Hypertension in

Pregnancy
Fitsum Ashebir
OUTLINE
Introduction
Physiology of CVS in pregnancy
Hypertensive disorders
Definition & classification
Pathophysiology
Risk factors & complications
Management

Summary
Introduction
Complicates 5-10% of all pregnancies
Ranks among the leading causes of maternal morbidity and mortality
(along with hemorrhage and infection)
The fetus and neonate also are at increased risk from complications.
Management & prognosis differs in the different forms of hypertension
during pregnancy. Therefore, it is important to distinguish the forms of
hypertension that may complicate pregnancy.
One of the major causes of maternal morbidity-mortality leading to
10–15% of maternal deaths especially in the developing areas of the
world.
Physiology of
CVS In pregnancy
Physiologic changes

Hormones- Estrogen, RAAS, plasma

expansion, Progesterone, human
chorionic sommatomammotropin [
human placental lactogen] the ‘growth
hormone’ of pregnancy
Physiologic changes
Physiologic changes
CO increase, decreased PVR and increased HR, stroke volume ,
increased VR from Uteroplacental circulation i.e. 24% SV, 15% HR, max
CO

Position stroke volume in supine decreases from 20 wks. onwards and

can reach nonpregnant levels at 40 wks.

Supine hypotension syndrome in 8% bradycardia, hypotension,

syncope, decreased capacitance of collateral veins.
Physiologic changes
 BP nadirs between 24-28 wks.
 Pulse pressure widens
 TPVR decreases up to 34% at 14 wk.
 hormones trigger NO, prostacyclin's and
adenosine
Blood flow distribution
Uterus
Kidneys
GFR = ↑50%

Breasts
Skin
Only 60% of women complain of urinary frequency despite increased
GFR due to retention by RAAS and ADH
Renal Physiology in pregnancy
 Definition

 Disorders must be excluded (Table 19–1). Blood pressure should be

measured in both arms with the patient in a sitting position and the arm at
the level of the heart
NHBPEP Classification
1. Chronic hypertension
2. Gestational hypertension
3. Preeclampsia
4. Eclampsia
5. Preeclampsia superimposed on chronic HTN
Classification
 Proteinuria
 1 sample per 24 hr.
 Mild ----- 300mg/24hr
 Severe ---- 5g/24hr

 At least 2 random urine

samples, 4 or more hrs. apart
 Mild----- >1+
 Severe ---- >3+

 Proteinuria of preeclampsia is episodic; i.e. dipstick measurements could reveal different

values during each measurement differing from each other in the same patient .
Gestational Hypertension
 Is the development of an elevated BP during
pregnancy (after 20 weeks gestational age) or in
the first 24 hrs. post partum
 Absence of proteinuria and other symptoms of
preeclampsia
 The BP returns back to normal by 6 weeks post
partum
 The commonest hypertensive disorder of
pregnancy.
Gestational Hypertension
 Diagnosis
 Sustained elevation of BP > 140/90 after 20 wks. of pregnancy
 No Proteinuria
 BP return to normal in < 12 wks. postpartum

Final Diagnosis- Only Postpartum

Reclassified as transient hypertension of pregnancy if
 Evidence for preeclampsia does not develop
 BP returns to normal by 12 weeks.
 Preeclampsia
It complicates 5-7% of all pregnancies
Preeclampsia is a multisystemic disease of pregnancy manifested by the
cardinal features of hypertension and proteinuria manifesting after the
20th week of pregnancy.
Mild preeclampsia: the diastolic BP remains below 110 mm Hg and the
systolic BP below 160 mm Hg .
Rarely appearing during the puerperium for the first time.

 Exception- Atypical eclampsia when eclampsia develops before 20 weeks of

gestation or after 48 postpartum
 May occur before 20 weeks in molar pregnancies and Antiphospholipid antibody
syndrome
 Sometimes labor does not start and convulsions recur again ‘intercurrent
eclampsia’ and carries a bad prognosis
Preeclampsia
In the absence of proteinuria preeclampsia should be
considered:
Gestational hypertension plus

Persistent cerebral symptoms

Epigastric or right upper quadrant pain plus nausea or vomiting

IUGR

Abnormal laboratory tests such as thrombocytopenia and elevated liver enzymes.

 Risk Factors for Preeclampsia
Age of the woman (<20yrs? or >35yrs)
Nulliparity
Family history of preeclampsia
Obesity
Hydatidiform mole
Polyhydramnios
Low socioeconomic status
Risk Factors
Spouse change
Multifetal gestation
Preeclampsia in previous pregnancy
Poor outcome in previous pregnancy
Preexisting medical—genetic conditions : Chronic HTN, Renal disease, Type
1DM, Thrombophilia's
Severe hypertension increases risk of

For the Mother For the fetus

heart attack poor placental transfer of oxygen

renal failure fetal growth restriction
cerebrovascular accidents preterm birth
Retinopathy placental abruption
Still birth

Neonatal death
Systemic Pathology and
Complications

Cardiovascular Generalized vasospasm; •Hypertension

system
Increased afterload; •Congestive heart failure

endothelial damage and •Generalized edema

fluid and protein leakage

Respiratory Pulmonary capillary endothelial •Non- cardiogenic

system damage and hypoprotienemia Pulmonary edema

left ventricular failure •Cardiogenic pulmonary

edema

22
 Systemic Pathology and
Complications
Hematologic Excessive consumption of platelets to repair
system endothelial damage; •Thrombocytopenia

RBC damage as they pass through the spastic •Microangiopathic

arterioles hemolytic anemia

Reno vascular Decreased GFR due to spasm; •Acute renal failure

system
renal glomerulo endotheliosis; •Proteinuria

renal damage •Hyperuricemia

Systemic Pathology and
Complications
Gastrointestinal Hepatocellular injury •Hepatic failure
tract
Coalescing focal hemorrhages •Sub capsular hematoma
Lead to hematoma collection •Acute liver rupture
under the Glisson’s capsule

Central nervous Cerebral hypoxia •Eclampsia

system
focal hemorrhages •Hemorrhagic stroke

secondary cerebral edema •Cerebral edema and

intracranial hemorrhages death due to coning
•Transient blindness –
retinal or cortical

24
 Systemic Pathology and
Complications
Blood volume Contracture of the total •Less tolerant to blood loss at
vascular space and overall delivery (easily develop PPH)
reduced blood volume •Less tolerant to fluid administration
(develop pulmonary edema)

HEELP syndrome Concomitant occurrence of

Microangiopathic hemolysis
Thrombocytopenia
Liver damage
 Preeclampsia
Diagnosis
Mild Preeclampsia
 Sustained elevation of BP > 140/90 after 20 wks. of pregnancy
 Proteinuria > 300mg/24hr or > 1+ dipstick

Severe Preeclampsia
 Persistent headache or other cerebral or visual disturbance
 Persistent epigastric pain, Fetal growth restriction
 Sustained elevation of BP > 160/110 after 20 wks. of pregnancy
 Proteinuria > 5g/24hr or > 3+ dipstick
 Oliguria of less than 400 mL in 24 hours
 Serum creatinine > 1.2 mg/dl (unless previously elevated)
 Thrombocytopenia- Platelets < 100,000/mm3
 Microangiopathic hemolysis (Inc. LDH) ,Elevated ALT or AST
 Pulmonary edema or cyanosis
Criteria for Severe
Preeclampsia
Criteria
1.
Blood pressure of ≥160 mm Hg systolic or ≥110 mm Hg diastolic, recorded on
at least two occasions at least 6 hours apart

2. Proteinuria of ≥5 g in 24 hours , >3+ on dipstick

3. Oliguria (≤400 ml in 24 hours)
4. Cerebral visual disturbances
5. Epigastric/RUQ pain, nausea, and vomiting
6. Pulmonary edema
7. Thrombocytopenia< 100,000/ml
8. Impaired liver function of unclear etiology
9 IUGR
 Pathophysiology
Heart: Generally unaffected; cardiac decompensation in the presence of
preexisting heart disease.
Kidney: Renal lesions (glomerular endotheliosis); GFR and RBF decrease;
hyperuricemia; proteinuria may appear late in clinical course; hypocalciuria;
alterations in calcium regulatory hormones; impaired sodium excretion;
suppression of renin angiotensin system.
Coagulation System: Thrombocytopenia; low antithrombin III; higher fibronectin.
Liver: HELLP syndrome (hemolysis, elevated ALT and AST, and low platelet count).
CNS: Fibrinoid necrosis, thrombosis, microinfarcts, and petechial hemorrhages,
primarily in the cerebral cortex, and Cerebral edema may be observed
Lungs: Pulmonary edema as a result of capillary leak, fluid overload (iatrogenic),
postpartum refill or CHF.
Pathophysiology
Pathophysiology
All pathologic features of preeclampsia recede upon delivery of the
placenta without any remnant disease or pathology

Development of hypertension is due to generalized vasoconstriction,

not activation of the RAAS: NO salt restriction
Etiology of preeclampsia
Etiology remains unknown
Possible etiologies:
Abnormal trophoblastic invasion
Coagulation abnormalities
Vascular endothelial damage
Cardiovascular maladaptation
Immunologic phenomena
Genetic predisposition
Dietary deficiencies or excesses
Pathophysiology
Etiology of preeclampsia is unknown
“ Disease of Theories”
1. Vascular theories
2. Hypoxic placenta theory
3. Immunological theory
4. Genetic theory
5. Nutritional theory
Vascular theory
Hypoxic placenta theory
 Immunologic theory
Placenta has both paternal and maternal antigen
Uterine arteries must be independent from ANS.
Achieved by two waves of trophoblastic invasion.
Genetic
Preeclampsia is a multifactorial, polygenic disorder

Because there is a pattern of inheritance

Spouses of men born from preeclamptic mother
Women born from preeclamptic mother
Mothers carrying fetuses with trisomy 13
 Characterization of Symptoms

Clinical manifestations
Clinical manifestations
Visual disturbances typical of preeclampsia are scintillations and
scotomata. These disturbances are presumed to be due to cerebral
vasospasm.
SOB – due to Pulmonary edema
Physical Findings in Preeclampsia
Increased Blood Pressure
Retinal vasospasm or Retinal edema
Right upper quadrant (RUQ) abdominal tenderness
Basilar crepitation's
Brisk, or hyperactive deep tendon reflexes
A sudden change in dependent edema, edema in nondependent areas
such as the face and hands
Rapid weight gain during serial weight measurement
Eclampsia
Diagnosis
Preeclamptic patient + Seizure (that cannot be attributed to other cause)
Occurs in 1-3 per 1000 of preeclamptic patients
GTC convulsions, mostly self limited (1-2 min)
May also result in coma.
Diagnosis Of Eclampsia
Clonic stage (1-2 minutes): Coma:
Convulsions Variable duration due to respiratory
and metabolic acidosis.
Tongue may be bitten
Deep coma may occurs (cerebral
face is congested and cyanosed hemorrhage).
conjunctiva congestion Labor usually starts shortly after the
fit.
blood stained froth from the
mouth
Stertorous breathing
temperature may rise
involuntary passage of urine or
stool
Gradually convulsions stop
Chronic hypertension
 It complicates 5% of pregnancies
 Hypertension before pregnancy, before 20th wk. of gestation or
persisting 12 weeks after delivery.
Chronic hypertension
Mild chronic hypertension
Mild hypertension
No End organ Damage

Severe chronic hypertension

Severe hypertension
End organ involvement (heart failure, stroke, renal failure)

Diagnosis
 Hypertension diagnosed before pregnancy
 Sustained elevation of BP > 140/90 before 20 wks. of pregnancy
 Hypertension persist after 12 wks. postpartum
Preeclampsia superimposed
on chronic hypertension
This complication occurs in 25% of patients with chronic HTN.

Diagnosis
 Hypertension before 20 wks. +
 Proteinuria (after 20 weeks)
 Evidence of maternal jeopardy
OR
 Hypertension and proteinuria before 20 wks. +
 Sudden increase in proteinuria or BP
 Thrombocytopenia
 H E L L P syndrome

Hemolysis Elevated Low Platelets

Liver enzymes

 Occurs in 5-10% of preeclamptic patients

 One of the signs to classify as severe preeclampsia
The HELLP syndrome
Hemolysis
Elevated Liver enzymes
Low Platelets
0.2 to 0.6 % of all pregnancies
Complicates 10% of cases of severe PE and up to 50% of cases of
eclampsia
Maternal mortality has been estimated to be as high as 2-24%
Perinatal mortality is equally high, ranging from 9 –39 %.
RUQ pain, nausea, vomiting, and malaise are common.
The hallmark of the disorder is Microangiopathic hemolysis
The HELLP syndrome...
The elevated liver enzyme levels in the syndrome are thought to be
secondary to obstruction of hepatic blood flow by fibrin deposits in the
sinusoids.
This obstruction leads to periportal necrosis and, in severe cases,
intrahepatic hemorrhage, subcapsular hematoma formation or hepatic
rupture.
The thrombocytopenia has been attributed to increased consumption
and/or destruction of platelets.
90%of patients present with generalized malaise, 65 % with epigastric pain,
30 % with nausea and vomiting, 31 percent with headache
Because of the variable nature of the clinical presentation, the diagnosis of
HELLP syndrome is generally delayed
Usually present with complications
Laboratory Diagnostic Criteria for
HELLP syndrome
Haemolysis
Abnormal peripheral smear : spherocytes, schistocytes, triangular cells and
burr cells
Total Bilirubin level > 1.2 mg/dL
Lactate dehydrogenase level > 600U/L

Elevated liver function test result

Serum aspartate amino transferase level > 70U/L
Lactate dehydrogenase level > 600 U/L

Low platelet count

Platelet count < 100 000/mm3
Conditions confusing with
HELLP syndrome
1. Acute fatty liver in pregnancy.
2. Hepatitis
3. Thrombocytopenia purpura
4. Hemolytic Uremic syndrome
5. Diabetic Ketoacidosis
6. Kidney stones
7. Peptic ulcer disease
 Investigations:
Baseline investigations:
Complete blood count
 Hematocrit (hemoconcentration
supports the diagnosis of
preeclampsia)
 PT, aPTT, platelet count
Urine albumin
Renal function tests – cr,
Liver function tests- SGOT, SGPT, LDH
Uric acid level
Ultrasound ( fetal growth and BPP)
Special Investigations:
Coagulation profile (if thrombocytopenia
or elevated liver enzymes)
Peripheral morphology if HELLP
syndrome suspected
Serum electrolytes in eclampsia
Chest x-ray
ECG in patients with pulmonary edema
and/or CHF
CT or MRI in patients with prolonged com
Complications of Eclampsia
In addition to known complications of severe preeclampsia, eclampsia
can develop the following complications
Aspiration
Trauma
Preterm labor
Higher risk of infections such as pneumonia
Fetal distress and asphyxia
Cerebral edema

51
Differential diagnoses of
eclampsia
Hypertensive encephalopathy
Seizure disorder
Hypoglycemia,
Hyponatremia
 TTP
Vacuities/angiopathy
 AFE
Cerebrovascular accidents
Hemorrhage
Meningitis/ encephalitis
Ruptured aneurysm or malformation
 Arterial embolism, thrombosis
 Venous thrombosis
 Hypoxic ischemic encephalopathy
 Angiomas
Management
Management
The stages of PIH are:-
Hypertension with proteinuria or edema
 Mild chronic
 Severe chronic
Mild pre-eclampsia
Severe preeclampsia,
Eclampsia
 Chronic hypertension
Clinical features- Two blood pressure readings greater than 90mm Hg and 4 hours
apart (± 140 mm Hg systolic). There will be no symptoms & hypertension is the only
sign at this stage.
Mild chronic
ANC every 2-4 wks until 34-36 wks. & weekly thereafter
BP , urine protein , fundal height , follow for IUGR if found admit and follow if
induction of labor is needed
Counsel for Symptoms of preeclampsia
If normal follow and wait normal labor

Restriction of dietary salt

Anti hypertensive medication is not usually necessary and the threshold for
initiation of anti hypertensive therapy
BP 150\100 without evidence of end organ involvement
BP 140\90 with evidence of renal involvement
 Chronic hypertension
Severe chronic
Anti hypertensive therapy
Check the effectiveness of medication
Check for evidence of superimposed preeclampsia
Delivery is accomplished after 38 wks or when fetal lung maturity is
demonstrated.
If exacerbation of chronic hypertension necessitates preterm delivery,
corticosteroids should be given to accelerate fetal lung maturity.
 Preeclampsia
Clinical Features- The DBP remains on 2 occasions 90 mmHg but <110mmHg,
Proteinuria of 2+ (or 1 ~ with specifications given in the definition)., no other
symptoms, signs or laboratory findings of severe pre-eclampsia.
Follow up during out pt. management of PE includes:
Urine protein daily
BP measurement daily
Fetal movement count daily
ANC follow up twice weekly where
 BP, DTR and fetal conditions are assessed
 Counsel about the danger signals and bed rest
 Encourage the woman to eat a normal diet (salt restriction should be discouraged)
 Orient on fetal movement counting (kick chart) daily, to be reported at ANC visits
 No medications (do not give anticonvulsants, anti hypertensive, sedatives or).
CBC and liver enzymes during each ANC visit
NST and serial fetal growth and amniotic fluid evaluation
 Mild preeclampsia
Vary depending on the gestational age
GA <37 weeks
 Outpatient 2x weekly ANC follow up (previous slide)
Admit the patient if outpatient follow up is not possible, close observation is
preferred, or preeclampsia progress rapidly
Monitor BP 2x daily and urine protein & weight daily (Weight gain must be = 0.45kg/wk.)
Auscultation of FHB & kick chart daily
Normal diet, no medication, no diuretics unless pulmonary edema or CHF develop

Out patient follow up if pressure is normal or she is stable

 If the signs remain unchanged ,keep the woman in the hospital
Consider early delivery if there are signs of growth restriction
Manage as severe preeclampsia if signs worsen
Mild preeclampsia
GA >= 37 complete weeks
If the woman's condition remains stable & no sign of IUGR, plan
delivery when the cervix is favorable.
If signs of fetal compromise, assess the cervix and expedite delivery
Favorable: rupture the membranes and with an amniotic hook or
Kocher clamp & induce labor (refer to inducation protocol).
Unfavorable: ripen the cervix or deliver by c\s
Severe preeclampsia
a)Clinical Features - includes any one or more of the following in variable
combination.
Diastolic blood pressure 2X 110mmhg after 20wks gestation & proteinuria of
>3 + (≥ 5gm in 24hrs)
Any of these manifestations of multi organ involvement
 Headache: -increasing frequency, unrelieved by regular analgesics
(frontal/occipital)
 Hyperreflexia (exaggerated deep tender reflexes)
 Clouding of vision (blurred vision/photophobia)
 Oliguria (<400 ml urine in 24hrs) (followed by rapid weight gain)
 Upper abdominal pain (epigastric or right upper quadrant pain)
 Pulmonary edema (rapid shallow breathing, cyanosis, rales).
Fetal growth restriction
Abruptio placenta
Severe preeclampsia
Disseminated intravascular coagulation (DIC) (bleeding, petechial)
HELLP syndrome (hemolysis, elevated liver enzymes & low platelets)
Eye changes: arteriolar spasm, edema, retinal detachment ( by fundoscopy).
Severe nausea & vomiting
Lab changes include
 Increased hematocrete (hemoconcentration
 Blood smear (----> hemolysis)
 Platelets < 100,000
 PT, PTT, Fibrinogen, FDP
 Serum uric acid (↑ ed)
 Serum creatinine (↑ ed)
 Significantly altered liver function tests
 Hyperbilirubinemia
 Elevated liver enzymes (AL T, AST, LDH)
Severe preeclampsia
The appearance of any of the above manifestations of multi-organ
involvement constitutes an obstetrical emergency (act accordingly).
If there are symptoms or signs of imminent eclampsia (such as headache,
blurred vision, vomiting, right upper quadrant pain, oliguria, exaggerated
DTR) manage as in eclampsia.
The steps of management include:
General measures - supporting the specific treatments
Prevent convulsion with magnesium sulfate or valium
Control hypertension
Delivery as soon as possible
 Severe preeclampsia
General measures
Admit the patient urgently, if not done before
Manage in left lateral position (relieves pressure on inferior vena cava)
Set up IV line and infuse fluids to replace estimated loss (from
bleeding, vomiting diarrhea, sweating) ( 500ml in 1st 1/2 hr.). then ongoing loss
+urine out put + insensible loss (700 ml/24 hrs. (PO & IV).
Monitor urine output (at least 30 ml/hr.) & proteinuria
Prepare for convulsion management (mouthpiece, airway, suction equipment,
mask & bag, oxygen)
Observe vital signs , FHB , & reflexes hourly
Check for pulmonary edema ; if it occurs, avoid fluids and use diuretic
(frusemide 40 mg IV )
Anti emetic – for nausea & vomiting
Anti pain- for RUQ pain, headaches
Severe preeclampsia
Stress Reduction
A component of maternal hypertension is adrenergic & may be modified by
stress reduction
Maternal discomfort must be minimized (as above & others)
Components of stress reduction includes
 Quiet, dimly lit, isolated room.
 Well planned management protocol
 Clear explanation of the management plan to patient and family
 Minimization of negative stimuli
 Consistent, confident team approach
Severe preeclampsia
Seizure prophylaxis
In all pre-eclamptics during labor & continued 12-24 hrs. after delivery
In all severe pre-eclamptics during admission and continued during period of
evaluation and observation
Give anticonvulsive therapy aggressively to prevent under treatment

Magnesium sulphate is the DOC for severe preeclampsia and eclampsia

Diazepam if the above isn’t available
Greater risk for neonatal respiratory depression
Severe preeclampsia
Anti hypertensive therapy
Goals
Minimize risk of maternal CVA (but does not necessarily reduce the risk of seizure
or prevent IUGR)
Maximize maternal condition for safe delivery
Gain time for further assessment
Facilitate vaginal delivery if possible
Prolong gestation where appropriate / feasible
Anti - hypertensive drugs should be used if the DBP remains at ≥ 110 mmHg
after 1 hr. of bed-rest & anti-convulsive treatment (also for DBP I00-109 mm
hg with other adverse manifestation)
The goal is to keep the DBP 90-100 mm hg) (< 110 mmHg in labor).
Severe preeclampsia
Anti hypertensive therapy
Acute or maintenance therapy

Hydralazine
DOC for acute therapy
Arteriolar dilator with rapid Iv onset
5-10 mg Iv slowly every 5 minutes until BP is lowered (diastolic <110)
OR 12.5mg 1M every 2hrs as needed.( If IV rout is not possible)
Hypotension with fetal compromise may occur in slow acetylaters &
hypovolemic patients(start with 5 mg Iv test dose)
s/e: flushing , headache or tachycardia
Severe preeclampsia
Nifedipine
Ca2+ -channel blocker, oral agent , with rapid onset of action (relaxes
vascular smooth muscle)
Alternative for acute therapy
5-10 mg sublingually as initial dose , followed by 5-10 mg if response
is inadequate in 30 minutes. Then continue as 10-20 mg PO every 6
hours.
For maintenance therapy 10-40 mg PO BID
S\e: edema ,flushing , headache, palpitation, magnesium sulphate
toxicity , tocolytics (may stop labor)
Severe preeclampsia
Methyldopa
Oral centrally acting a-receptor agonist
DOC for maintenance therapy
Minimal side effect & safe
500-3000 mg PO in 2-4 divided doses per 24 hours
Other alternative drugs for maintenance therapy include: Nifedipine ,
Hydralazine or Atenolol PO

ACEIs are C\I in pregnancy : fetal hypercalvaria , renal defects ,anuria ,

and fetal & neonatal death
Diuretics should be avoided with few exceptions
Eclampsia
Treatment of eclampsia is symptomatic & consists of six aspects:
1. General measures
2. Control of convulsions (to stop ongoing convulsion & prevent repeated
convulsion)
3. Correction of hypoxia & acidosis-by clearing airway & giving O2 by mask
at 6L/min
4. Blood pressure control & stabilization of the condition of the mother &
fetus
5. Fluid balance & diuresis
6. Delivery & intra partum/post partum care
Eclampsia
General measures
Set up IV line
Position the patient on her side (left lateral) & in Trendelenburg (head
down) position to reduce risk of aspiration of secretions, vomits or
blood
Aspirate the mouth & throat as necessary & ensure open airway
Give oxygen by mask at 6L\Min
Avoid tongue bite
Monitor urine output & protein
Observe vital signs , FHB & reflexes frequently and check for
pulmonary edema
The patient has to be kept in the eclampsia room (quiet ,intensive
care with attendant always beside the patient)
Administration of prophylactic IV antibiotics is beneficial
 Eclampsia
Anticonvulsant therapy
To stop the ongoing convulsion & prevent repeated attacks
Magnesium sulphate is the DOC- Magnesium is NMJ blocker
 Follow up RR, urine output, reflex
 In case of respiratory arrest
 Assist ventilation
 Give calcium gluconate 1g (10 ml of 10% solution) Iv slowly until respiration
begins
Before repeat administration, ensure that:
 Respiratory rate is at least 16 per minute.
 Patellar reflexes are present.
 Urinary output is at least 100 ml over 4 hours.
Withhold or delay drug if:
 Respiratory rate falls below 16 per minute.
 Patellar reflexes are absent.
 Urinary output falls below 30 mL per hour over preceding 4 hours.
Eclampsia
Eclampsia
Diazepam
Effective alternative drug
But it increases the risk of respiratory depression & newborn asphyxia in
babies who, may already be suffering from the effects of Uteroplacental
ischemia & pre term birth & the effect may last several days
 A 10 ml syringe can be used to install the drug into rectum
Eclampsia
Antihypertensive therapy
To keep the diastolic pressure<110 mm Hg & prevent cerebral hemorrhage

Fluid balance & diuresis

Keeping strict input & output record is essential and determine serum
electrolyte, if possible.
For unconscious patient, 5% DW (1000ml) & ringer's Lactate (500ml) are
infused for maintenance of nutrition & fluid balance during 24hrs. (or
alternatively urine output plus insensible loss of 700ml)
Replace extra fluid loss through vomiting, diarrhea, sweating or blood loss
Nothing by mouth is allowed (if unconscious); when the patient becomes
conscious & can drink, oral feeding of fluid is started.
Lasix 20mg IM is given for diuresis (especially after delivery)
Eclampsia
Delivery
Regardless of gestational age
Eclamptics usually proceed to labor spontaneously while having
convulsions
Delivery should occur with in
 24 hrs. of the onset of symptoms in severe preeclampsia ,
 12 hrs of the onset of convulsions in eclampsia
If vaginal delivery isn’t possible with in this time limit , delivery
should be by c/s
Indications for delivery
Pregnancy at >37 wks. depending on the favorability of the cervix
Gestation >34 wks. with severe preeclampsia
Severe preeclampsia remote from term(28 or 30)
Gestational age from 32-34 wks with severe hypertension not responding to initial
observation & treatment
Gestation<34 wks. (urgent delivery within 12-24 hrs.)
Severe hypertension not responding to RX
Symptoms unresponsive to appropriate therapy i.e. Severe headache or visual
disturbance, Nausea, vomiting or RUQ / epigastric pain
Suspected fetal compromise
Eclamptic-convulsions
Lab. Evidence of end organ involvement despite good blood pressure control,
Decreasing platelets or increasing liver function enzymes, Severe proteinuria
Indications for delivery
Route of delivery
Depends on gestational age , fetal condition & presentation , cervical and
maternal condition

Vaginal delivery
Vaginal delivery by inducing ARM & oxytocin where needed under the
following conditions
 If the cervix is ripe
 If the fetus is dead or extremely premature for survival
 With rapid progress in labor
C\S can be performed if labor has not begin within 6-12 hrs. or if the
progress of labor is poor
Cesarean delivery
Cesarean delivery
If the cervix is unfavorable
With poor progress of labor
If the patient has not entered active labor within 8 hrs of induction of labor in
women with pre-eclampsia or eclampsia
Evidence of fetal distress and other obstetric indications
Use of Anesthesia
Do not use local anesthesia or ketamine in women with pre-eclampsia or
eclampsia.
General anesthesia with thiopental, succinyl cholines & nitrous oxide is
preferable
Spinal anesthesia can be used, with adequate IV fluid loading (500- 1000ml),
to reduce the risk of hypotension (except in patients with thrombocytopenia
(platelets <100,000) or bleeding disorders).
 Management of hypertension
during labor
Absolute bed rest in LLP, is essential

Proper sedation is important as hypertension & risk of convulsion tends to increase in labor

Anti hypertensive drugs (usually hydralazine or nifedipine) should be employed, as necessary, to regulate
diastolic blood pressure between 90& 110 mm hg

Glucose therapy is useful

Careful monitoring of FHB, maternal conditions & progress of labor is essential with augmentation as
required

The second stage should be shortened by episiotomy & low forceps (or craniotomy with dead baby), in
severe cases (avoid difficult vaginal delivery).

Pudendal block or perineal infiltration analgesia along with injection of diazepam is often employed .

Prevent PPH-(Manage third stage actively using Oxytocin), watch closely for at least 2hrs after delivery, for
complications such as shock, PPH & eclampsia

Neonatal care is needed for premature & those with IUGR for respiratory distress
 Postpartum care
Anticonvulsive therapy should be maintained for 24-48 hrs. after delivery or the
last convulsion , whichever occurs last
Continue anti hypertensive therapy as long as the DBP ≥ 110mmhg
Continue to monitor urine output & check for coagulation failure , LFT, RFT if
possible
Postnatal follow up for the Rx of HTN & possible complications e.g. pelvic and UTI
or pneumonia
Treatment of complication
i. DIC - minimize trauma; transfuse with fresh whole blood or fresh frozen plasma
ii. Acute renal failure (persistent oliguria for> 48hrs after delivery, despite adequate
fluid & diuretics). Restrict fluid intake to 500ml plus ongoing loss, consider referral if
no improvement
iii. Pulmonary edema - keep in propped up position, give O2 (100%), restrict fluid
intake (2.5 l/day) give Furesemide 40-100mg IV & Aminophylline 480mg IV slowly).
SUMMARY
Summary
 Principles of Management

Summary
 SUMMARY
Summary
Challenges in diagnosis
Nadir of BP during 2nd trimester
Mild preeclampsia has no symptoms

Routine blood pressure measurements, weight gain surveillance and

check for symptoms and proteinuria are performed to detect
preeclampsia early.