Gestational Hypertension

▪ for the first time after mid-pregnancy → Blood pressure reaches 140/90 mm Hg or greater + proteinuria is not identified.
▪ by 12 weeks postpartum → Transient hypertension and blood pressure returns to normal
 Women with gestational hypertension are at risk for progression to either severe hypertension, pre-eclampsia, or eclampsia
 Close fetal monitoring is necessary.
 In absence of progression to severe hypertension or pre-eclampsia
women with gestational hypertension can continue pregnancy until term.
 During labor and immediately postpartum, they do not require seizure prophylaxis because rate of eclampsia < 1 in 500.

Preeclampsia
Definition:

 pregnancy-specific syndrome characterized by widespread vascular endothelial malfunction and vasospasm

after 20 weeks' gestation (except in V.M.)
 It is clinically defined by hypertension and proteinuria, with or without pathologic edema.

Incidence: 5-15 % of all pregnancies (most common medical disorder).

Risk Factors:

▪ Age: Extremes of child bearing period.

▪ Parity: More in primigravida, elderly multipara
▪ Race: More in black races.
▪ Genetic: More with past history or family history of PET
▪ Socioeconomic status: Low socioeconomic status.
▪ Obesity (causes DM and HTN).
▪ Malnutrition: Fe, protein, Ca, deficiency.
▪ Medical disorders: DM, chronic hypertension and chronic nephritis
▪ Obestetric disorders: Vesicular mole and multiple pregnancies

Pathology:

1- Segmental Vasospasm: 2- Hemodynamic changes

▪ generalized segmental vasospasm of small & medium sized arterioles →  after-load caused by hypertension
↑ peripheral resistance→ HPN. leak of blood constituents  peripheral resistance → CO
including platelets and fibrinogen subendothelially
leading finally to degeneration, Hemorrhage and necrosis of organ supplied.
3- Blood volume
relative hemoconcentration leading to relative increase in Hematocrit value.
dt vasospasm and  capillary permeability (excessive shift of the intravascular fluid to the extravascular compartment).
a) Blood components changes:( in severe preeclampsia and eclampsia)
Blood cells: Coagulation disturbance:
• Erythrocytes may display bizarre shapes factor VIII consumption + fibrin degradation products
undergo rapid hemolysis. → risk of DIC
•  eosinophils, which denote immunological nature. Fluid &Electrolyte changes:
• Thrombocytopenia (Platelet count < 100,000/mL). ▪ Na+ & H20 retention
▪ After eclamptic fits, there is lactic acidosis.
4- Brain: Brain edema, Hemorrhage and infarctions
5- Visual Changes and Blindness:
o Reversible Scotomata, blurred vision common with severe preeclampsia
o In retina → ischemia, infarction, and detachment.
o Rarely, extensive cerebral infarctions → total or partial visual defects
6- Kidney 7- Liver (usually in severe cases):
• Glomerular endotheliosis (pathognomonic) • Asymptomatic elevations of serum transaminase levels
glomerular cell swelling, mesangeal cell proliferation and (AST and ALT)
fibrin-like deposits intra and subendothelially. • Lobular infarctions
• Renal tubular nercrosis(reversible) • Hemorrhages of infarctions → subcapsular hematoma
• Cortical necrosis(irreversible) • Rupture of subcapsular hematoma
8- Utero-placental Perfusion:
• Failure of the 2nd wave of trophoblastic invasion
• Acute atherosis associated with intravascular thrombosis → vascular occlusion →may progress to placental infarctions.
• Similar pathology is detected in cases of placental abruption.
•  in placental perfusion and IUGR.

Diagnosis:

Signs:→usually precedes symptoms (disease of signs)

A. Hypertension:( BP>140/90 mm Hg after 20 weeks' gestation).

Preacuations:
• Blood pressure measured in left lateral or semi-sitting position.
• Blood pressure measured twice, 4 hours apart
B. Oedema
Occult Manifest
• excessive weight gain > 2 pound / week or pitting oedema (dependent )
• > 2 pounds/month
C. Proteinuria >300 mg/24 hours or >1+ dipstick

Symptoms:→ late and indicate severe disease

• Eye: Blurring of vision, flashes of light or complete blindness(usually reversible).

• Headache either (occipital) due to hypertension or (frontal)due to cerebral edema.
• Epigastric pain due to enlargement of subcapsular hematoma &Rt hypochondrial pain.
• Persistent nausea and vomiting due to congestion of gastric mucosa.
• Oliguria or even anuria.
• Lower limb oedema.
• ↓ fetal movement.

Criteria of Severe preeclampsia:

▪ B.P. ≥ 160/110 on 2 occasions at least 6 hours apart.

▪ Proteinuria ≥5 g in a 24-hour urine specimen or ≥3+ dipstick on 2 random urine samples collected at least 4 hours apart.
▪ Persistent headache
▪ Cerebral or visual disturbances.
▪ Pulmonary edema or cyanosis. HELLP syndrome
▪ Epigastric or right upper quadrant pain. ▪ H = Haemolysis (bilirubin ≥ 1.2 mg/dl)
▪ Impaired liver function. ▪ EL = Elevated liver enzymes
▪ Oliguria <500 ml in 24 hours ▪ LP = Low platelets count < 100,000/mm
▪ Serum creatinine >1.2 mg/dL unless known to be previously elevated → the most significant sign.
▪ Thrombocytopenia
▪ Fetal growth restriction (Asymmetrical).
 Complications

Fetal Maternal:
▪ Iatrogenic prematurity and its complications. ▪ Central nervous system
▪ IUGR Cerebral hemorrhage(commonest cause of death)& edema,
▪ IUFD Cortical blindness
▪ Respiratory system: Laryngeal edema, Pulmonary edema
▪ Renal system: renal failure
▪ Liver: Jaundice, Hepatic infarction, Hepatic rupture
▪ Coagulation system: DIC, Micro-angiopathic hemolysis.
▪ Eclampsia .
▪ Placenta: Red infarction, Retroplacental bleeding + abruptio placentae
▪ Remote : residual HPN, residual proteinuria& recurrence.
Investigations

Prediction→ Persistant notch on uterine artery Dopler at 20-24 weeks gestation

Labouratory findings:
▪ Renal function (deteriorated only in severe cases):
▪ CBC:
 ↑Serum uric acid + ↑Creatinine + ↑BUN.
  hematocrit value
 ↓Creatinine clearance
 Microcytic hemolytic anemia
▪ Liver functions
 Thrombocytopenia.
 ↑liver enzymes (ALT&AST) + ↑ LDH.
▪ Urine analysis: Oliguria, proteinuria, hypocalciuria.
▪ Coagulation profile is disturbed in DIC
Other investigation:

• Fundus examination to diagnose

retinal spasm (early finding) ,detachement & Hge .
• CT skull to diagnose intracranial complications.
• U/S& Doppler for diagnosing placental abruption, fetal life, age, weight, anomalies, wellbeing, V. mole, twins, hydramnios.

Differential diagnosis:
4. D.D of HELLP syndrome
1. D.D of hypertension with pregnancy: ▪ Acute fatty liver in pregnancy
▪ PIH, preeclampsia and superimposed preeclampsia. rare disease with unclear etiology + poor prognosis
▪ Essential hypertension & 2ry hypertension: Acute, rapidly progressing liver failure
▪ Chronic nephritis. with heavy hepatic infiltration with fat.
▪ Thyrotoxicosis(systolic HPN). ▪ Viral or drug induced hepatitis.
▪ Coarctation of aorta (differential HPN ). ▪ Thrombocytopenic purpura.
▪ Pheochromocytoma ▪ Hemolytic-uremic syndrome
(medulla of suprarenal gland, diagnosed by ↑VMA) Very rare & poor prognosis→ severe acute renal failure,
2. D.D of edema with pregnancy microangiopathic hemolytic anemia, thrombocytopenic purpura.

Unilateral bilateral
DVT Physiological Pathological
Cellulitis "pregnancy" ▪ Preeclampsia
▪ Renal,hepatic,cardiac,nutritional + angioneurotic
3. D.D of proteinuria with pregnancy:
▪ Contamination of the specimen with vaginal discharge( commonest cause).
▪ Urinary tract infection. ▪ Orthostatic proteinuria (rare and insignificant)
▪ Preeclampsia. present at the end of day and
▪ Renal hypoxia as in cases of CHF and severe anemia. disappears at morning dt stretch of left renal vein
▪ Anaemia. over 5th lumbar vertebrae in standing position
▪ Congestive heart failure. dt lumbar lordosis.
▪ Rarely in severe cases with hyperemesis gravidarum.
Prevention of pre-eclampsia:

▪ A variety of strategies used to prevent or modify the severity of preeclampsia have been evaluated.
▪ In general, none of these has been found to be clinically efficacious.
Examples → Dietary calcium , vit D + low-dose aspirin,

Management in table between pre / eclampsia

 Eclampsia
Def

▪ development of convulsions or unexplained coma during pregnancy or postpartum in patients

with signs and symptoms of preeclampsia.

Pathology:

▪ As pre-eclampsia and Cerebral Pathology which may be cerebral edema, ischemia or infarction
leading to hypertensive encephalopathy manifested by convulsions

Course of eclamptic seizures: 4 stages of an eclamptic event:

Premonitory stage (30 seconds): Tonic stage ( 15 to 20 seconds )

▪ eyes are rolled up Generalized tonic spasm with episthotonus.
▪ face and hands → twitches ▪ patient is cyanosed dt transient asphyxia
dt spasm of respiratory muscles.
Clonic stage (1 minute): Coma stage:(variable duration)
▪ muscles begin alternating ▪ respiratory and metabolic acidosis
between contracting and relaxing in rapid sequence. ▪ In rare cases, coma persist and woman never awake.
▪ tongue may be bitten, foam appears at mouth  usually denotes massive cerebral Hge
with bloody frothy discharge.
▪  temperatue.
Types:

▪ Antepartum (65%) Intrapartum (20%) Postpartum (15%)

▪ Eclampsia always should be considered in any pregnant patient with a seizure episode.

Complications as PE +Asphyxia (aspiration pneumonia)

Investigations: The same as pre-eclampsia AND

1. CT Scanning:
Cerebral edema,hemorrhage(Cerebral ,intraventricular hemorrhage, parenchymal hemorrhage)& Cerebral infarction
2. Magnetic Resonance Imaging of brain
3. Electroencephalography and CSF Studies

Differential diagnosis:

D.D of convulsions with pregnancy: D.D of coma with pregnancy:

▪ Eclampsia + Epilepsy + Hysteria. ▪ Hyperglycemic or ketotic coma.
▪ Meningitis & encephalitis. ▪ Hypoglycemic coma.
▪ Tetanus.Tetany. ▪ Alcoholic coma
▪ Strychnine poisoning. ▪ Cholemic coma.
▪ Brain tumors. ▪ Cerebral coma.
▪ Uremia ▪ Uremic coma.
Prevention:

 Proper management of preeclampsia

 Prophylactic magnesium sulfate( MgSO4) is recommended in severe preeclampsia and continued for 24 hrs postpartum.

Emergency management of eclamptic fit:

▪ Maintain patent airway

▪ Place the patient in the left lateral position
positioning  risk of aspiration
help improve uterine blood flow by relieving obstruction of the vena cava by the gravid uterus.
▪ Protect patient against injury during seizure by
padding, using a padded tongue blade between the teeth, and suction secretions as needed.
▪ Most eclamptic convulsions stop spontaneously and therefore no acute medical treatment is necessary.
If seizure persists
benzodiazepine (lorazepam or diazepam 5 mg over 60 seconds intravenous or magnesium sulphate 1-2 gm intravenous).

Subsequent pregnancy outcome:

▪ Women with a history of eclampsia are at increased risk for all forms of pre-eclampsia in subsequent pregnancies.
 Preeclampsia eclampsia
Expectant treatment (medical ) Medical
General General
1. Rest 1. Rest : single , quiet semidark room equipped + suction apparatus , mouth gag.
2. Diet : NPO.
2. Observations: 3. Observation :
• Frequently → vital signs , symptoms , urine output • Maternal coma duration , convulsion number & vital signs.
• Lab. Investigation (KFT , LFT , CBC, …etc). • fetal U/S. to document fetal viability.
• U/S & assessment of fetal wellbeing 4. Drugs →
3. Specific: Control of hypertension: Antihypertensive
Parenteral drugs (in severe cases) parentral (Hydralazine or labetalol)
• Hydralazine → peripheral vasodilator → palpitation. to maintain systolic BP between 140 - 160 mm Hg
• Labetalol → alpha1 and none selective beta adrenergic blocker. diastolic BP between 90 - 110 mm Hg
Oral anti-hypertensive: Anticonvulsants → Magnesium Sulfate, valium , Na thiopental &epanutin
• Alpha methyl DOPA (aldomet) Second-Line Medications:
acts centrally Max. • Diazepam + Clonazepam .
dose is 2 g/day • Phenytoin (epanutin) to prevent and treat convulsions.
SE→ postural hypotension, depression, night mares Although it widely used anticonvulsant drug, its use in eclampsia is limited
less commonly cholestatic jaundice + hemolytic anemia (+ve coombs test).  Care must be taken not to  the BP too drastically;
• Beta blockers → labetalol . + CCB → nifedipine an excessive  → inadequate uteroplacental perfusion and fetal distress
Obstetric 5. Complications:
Timing • Glucose → nutrition , supports liver.
Mild cases: Severe cases: • Atropine→↓ bronchial secretion.
▪ GA ≥ 37 wks: ▪ Gestational age ≥ 34 weeks • Digitalis→ in H.F. *Diuretics only in the setting of pulmonary edema.
termination of pregnancy T.O.P. • Oxygen
▪ Gestational age < 37 wks: ▪ Gestational age < 34 weeks: Obstetric
expectant till maturity then management is controversial Timing
termination TOP or conservative till 34 wk.  3 – 6 hours to stabilize general condition then termination.
Method (VD Vs CS.) Method
• vaginal delivery should be attempted if no indications for cesarean delivery. ▪ based on obstetric indications however vaginal delivery is preferable .
Postnatal care ▪ Cesarean delivery may be considered in patients with
▪ Continue antenatal antiHTN ttt (If methyldopa used, stop within 2 days of birth) unfavorable cervix // gestational age of 30 weeks or less.
▪ Stop antihypertensive treatment if BP falls to < 130/80 mmHg. ▪ vaginal delivery → same precautions as PE
▪ Measure BP at least 4 times a day while inpatient. Postpartum
▪ Measure platelet count, transaminases and creatinine 48-72 hours after birth. Parenteral magnesium sulfate
▪ Postnatal review (6-8 weeks after birth) continued for at least 24 hours after delivery or
✓ Offer medical review for at least 24 hours after last convulsion.
✓ Offer referral for specialist assessment if antihypertensive ttt still needed. oral antihypertensive as labetalol or nifedipine
✓ Repeat platelet count, transaminases and serum creatinine measurements to keep systolic BP < 155 mm Hg and
if indicated. diastolic BP < 105 mm Hg.
✓ Referral for specialist kidney assessment, if proteinuria ≥ 1+ (Nifedipine offers benefit of improved diuresis in the postpartum period).
 Rest of Ttt of PE

Indications for stopping conservative management in severe Preeclampsia:

Fetal
▪ Severe growth restriction
▪ Persistent severe oligohydramnios (AFI < 5 cm)
▪ Biophysical profile ≤4 done 6 hr apart
▪ Reversed end-diastolic umbilical artery flow
▪ Fetal death
Maternal
▪ Persistent severe headache or visual changes; eclampsia
▪ Shortness of breath; chest tightness , pulmonary edema
▪ Uncontrolled severe hypertension despite treatment
▪ Oliguria < 500 mL/24 hr or serum creatinine ≥1.5 mg/dl
▪ Persistent platelet counts < 100,000/mm3
▪ Suspected abruption, progressive labour, and/or ruptured membranes

Method (VD Vs CS.)

• vaginal delivery should be attempted if no indications for cesarean delivery.

1st stage 2nd stage 3rd stage 4th stage:

(continuous mat.& fetal monitoring) shorten with forceps or ▪ Ergometrine is contraindicated Observe for fits +PPH
▪ Oral Anti-hypertensives replaced by IV drugs ventouse. as causes v.c →  BP. for at least 24 hrs after delivery.
(DBP maintained on 80-100 mmHg) ▪ oxytocin
▪ Anticonvulsant drugs ( MgSO 4) to prevent PPH
started (in severe preeclampsia)

Magnesium Sulfate
is the drug of choice to treat and prevent subsequent convulsion
Dose: Loading dose Maintenance dose
4-6 gm in 100ml fluid IV initially over 15-20 min. 1-2g/hr to maintain effect with close monitoring of mg level in serum every 4 6hrs.
(Therapy is stopped 24hrs after delivery).
Mechanism: • Anticonvulsant
 CNS depression . • Vasodilator
 inhibits release of Acetyl choline at motor end plate. • diuretic
 inhibits intracellular ca influx .
Toxicity 8mEq/L 12mEq/L > 15 mEq/L
• patellar reflex is lost. respiratory depression. • cardiac conduction is disturbed
• myometrial inhibition starts • death may occur
Treatment →calcium gluconate or calcium chloride (antidote),
1 gm intravenously, along with withholding further magnesium sulfate Maintain levels between 4 and 7 mEq/L (4.8 to 8.4 mg/dL).
Before giving dose, the following should be confirmed:
o Present patellar reflex + Respiratory rate> 16/min . + Urine output >100 ml/4hrs.
 Superimposed pre-eclampsia on chronic hypertension
▪ New onset proteinuria in hypertensive women after 20 weeks' gestation, or
▪ sudden increase in proteinuria or blood pressure

Chronic Hypertension
Def

▪ hypertension present at booking visit or

▪ before 20 weeks or
▪ if woman is already taking antihypertensive medication when referred to maternity services.

Etiology

▪ Primary (essential): 90%

▪ Secondary to one or more underlying disorders:
✓ Renal disease (glomerulo-nephritis, interstitial nephritis, polycystic kidneys, renal artery stenosis)
✓ Endocrine disorders (DM with vascular involvement, pheochromocytoma, thyrotoxicosis, Cushing’s disease, hyperaldosteronism)
✓ Collagen vascular disease (lupus, scleroderma)
✓ Coarctation of the aorta.

Classification:

• Mild.
• Severe
Systolic and diastolic BP of at least 180 mm Hg or 110 mm Hg, respectively

Effect of pregnancy on chronic hypertension:

▪ In most women with chronic hypertension, blood pressure  in early pregnancy and then  during 3rd trimester
to levels somewhat above those in early pregnancy.

Effect of chronic hypertension on pregnancy

Fetal Maternal
• IUGR • Superimposed Pre-eclampsia
• Preterm Delivery • Placental Abruption
• Life-threatening complications such as
hypertensive encephalopathy, cerebral hemorrhage- retinopathy
acute renal failure - Pulmonary edema,

Management

Pre-conceptional Evaluation

▪ Women with chronic hypertension should ideally be counseled prior to pregnancy.

▪ Renal and cardiovascular function should be assessed.
▪ Ophthalmological evaluation and echocardiography in those with long-term hypertension.
▪ Most clinicians believe that pregnancy is relatively contraindicated in women who have:
✓ Persistent diastolic pressures of 110 mm Hg despite therapy, require multiple anti-hypertensives,
✓ Serum creatinine level of >2 mg/dl.
✓ Prior cerebrovascular thrombosis or hemorrhage, myocardial infarction, or cardiac failure.
 Antenatal
• Blood Pressure Control:
Pregnant women with severe hypertension must be
treated for maternal indications
regardless of pregnancy status
Antihypertensive Drugs:
1. Adrenergic-Blocking Agents
methyldopa – Labetalol
2. Calcium-Channel Blockers: Nifedipine
3. Vasodilators: Hydralazine
4. Diuretics: Thiazide- furosemide. avoided
as their use reduce plasma volume expansion.
5. ACE Inhibitors: avoided once pregnancy is
established. Because of adverse fetal effects
aim is to keep blood pressure < 150/100 mmHg, but
with diastolic pressure not < 80 mmHg.
• Fetal monitoring
U/S evaluation and cardiotocography.
Intrapartum Postpartum:
• Timing of birth: • Continue antenatal antihypertensive ttt.
✓ Uncomplicated cases: wait labour at term. • If woman has taken methyldopa
✓ Refractory severe chronic hypertension: stop within 2 days of birth
termination after a course of corticosteroids restart antihypertensive ttt that taking
(if required) has been completed. before pregnancy.
• Prophylaxis against convulsions: • Review log term antiHTN ttt
Magnesium sulfate prophylaxis is recommended for 2 weeks after pegnancy
prevention of eclampsia with chronic HTN
who develop severe gestational hypertension.
dose and duration is the same as in preeclampsia.
• Control of severe hypertension:
intravenous hydralazine or labetalol.
• Vaginal delivery is usually preferable,
Cs performed for usual obstetrical indications.