PRINCIPLES AND MANAGEMENT OF PRE-ECLAMPSIA Flashcards
Definition of Pre‐eclampsia
Pre‐eclampsia is a multi‐organ syndrome of pregnancy that manifests after 20 weeks’ gestation with new‐onset hypertension and proteinuria in a previously normotensive patient.
It may be defined as systolic blood pressure greater than 140mmhg and diastolic blood pressure greater or equals to 90mmhg in a previously normotensive patient.
Pre-eclampsia may occur before the 20th week of pregnancy in a patient with molar pregnancy.
CLASSIFICATION of Pre-eclampsia
MILD PRE-ECLAMPSIA:
•This is diagnosed when after resting, the mother’s diastolic blood pressure rises 15-20 mmHg above the basal blood pressure recorded in early pregnancy or when the diastolic blood pressure rises above 90 mmHg.
SBP: 140-159mmhg
DBP: 90-109mmhg.
SEVERE PRE-ECLAMPSIA:
•SBP 160 mmHg or higher OR DBP 110 mmHg or higher on 2 occasions at least six hours apart in a woman at rest or DBP 120mmHg on one occasion
Aetiology
The exact cause of pre-eclampsia is not known. Experts believe it begins in the placenta.
Causes of this abnormal development may include:
•Insufficient blood flow to the uterus
•Damage to the blood vessels
•A problem with the immune system ( Autoimmune disorders)
•genetic factors
Imbalance between thromboxane A and Prostacyclin
•failure of 2nd phase trophoblastic invasion
Risk factors
Maternal-related factors
* >35 years or <20 years
* Black race
* Family Hx of preeclampsia
* Nulliparity
* Previous hx of preeclampsia/ eclampsia
* New male partner
Pregnancy-associated factors
* Multiple gestation
* Hydatidiform mole
* Hydrops fetalis
* Hyperplacentosis
* Oocyte donation or donor insemination (ART – IVF)
* Structural congenital anomalies
* Chromosomal abnormalities
Medical related factors
* Pre-existing hypertension
* Renal disease
* Diabetes(pre-existing or gestational)
* Antiphospholipid syndrome
* Connective tissue diseases
* Inherited thrombophilia…associated with early onset PIH
*Obesity
Pathophysiology of preeclampsia
In preeclampsia, Failure of trophoblastic cells to invade the maternal spiral arteries at 12th week of gestation to remodel spiral arteries from low capacity high resistance to high capacity low resistance. They may be narrower than normal and less efficient at delivering blood.
The impaired blood flow in the placenta triggers a series of events that can lead to hypertension in preeclampsia.;
•Reduced blood flow: leading to uteroplacental hypoxia.
•Ischemia and tissue damage: Ischemia causes cellular damage and the release of toxins into the mother’s bloodstream.
•Vasoconstriction: The toxins causes release of Thromboxin A2 (vasoconstrictor), which increases peripheral resistance, making it more difficult for blood to flow through the vessels
•Increased blood pressure: The vasoconstriction and reduced blood flow trigger the body’s response to increase blood pressure to overcome the resistance. This results in hypertension.
Endothelial dysfunction: causing further constriction and reducing the flexibility of blood vessels. Note: in preeclampsia, there is widespread epithelial damage. This leads to inflammation, realease of cytokines, reduced oncotic pressure, extravasation of fluid (leakage), pre-eclamsic symptoms.
Organ damage: The combination of the effects can lead to damage in various organs, such as the liver and kidneys.
N/B: The body’s compensation response in pregnancy is aimed at protecting the fetus not the mother.
Clinical presentation
Hypertension
Proteinuria
In severe ; oliguria, upper right epigastric pain, pulmonary edema, cerebral/ visual disturbances, impaired liver function, thrombocytopenia.
Investigation
- FBC:↓ Hb - haemolysis,↓ platelets - HELLP. ↑ Hb(polycytaemia – is indicative of severe disease
- E & U:↑ urea,↑ creatinine,↑ uric acid - renal affectation and possible chronic hypertension,
- Hourly urine output and urinalysis.
- LFTs:↑ ALT,↑ AST, ↑ bilirubin - HELLP.
- Clotting studies: Usually deranged
- Blood glucose: to rule out hypoglycemia
- Abdominal ultrasoundmay be performed to estimate the gestational age, detect IUGR and to rule out placental abruption which can complicate eclampsia.
- Continuous CTG monitoringis likely to indicate evidence offetal distressandbradycardia.
- It may be necessary to rule out other causes of seizures if there is any doubt regarding the diagnosis of eclampsia using E.E.G, cranial CT/ MRI
- Others – Biophysical profile
- Doppler study.
Complications of pre-eclampsia
•Fetal growth restriction
•Placental abruption
•Preterm birth
•HELLP syndrome
•Eclampsia
•Cardiovascular disease
Acute renal failure
•DIC
•Hyperpyrexia
Prevention of pre-eclampsia
•low dose (75–150 mg) aspirin as prophylaxis (reduce the risk of pre-eclampsia) from 12 weeks gestation until delivery in high risk women.
•Control Hypertension
•Control Diabetes mellitus
•Advise early antenatal care
•Vit. C and Vit. E acts as antibiotics
•Mg and calcium supplements in high risks patients or those with low dietary intake
•Uterine artery Doppler screening for uterine artery resistance
Management ;
MILD PIH remote from term
outpatient management@ the ANC can be done with oral Antihypertensive e.g. methyldopa, nifedipine, labetalol
AIM IS to get the pregnancy as close to term as possible
SFH is measured @ each visit to detect IUGR - Serial USS to diagnose IUGR
Urinalysis is done @ each visit
Management ;
MILD PIH @ term:
elective delivery – if there is no contraindication to vaginal delivery, IOL
Management;
Severe pre-eclampsia
- Admit patient
Close monitoring of mother – vital signs, input/output,
Fetal monitoring – intermittent auscultation, FBPP, CTG - Antihypertensive – parenteral in acute situation (Hydralazine, labetalol)
- Anticonvulsant (Magnesium sulphate) [prevention of fit]
- Immediate delivery after stabilization (Induction or C-Section)
