consider thromboprophylaxis.

Delivery: Consider optimum mode and timing of delivery, consult with anaesthetists, correct positioning, fluid management, consider antibiotic prophylaxis (structural defects).

Post-partum: Increase surveillance (period of haemodynamic change).

COMPLICATIONS

Maternal: Progression of disease, VTE, pulmonary oedema, death.

Fetal: PTL, ↑ congenital heart disease (if maternal congenital heart disease), IUGR, effects of teratogenic drugs for anticoagulation, fetal death.

PROGNOSIS

High risk of maternal mortality if LVEF <40% or LVF. Pulmonary hypertension: 20–50% maternal mortality rate. Eisenmenger’s: 50% maternal mortality rate. Patients with Marfan’s syndrome with aortic root >4–4.5 cm are advised against pregnancy.

Chronic hypertension in pregnancy

DEFINITION

Hypertension that is either present prior to conception (detected before 20/40) or persists after pregnancy.

AETIOLOGY

Essential hypertension in >90–95% (cause unknown). Remainder are secondary to: endocrine (Cushing’s, phaeochromocytoma, CAH), renal (renal artery stenosis, chronic renal disease), vascular (e.g. coarctation of aorta).

ASSOCIATIONS/RISK FACTORS

Increasing age, ethnicity (Afro-Caribbean), obesity, smoking, diabetes, family history, pre-eclampsia.

EPIDEMIOLOGY

Affects 1–5% of pregnancies.

HISTORY

Largely asymptomatic.

EXAMINATION

Blood pressure may be normal in first trimester due to ↓ systemic vascular resistance. Secondary causes include renal bruits, radiofemoral delay.

PATHOLOGY/PATHOGENESIS

Chronic systemic inflammatory response increases susceptibility to pre-eclampsia. Placental pathology similar to pre-eclampsia (arterial occlusive changes, excess villous syncytial knots, infarction etc.) leads to hypoperfusion of the maternal space.

INVESTIGATIONS

Bloods: FBC, U&E, LFT, Urate.

Urinalysis: For proteinuria. If secondary causes are suspected: urinary catecholamines, renal artery USS and so on.

Fetus: Serial USS for fetal growth.

MANAGEMENT

Medication: Convert to non-teratogenic medications: methyldopa, nifedipine, labetalol (note: ACE inhibitors are teratogenic), aspirin 75 mg od (↓ risk of pre-eclampsia/IUGR).

Other: Monitor for pre-eclampsia, serial USS for fetal growth, uterine artery Dopplers at 24/40 (predicts pre-eclampsia).

COMPLICATIONS

IUGR, superimposed pre-eclampsia (25%), placental abruption, prematurity.

PROGNOSIS

Raised maternal and perinatal morbidity is related to superimposed pre-eclampsia.

Cord prolapse

DEFINITION

Descent of the umbilical cord through the cervix past the presenting part in the presence of ruptured membranes: an obstetric emergency.

AETIOLOGY

Potential space (e.g. unengaged presenting part) allows descent of the cord past the presenting part.

ASSOCIATIONS/RISK FACTORS

Breech presentation, abnormal lie, multiple pregnancy (second twin), prematurity, low birthweight, unengaged presenting part, polyhydramnios, ARM.

EPIDEMIOLOGY

Affects 0.1–0.6% of pregnancies.

HISTORY

An abnormal FHR is detected, often after membrane rupture.

EXAMINATION

Cord is felt or seen through the cervix below the presenting part.

PATHOLOGY/PATHOGENESIS

Compression of the cord by the presenting part and arterial spasm prevents blood flow through the cord, causing asphyxia.

INVESTIGATIONS

Unnecessary.

MANAGEMENT

Place patient in Trendelenberg or knee–chest position. Manually elevate the presenting part (this may also be achieved through bladder filling). Emergency delivery is necessary, usually via Caesarean section. The neonatal team should be present at delivery.

COMPLICATIONS

Hypoxic–ischaemic encephalopathy, fetal death.

PROGNOSIS

Perinatal mortality rate is 91 per 1000, higher if it occurs outside hospital.

Diabetes in pregnancy

DEFINITION

Pre-existing or new-onset diabetes in pregnancy.

AETIOLOGY

Pre-existing: Type 1 – failure of pancreas to produce insulin; type 2 – relative insulin deficiency associated with increased peripheral insulin resistance.

Gestational diabetes (GDM): Altered glucose tolerance in pregnancy.

ASSOCIATIONS/RISK FACTORS

GDM: ↑ maternal age, ethnicity (South Asian, Middle Eastern, Afro-Caribbean), obesity, smoking, PCOS, family history, previous macrosomic baby.

EPIDEMIOLOGY

Prevalence is 2–5% but estimates vary. GDM accounts for 90% of diabetes in pregnancy.

HISTORY

Pre-existing: Usually known to mother.

GDM: Usually asymptomatic, detected on screening.

EXAMINATION

Abdomen: Fundal height (macrosomia/polyhydramnios).

PATHOLOGY/PATHOGENESIS

Type I: Autoimmune destruction of pancreatic islet cells.

Type II: Genetic component + influence of age and obesity on peripheral insulin resistance.

GDM: ↑ insulin resistance in pregnancy (↑ secretion of insulin antagonists, including HPL, glucagon and cortisol), altered carbohydrate metabolism, failure of normal pregnancy increase in insulin production.

Fetus: Hyperglycaemia in early pregnancy may affect development (congenital abnormalities); hyperglycaemia causes fetal hyperinsulinaemia and macrosomia.

Neonatal: Hypoglycaemia can occur (withdrawal of maternal glucose while fetal insulin levels remain high).

INVESTIGATIONS

Delivery: Aim for delivery after 38 completed weeks of pregnancy. Sliding scale in labour.

Pre-existing: Detailed anomaly scan, fetal cardiac scan, ophthalmic examination.

GDM: Screening (universal or selective) by GTT at 26–28/40.

MANAGEMENT

Pre-existing

Preconceptual: Optimisation of glucose control.

Medical: Optimise diet, consider converting oral hypoglycaemics to insulin. Likely to require increasing doses of insulin.

Pregnancy: Capillary blood glucose monitoring, monitor for pre-eclampsia, serial USS for fetal growth.

Delivery: Sliding scale in labour.

Postpartum: Return to pre-pregnancy doses of medications.

GDM

Medical: Diet control. Persistent hyperglycaemia may require insulin treatment.

Pregnancy/delivery: As for pre-existing.

Postpartum: Stop insulin after delivery, fasting blood glucose 6/52 postpartum.

COMPLICATIONS

Maternal: Progression of pre-existing nephropathy/neuropathy/retinopathy, miscarriage, pre-eclampsia, operative delivery.

Fetal/neonatal: Congenital abnormalities (pre-existing only), fetal death, polyhydramnios, polycythaemia, macrosomia (+ traumatic delivery), respiratory distress syndrome, neonatal hypoglycaemia, neonatal jaundice.

PROGNOSIS

Dependent on adequacy of control.

GDM: 70% recurrence in future pregnancies, ↑ risk (40–60%) for type 2