Case 2: Claire McFadden Pt 2 - Preeclampsia + HELLP

Primary Pregnancy Care

General + Community-based

Content:

• Prenatal care

• Preconception care

• Postpartum care

Providers:

• Midwives

• Family physicians

• Obstetricians

Secondary Pregnancy Care

Specialty care

Content:

• > 20 weeks referral

• Risks + complications

  • Preeclampsia

  • Placenta previa

  • Pregestational diabetes

  • Chronic HTN

Providers:

• Obstetrician

• Maternal-fetal medicine

Tertiary Pregnancy Care

Subspecialty care

Content: High risk

• Placenta accreta: Placenta attaches deeply in uterine wall + does not separate properly after birth

• Placenta previa

• Severe preeclampsia

• HELLP syndrome

Providers:

• Obstetrician

• Obstetric anesthesia

• Maternal-fetal medicine

• Subspecialists

Pregnancy Changes: Etiology

1. Increased plasma volume = Hemodilution

2. Hypercoagulable state

3. Placental/hormonal changes = Affect liver, kidneys, metabolism

Hemodiluation Effects: Labs

Decreased:

• Hb

• Platelets

• Albumin

Increased:

• WBC

Hypercoagulability Effects: Labs

Decreased: Antithrombin + Protein S

Increased: Fibrinogen + Clotting Factors

Normal: PT/INR + PTT

Hormonal Effects: Labs

Increased:

• Alkaline phosphatase

• AST/ALT

• Lipids

Decreased:

• Bilirubin + GGT

• Creatine

• TSH

  • 1st trimester

• Free T4

  • 2nd-3rd trimester

3rd Trimester Antenatal Care: Maternal Health

HTN

Rhesus antibody

• Indications:

  • Rh- nonsensitized

  • 28 weeks

• Treatment: Anti-D Ig

3rd Trimester Antenatal Care: Infections

Screening

Vaccines

Treatments

3rd Semester Infections: Screening

Group B strep (GBS) swab + culture

• 36 - 37 weeks

STI:

• Chlamydia

• Gonorrhea

• HIV

• Syphilis

• Hep B

3rd Semester Infections: Vaccines

Tdap

RSV: If not given previously

3rd Semester Infections: Treatments

HSV Antivirals: For history of genital HSV

• Ex: Acyclovic, valacyclovir

GBS+: During delivery

• Beta-lactam

  • Ex: Pencillin G, ampicillin

• Penicillin Allergy: Cefazolin, clindamycin

3rd Trimester Antenatal Care: Fetal Surveillance

Position

Kick count

Nonstress test (NST)

Contraction stress test (CST)

BPP US

3rd Trimester Fetal Surveillance: Position

Leopold maneuvers

• ≥ 36 weeks

• Determine:

  • Fetal lie (direction)

  • Fetal presentation (cephalic vs breech)

  • Fetal position (anterior vs posterior)

  • Fundal height

US: Confirm fetal + placental position

3rd Trimester Fetal Surveillance: Kick Count

No reduction = Good

3rd Trimester Fetal Surveillance: NST

Measure FHR response to movement for 20 mins

• Electronic FHR monitor

Reactive:

• Normal

• ≥ 2 FHR accelerations

Nonreactive:

• Abnormal

• < 2 FHR accelerations

3rd Trimester Fetal Surveillance: CST

Measure FHR response to uterine contractions

• Cardiotocography

Neonatal Hypoglycemia: Description

Low blood glucose in newborn

Neonatal Hypoglycemia: Epidemiology/Etiology

Risk factors…

• Hyperinsulinemic hypoglycemia (GDM)

• Prematurity

• Intrautrine growth restriction

Neonatal Hypoglycemia: Pathophysiology

Storage + production insufficiency

Increased glucose use

Neonatal Hypoglycemia Pathophysiology: Storage + Production Insufficiency

1. Insufficient glycogen storage + hyperinsulinemia = Impaired hepatic glycogen → glucose

2. Hypoglycemia

Neonatal Hypoglycemia Pathophysiology: Increased Glucose Use

1. Maternal hyperglycemia = Fetal hyperglycemia = Beta cell hypertrophy + hyperfunction

2. Neonatal hyperinsulinemia → Delivery = Decrease maternal glucose supply

3. Hypoglycemia

Neonatal Hypoglycemia: Clinical Presentation

Usually asymptomatic

Autonomic symptoms

• Tachycardia

• Sweating

• Tremors

Neurological symptoms

• Hypotonia

• Irritability

• Poor feeding

Neonatal Hypoglycemia: Investigations

Glucose levels

• < 45h: < 2.2-2.5 mmol/L

• > 48h: < 2.8 mmol/L

Neonatal Hypoglycemia: Treatment/Management

Monitor glucose

Oral/IV glucose

Utero-Placental Insufficiency: Description

Fetomaternal circulation disorder = Decreased blood flow to placenta + impair substance exchange

Utero-Placental Insufficiency: Epidemiology/Etiology

Risk factors…

• Smoking

• DM

• HTN

• Severe anemia

• Anorexia

• Preeclampsia

• Rh incompatibility

Utero-Placental Insufficiency: Clinical Presentation

Decreased/no fetal movements

Decreased symphysis-fundal height

Utero-Placental Insufficiency: Treatment/Management

Treat underlying cause

Fetal surveillance

Low-dose ASA

Utero-Placental Insufficiency: Complications

Preeclampsia

Fetal growth restriction

Placental abruption: Premature placental separation before delivery

Preterm labour

Oligohydramnios: Blood shunt to brain not kidneys = Less amniotic fluid

Preeclampsia: Description

New gestational HTN with proteinuria + end-organ function

Preeclampsia: Types

Superimposed Preeclampsia: Preeclampsia + Chronic HTN

Eclampsia: New seizures from pregnancy-related HTN

HELLP Syndrome: Life-threatening preeclampsia

• Hemolysis

• Elevated Liver enzymes

• Low Platelets

Preeclampsia: Etiology

Unknown

Combination: Genetics, environment, nutrition, immunology

Preeclampsia: Epidemiology

Risk factors…

• PMHx

  • Thrombophilia

    • Antiphospholipid syndrome

  • DM/GDM

  • Chronic HTN

  • Chronic renal disease

    • CKD

    • SLE

  • Obesity

  • Previous preeclampsia

• Pregnancy-Related

  • Nulliparity

  • Multiple gestation

  • Hydatidiform mole: Molar pregnancy

    • Benign uterine tumor

• FMHx

• Maternal age < 20 + > 35 years

Preeclampsia: Pathophysiology

1. Reduced uterine spiral arteries → Blood vessels = Decidual vessel atherosis + High pressure and pulsatile flow → Placenta

• Atherosis: Arterial wall fibrinoid necrosis + lymphocytic infiltration

2. Arterial HTN + Systemic vasoconstriction + Endothelial dysfunction = Placental hypoperfusion

3. Release vasoactive substances 

• Ex:

  • VEGF

  • Placental growth factor

• Increase maternal BP = Ensure sufficient fetal blood supply

• Endothelial lesions = Microthrombosis

4. Chronic hypoperfusion = Uteroplacental insufficiency + fetal growth restriction

Preeclampsia: Clinical Presentation

Asymptomatic

Nonspecific symptoms

• Headaches

• Visual changes

• RUQ/epigastric pain

• Edema: Frank-starling mechanism → Increased hydrostatic pressure + decreased oncotic pressure

  • Legs

  • Pulmonary

Urinary symptoms

• Proteinuria

• Oliguria

Preeclampsia: Investigations

Rapid weight gain/edema

BP

Urine studies

Blood tests

Fetal assessment

Preeclampsia Investigations: BP

≥ 140/90

Severe: ≥ 160/110

Preeclampsia Investigations: Urine Studies

24h urine collection

• Proteinuria

Protein:Creatinine ratio

• ≥ 0.3

Dipstick

• Proteinuria

• > 2+ protein

Preeclampsia Investigations: Blood Tests

CBC

• Low Hb

Liver enzymes

• Increased AST/ALT

Renal function

• Decreased eGFR

Preeclampsia Investigations: Fetal Assessment

Cardiotocography: Monitor FHR + uterine contractions

Doppler US

• Abnormal uterine artery flow: Bilateral notches

• Oligohydramnios

• Fetal growth restriction

Preeclampsia: Treatment/Management

Nonpharmacological

Pharmacological

Preeclampsia Management: Nonpharmacological

Indications: Mild/moderate

Frequent prenatal visits

Deliver ≥ 37 weeks

Preeclampsia Treatment: Pharmacological

Antihypertensives

Mg2+ sulfate

Preeclampsia Treatment: Antihypertensives

Decreased SBP 20%

Mild/Moderate:

• Beta blockers: Labetalol

• CCB: Nifedipine

• Alpha agonist: Methyldopa

Severe: Urgent control

• Labetalol

• Nifedipine

• Hydralazine: Peripheral vasodilator

Preeclampsia Treatment: Mg2+ Sulfate

Seizure prophylaxis

Preeclampsia: Complications

Seizures

AKI/acute renal failure

Placental abruption

Fetal growth restriction

Preterm birth

ARDS

Stroke

Preeclampsia Complications: Eclampsia

Seizures

Pathophysiology: HTN = Vasoconstriction + Endothelial damage = Microthrombi = Vasospasms in CNS

Preeclampsia Complications: AKI

Pathophysiology: HTN = Vasoconstriction + Glomerular endothelial swelling = Glomerular endotheliosis (damage from swelling)

• Renal/intrinsic AKI

AKI: Clinical Presentation

Confusion + lethargy

Oliguria/anuria

Proteinuria

Edema

Uremia

• Nausea

• Asterixis

AKI: Complications

Uremia: Waste retention

Electrolyte abnormalities

• Hyperkalemia

• Hyperphosphatemia

• Hypocalcemia

Metabolic acidosis

HELLP Syndrome: Description

Life-threatening preeclampsia

• H: Hemolysis

• EL: Elevated Liver enzymes

• LP: Low Platelets

HELLP Syndrome: Etiology

HE’S Virchow

• H: Hypercoagulability

  • From pregnancy

    • Hormonal increase in clotting factor production

    • Decreased protein S production

    • Decreased antithrombin activity

• E: Endothelial damage

  • Promote plaque/thrombus formation

• S: Stasis

  • Vasodilation = Decrease venous flow

  • Iliac vein compression from uterus

Normal Hemostasis

1. Primary: Endothelial injury = Expose collagen + von Willebrand factor (vWF) = Increase platelet aggregation → Platelet plug

2. Secondary: Coagulation cascade activation = Clotting factors form fibrinogen → fibrin mesh over clot = Stabilization

3. Fibrinolysis: Plasminogen → Plasmin by tPA = Degrade fibrin

HELLP Syndrome: Hemolysis Pathophysiology

Microangiopathic hemolysis (MAHA)

1. HTN = Microthrombi in blood vessels = Damage erythrocytes = Hemolysis

HELLP Syndrome: Elevated Livery Enzymes

HTN = Vasoconstriction + Microthrombi formation = Obstruct liver sinusoids = Liver cell damage

HELLP Syndrome: Low Platelets

Disseminated Intravascular Coagulopathy (DIC)

1. HTN = Vasoconstriction + Microthrombi formation = Overactivate secondary hemostasis

2. Increase coagulation cascade = Platelet + coagulation factor consumption

HELLP Syndrome: Clinical Presentation

Nausea/vomiting

Diarrhea

RUQ pain

Rapid deterioration

• DIC

• Pulmonary edema

• Acute renal failure

• Stroke

• Placental abruption

HELLP Syndrome: Investigations

Blood tests

Coagulation panel

Blood smear

Fetal assessment

• Same as preeclampsia

HELLP Syndrome Investigation: Blood Test

CBC

• Low Hb

• Low platelets

Liver enzymes

• Increased AST/ALT

Bilirubin

• Increased indirect

LDH

• Increased

HELLP Syndrome Investigations: Coagulation Panel

DIC

• D-dimer: Increased

• PT/aPTT: Increased

• Fibrinogen: Decreased

HELLP Syndrome Investigations: Blood Smear

Hemolysis

• Schistocytes

HELLP Syndrome: Treatment/Management

Pharmacological

Delivery

HELLP Syndrome Treatment: Pharmacological

Antihypertensives

Blood products

Mg2+ sulfate

HELLP Syndrome Treatment: Antihypertensives

Beta blocker: Labetalol

CCB: Nifedipine

Hydralazine: Peripheral vasodilator

HELLP Syndrome Treatment: Blood Products

Platelets

Packed RBCs

FFP

HELLP Syndrome Treatment: Mg2+ Sulfate

Seizure prophylaxis

HELLP Syndrome Treatment: Delivery

≥ 34 weeks: Immediate

24-34 weeks: Corticosteroids → Fetal lung maturity

• Stable = Delay delivery 24-48h

Newborn Screening: Description

Identify infants at high risk for treatable disorders

Newborn Screening: Method

Heel poke

• Sample blood from heel

• > 24h

Newborn Screening: Conditions Screened

Inborn errors of metabolism

• Amino acid disorders

  • Phenylketonuria

  • MSU disease

• Fatty acid oxidation disorders

  • Acylcarnitine defects

• Carbohydrate disorders

  • Galactosemia

• Biotinidase deficiency

Endocrine disorders

• Congenital hypothyroidism

• Congenital adrenal hyperplasia

Hemoglobinopathies

• SCD

• Thalassemia

CF

Immunodeficiences

• SCID

NM disease

• Spinal muscular atrophy