Pre eclampsia

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Preeclampsia

Definition

Preeclampsia is defined as de novo hypertension (BP ≥140/90 mmHg systolic or ≥90 mmHg diastolic) after 20 weeks of gestation in a previously normotensive woman, combined with proteinuria (≥300 mg/24h, protein:creatinine ratio ≥0.3, or dipstick ≥1+) or evidence of end-organ dysfunction.

Importantly, proteinuria is no longer required for diagnosis if other criteria of end-organ damage are present. - Tintinalli's Emergency Medicine

Classification of Hypertensive Disorders in Pregnancy

Disorder	Key Features
Gestational hypertension	BP ≥140/90 after 20 wks, no proteinuria, no end-organ damage
Preeclampsia without severe features	HTN + proteinuria or end-organ dysfunction
Preeclampsia with severe features	(see criteria below)
Eclampsia	New-onset seizures in preeclampsia, no other cause
HELLP syndrome	Hemolysis + elevated liver enzymes + low platelets - a severe variant
Superimposed preeclampsia	Preeclampsia developing in a patient with chronic hypertension

Diagnostic Criteria

Preeclampsia (basic)

BP ≥140 mmHg systolic or ≥90 mmHg diastolic, measured on 2 occasions ≥4 hours apart
Onset after 20 weeks in a previously normotensive patient
PLUS one or more of:
- Proteinuria ≥300 mg/24h
- Thrombocytopenia (<100,000/μL)
- Renal insufficiency (creatinine >1.1 mg/dL)
- Liver dysfunction (transaminases >2x normal)
- Pulmonary edema
- Cerebral or visual disturbances

Severe Features

Any one of the following qualifies:

Systolic BP ≥160 mmHg or diastolic BP ≥110 mmHg on 2 occasions ≥4 hours apart (while at bed rest)
Thrombocytopenia (<100,000 platelets/mL)
Impaired liver function (liver enzymes >2x normal) or persistent right upper quadrant/epigastric pain unresponsive to medication
Progressive renal insufficiency (creatinine >1.1 mg/dL or doubling of creatinine)
Pulmonary edema
New-onset headache unresponsive to medication, or visual symptoms

- Tintinalli's Emergency Medicine; Harrison's 22E

Pathophysiology

The precise mechanism is not fully understood. Multiple converging factors are implicated:

Abnormal placentation / uteroplacental ischemia - inadequate trophoblast invasion of spiral arteries leads to a high-resistance, low-flow placental bed. This is the primary trigger.
Angiogenic imbalance - the ischemic placenta releases excess sFlt-1 (soluble fms-like tyrosine kinase 1, an anti-angiogenic factor) and reduced PlGF (placental growth factor, a pro-angiogenic factor). The sFlt-1 binds and neutralizes circulating VEGF and PlGF, causing systemic endothelial dysfunction.
- An sFlt-1/PlGF ratio ≥40 is associated with increased risk of developing severe features within 2 weeks.
- PlGF <100 pg/mL before 35 weeks rules out need for delivery due to preeclampsia within the next 2 weeks with 98% probability.
- sFlt-1:PlGF <38 has a 99% negative predictive value for preeclampsia within 1 week.
Endothelial dysfunction - widespread vascular endothelial injury leads to increased vascular permeability, vasoconstriction, and activation of the coagulation cascade.
Exaggerated maternal inflammatory response - intravascular inflammation and syncytiotrophoblast stress.

- Harrison's 22E; Barash's Clinical Anesthesia 9e; Comprehensive Clinical Nephrology 7e

Systemic Effects

System	Effect
Neurologic	Focal vasoconstriction causing hypoperfusion; cerebral edema; headache, vertigo, cortical blindness, hyperreflexia, seizures. Cerebral hemorrhage is a leading cause of death.
Renal	Proteinuria, renal insufficiency (glomerular endotheliosis)
Hepatic	Elevated transaminases, right upper quadrant pain, hepatic capsule rupture (rare but catastrophic)
Hematologic	Thrombocytopenia (approximately 50% of cases), microangiopathic hemolysis in HELLP
Cardiovascular	Hypertension, increased SVR, pulmonary edema
Uteroplacental	IUGR (10-25%), placental abruption (1-4%), fetal growth restriction

HELLP Syndrome

A severe form of preeclampsia dominated by hepatic and hematologic abnormalities. Proteinuria may be absent.

Diagnostic criteria:

Hemolysis: schistocytes on blood film, elevated bilirubin, high LDH, low haptoglobin
ELevated liver enzymes: AST >70 U/L or >2x upper limit of normal
LP Low platelets: <100 x 10⁹/L

Maternal mortality ~1%; perinatal mortality 7-34% (gestational age-dependent). Delivery is generally indicated. - Comprehensive Clinical Nephrology 7e

Risk Factors

Nulliparity
Multiple gestation (10-20% twins; 25-60% triplets; up to 90% quadruplets) - primarily due to larger placental mass
Preexisting diabetes mellitus (2-4x higher risk), especially with nephropathy, long duration (>20 years)
Chronic hypertension
Prior history of preeclampsia
Obesity, thrombophilias, antiphospholipid syndrome
Assisted reproductive technology

Prediction / Screening

First-trimester combined screening can predict early-onset preeclampsia:

Maternal risk factors alone: ~50% detection
- Biochemical markers (PAPP-A, PlGF): ~75%
- Biophysical markers (uterine artery pulsatility index, mean arterial pressure): ~90%
- Both biochemical and biophysical: ~95%

- Comprehensive Clinical Nephrology 7e

Management

Definitive Treatment

Delivery of the fetus and placenta is the only cure. All management decisions balance maternal risk against fetal prematurity risk.

Situation	Recommendation
Preeclampsia without severe features	Expectant management to 37 weeks, then deliver. Close monitoring, fetal surveillance, limited activity.
Preeclampsia with severe features ≥34 weeks	Deliver
Preeclampsia with severe features <34 weeks	Expectant management in a tertiary center may be appropriate if no indications for earlier delivery
Indications for delivery before 34 weeks	Unrelenting symptoms, worsening labs, severe BP refractory to treatment, severe FGR, placental abruption

Antihypertensive Therapy

Acute severe hypertension (BP ≥160/110 mmHg) requires timely treatment to reduce CVA risk:

Labetalol IV - first-line agent (20 mg IV bolus; titrate)
Hydralazine IV/IM (5 mg IV/IM) - first-line alternative
Nifedipine 10-30 mg PO (not FDA-approved for this indication, but widely used)

Chronic/non-severe hypertension in pregnancy:

Labetalol (100 mg PO BID, maintenance 200-400 mg BID)
Methyldopa (250 mg q6h, max 3 g/day)
Long-acting nifedipine (30 mg PO daily, up to 120 mg/day)
Target BP: 140-150/90-100 mmHg (do not over-lower - placental perfusion risk)

Contraindicated: ACE inhibitors and ARBs (teratogenic - affect fetal kidneys, lungs, skull)

Seizure Prophylaxis / Treatment

Magnesium sulfate is the agent of choice for seizure prevention in severe preeclampsia and for treatment of eclampsia
Not covered in detail above snippets but universally endorsed in guidelines

Prevention

Low-dose aspirin (60-162 mg/day):

Initiated between 12 and 16 weeks (by 16 weeks for best effect, up to 28 weeks)
Recommended for high-risk women (ACOG, SMFM, ADA criteria)
In women with T1DM or T2DM, aspirin reduces preeclampsia incidence by ~50% and IUGR by 20%
Recommended by ACOG, SMFM, and ADA

- Harrison's 22E; Creasy & Resnik's Maternal-Fetal Medicine

Complications

Complication	Approximate Rate
Abnormal liver function / thrombocytopenia	10-20%
Acute kidney injury	1-5%
Placental abruption	1-4%
Fetal growth restriction	10-25%
Pulmonary edema	<0.5%
Neurologic damage	<1%
Progression to eclampsia (untreated)	~1%
Hepatic capsule rupture	Rare, catastrophic
CVA (stroke)	Risk increased with severe-range BP

Postpartum Considerations

Preeclampsia and HELLP usually resolve rapidly after delivery, but may be delayed. Monitor closely until labs and BP normalize (may take days to weeks).
Some patients require antihypertensives for the first time postpartum - treat if BP >140/90 mmHg.
If no improvement by postpartum day 3 and DIC excluded, consider plasma exchange (for TTP-like picture).
Long-term risk: Women who have had preeclampsia are at significantly increased risk for chronic hypertension, cardiovascular disease, chronic kidney disease, and diabetes mellitus later in life. Cardiovascular risk reduction counseling is indicated at postnatal visits.

Sources: Harrison's Principles of Internal Medicine 22E; Tintinalli's Emergency Medicine; Creasy & Resnik's Maternal-Fetal Medicine; Comprehensive Clinical Nephrology 7e; Barash's Clinical Anesthesia 9e; Goldman-Cecil Medicine

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