Clinical consequences of poor placentation

6th leading cause of direct maternal deaths (6 deaths over 3 years) • Commonest medical problem in pregnancy: – Gestational hypertension = 10% – PE = 2-5% – Severe PE= 1% – Eclampsia at a 2% death rate • Leading cause of iatrogenic prematurity • Immediate risks of eclampsia, stroke and heart failure • Life-long risk of cardiovascular disease

high risk factors: Previous pre-eclampsia Chronic hypertension Autoimmune disease Diabetes mellitus Chronic kidney disease Moderate risk factors Nulliparity Age >40 Pregnancy interval >10yr BMI >35 Family hx pre-eclampsia Multifetal gestation

Defective spiral artery remodelling Causes placental hypoperfusion diseased placenta releases pro-inflammatory proteins into maternal circulation diseased placenta releases pro-inflammatory proteins into maternal circulation this causes systemic vasoconstriction and endothelial dysfunction causes hypertension and end organ damage Remember HELLP Hameolysis Elevated Liver enzymes Low Platelets

Normal: • Normal • Trophoblasts invade maternal vessels • Narrow spiral arteries remodelled • Wide-bore low-resistance vessels deliver large amounts of maternal blood • Nutrient and oxygen delivery to foetus PE: Deficient trophoblast invasion • Spiral arteries not remodelled • High-resistance placental bed • Poorly perfused hypoxic placenta • Deficient nutrient and oxygen delivery • Release of inflammatory cytokines (IL, TNF etc) • Maternal endothelial dysfunction: – Increased vascular reactivity and vasospasm – Increased capillary permeability and reduced intravascular volume

Feto placental demands can sometimes be under excessive demand These can include foetal macrosomia, twin pregnancies, prolonged pregnancy excess weight gain This can have a negative impact on cardiovascular health causing cereobrovascular/cardiovascular morbidity or CKD In the foetus some factors cause proteinuria, cerebral oedema and liver dysfunction and foetal growth restriction Poor cardiac reserve can be due to maternal age, obesity, ethnicity, diabetes, auto-immune diseases, chronic hypertension and chronic kidney disease, also causing problems with cardiovascular function this causes foetal growth restriction in the foetus

Maternal effects: Cerebral oedema: eclampsia – Vasospasm: hypertension, renal failure – Endothelial injury: low platelets, disseminated intravascular coagulopathy (DIC) – Albumin leakage: proteinuria, pulmonary oedema Foetal effects: Growth restriction Prematurity Placental abruption foetal death

Hypertension Threshold >140/90 mmHg Hypertension Baseline Normotensive <20 weeks (BUT can have superimposed PE on background of Chronic HTN) Proteinuria >300 mg/24 hrs OR Protein:Creatinine ratio (PCR) >30 mg/mmol OR +2 urine dipstick Proteinuria a prerequisite for diagnosis No Other clinical criteria for diagnosis: Yes • Renal Creatinine >90 μmol/litre • Liver Liver enzymes: ALT or AST >40 IU/L, +/- RUQ or epigastric pain • Neurological Eclampsia, altered mental status, blindness, stroke, clonus, severe headaches or persistent visual scotomata • Haematological Platelets <150,000 x 109/L, Disseminated Intravascular Coagulopathy (DIC) or haemolysis • Uteroplacental Fetal growth restriction, abnormal umbilical artery Doppler waveform analysis, or stillbirth.

• No symptoms • Headaches • Flashing lights • Epigastric pain • Nausea / vomiting • Confusion • Hypertension – Use the right cuff size – Disappearance of sounds • Proteinuria • Brisk jerks

• 24-hr urinary protein OR spot protein:creatinine ratio • Platelet count • LFT - Liver enzymes (ALT) • U&E - Creatinine • Clotting tests • Fetal assessment – Ultrasound for growth and Dopplers +/- CTG

Hospitalization is recommended for monitoring • At least twice daily blood pressure measurements • PE bloods: frequency depends on the severity • Symptoms of severe PE

Complications of prematurity • Possibility of failed induction needing Caesarean section • Attempts to prolong pregnancy are justified for pre-term PE • Severe uncontrolled PE needs delivery after stabilization Authors concluded that induction of labour should be advised for women with mild PE or mild gestational hypertension at a gestational age beyond 37 weeks

Diastolic BP ≥ 110 mm X 2 • Systolic BP ≥ 160 mm X 2 and • ≥ ++ proteinuria • Signs or symptoms of imminent eclampsia – Hyper-reflexia (neuronal irritability) – Frontal headache – Blurred vision (cerebral vasospasm) – Epigastric tenderness (tension on liver capsule)

Magnesium sulphate to women with preeclampsia reduces the risk of an eclamptic seizure. • Women allocated magnesium sulphate had a 58% lower risk of an eclamptic seizure (58% reduction 95% CI 40–71%). • Maternal mortality lower in treatment group (11/5055 vs 20/5055) • Reduced risk of placental abruption (RR 0.67, 95% CI = 0.45 – 0.89)

Carefully assess women with signs or symptoms of preeclampsia • Assess need to continue anti-hypertensives • Arrange appropriate follow-up • An assessment of BP and proteinuria by the general practitioner at the 6 weeks postnatal check is recommended. • If hypertension or proteinuria persists then further investigation is required. Women whose pregnancies have been complicated by severe preeclampsia or eclampsia should be offered a formal postnatal review to discuss the events of the pregnancy. • Pre-conceptional counseling should be offered where the events that occurred, any risk factors and any preventative therapies can be discussed.

Pre-eclampsia can kill • The severity and progression of the disease are variable • Both mother and fetus are at risk • Is a multi-organ disease • Severe pre-eclampsia needs multi-disciplinary input • The only cure is delivery