This document provides an overview of hypertensive disorders in pregnancy. It begins with an introduction stating that hypertensive disorders are a leading cause of maternal and neonatal morbidity and mortality. It then covers the classification, diagnosis, risk factors, pathophysiology, clinical presentation, and management of the main types of hypertensive disorders - gestational hypertension, preeclampsia, chronic hypertension, and preeclampsia superimposed on chronic hypertension. Preeclampsia is described as a pregnancy-specific syndrome caused by reduced organ perfusion from vasospasm and endothelial dysfunction. The management of hypertensive disorders focuses on delivering the baby to resolve the condition, while controlling blood pressure and preventing seizures in severe preeclampsia

1. HYPERTENSIVE DISORDERS IN
PREGNANCY
GIRMACHEW T.(MD)
OBGY
MAY 22, 2018
GONDAR, ETHIOPIA

2. Outline
Diagnosis of HTN
Introduction
Classification
Pathophysiology and risk factor
Clinical presentation
Management

3. Introduction
 Most common medical complication
 Incidence 7-10% all pregnancies
70 % Preeclampsia- Eclampsia
30 % Chronic HTN
0.05 Eclamosia
 Major cause of maternal and perinatal mortality &
morbidity.

4. Classification
1) Gestational HTN( transient HTN)
2) Preeclampsia- Eclampsia syndrome
3) Chronic HTN
4) Preeclampsia superimposed on chronic HTN

5. Diagnosis
Hypertension:
Systolic BP > 140 or DBP > 90 mmHg. Measured
on any two occasions > 6hrs apart
or
One DBP> 110 mmHg

6. Proteinuria
Urine protein > 300mg/24hr or
30mg/dl(1+dipstick) or 0.1gm/L in at least two
random urine sample
Urine protein : creatinine ratio > 0.3
Edema No longer part of diagnosis
* wt gain >1kg/ week & pathological edema are↑
warning sign

7. Gestational Hypertension
Definition
B/P > 140/90 mmHg for first time during pregnancy
after 20 wks G.A or first 24 hrs post partum.
 No proteinuia
 Mild HPN & must return with in 12 weeks postpartum
 It is a diagnosis of exclusion
 Final dx made only postpartum.
Pregnancy outcome similar to normotensive pregn

8.  At risk of progression to PE or eclampsia
 Close observation of maternal & fetal condition
 In absence of severe HPN or PE can continue
pregnancy till term

9. Preeclampsia
Definition
 new onset of hypertension after 20 weeks of
gestation and
1. Proteinuria
2.Trombocytopenia(<100,000/ml)
3.Renal insuficiency….cr>1.2 mg/dl or doubling of base
line
4.Liver involvement….transaminase elivation
5.Cerebral symptoms…headache, visual disturbance,
convulsion
6.Pulmonary edema

10.  pregnancy specific syndrome of reduced organ
perfusion secondary to vasospasm and endothelial
activation.
incidence nullipara = 3-7% multipara 0.8-5%

11. Superimposed upon chronic HTN
HTN and no proteinuria <20 weeks:
 New onset proteinuria after 20 weeks of GA
HTN and protienuria <20 weeks:
Sudden increase in proteinuria
Sudden increase in BP in woman whose BP was well
controlled
Thrombocytopenia ( <100,000/ml)
Increase in ALT or AST to abnormal levels

12. Chronic HTN
BP > 140/90 mmhg before px or diagnosed before
20 weeks of GA or diagnosed after 20 weeks of GA
and persists after 12 weeks postpartum
Other associated findings
 Retinal change
 Cardiac
 Renal diseaese
 Other medical illness

13. Risk factors for PE
• Nulliparity
• Obesity
• Age <20 or > 35 yrs(chronic HTN and superimposed
PE)
• Multiple gestation
• Low socioeconomic status
• GTD
• Poor outcome of previous pregnancy (IUGR, SB
,abruption)
• ART( assisted reproductive technology)
• Race , ethinicity, genetics

14. Pre-existing medical conditions
 Chronic HTN
 Renal disease
 DM (type I)
 Thrombophilias (APA, protein C,S deficiency )
Smoking is it a risk factor or protective?

15. Classification of PE
Non severe PE Severe PE
BP >160/110 mmhg
Proteinuria of >5g/24 hr
Oliguria <500ml/24 hrs
Thrombocytopenia
Elivated liver function test with
persistent epigastric or RUQ pain
Pulmonary edema
Persistent severe cerebral or visual
disturbances
Convulsion
HELLP syndrome and DIC
BP >140/90
mmhg
Proteinuria of
300mg/ 24 hrs or
1+ on dipstich

17. Etiology & pathogenesis
Etiology – Unknown
Known as disease of theory
Some of theories
• Abnormal trophoblast invasion
Coagulation Abnormalties
Vascular endothelial damage
Immunologic theory
Placental toxin theory……toxemia of pregnancy
Genetic predisposition
Dietary deficiencies ….calcium and antioxidant
deficiencies

18. Any theory has the following charactersitics
1. Exposed to chorionic villi for the first
time….nulliparous
2.Exposed to superabundance of chorionic villi…twins
and GTD
3.Preexisting condition of endothelial cell
activation/inflammation….DM/renal/
cardiovascular disease
4.Genetically predisposed to HTN developing during
pregnancy…family hx

19. Abnormal Trophoblast invasion
Defective vascular response to placentation due to
inhibition of 2nd wave of endovascular trophoblast
occur often 16 week

20. Trophoblastic invasion of spiral arterioles leads to
the destruction of the muscularis layer which is
replaced by trophoblastic cells which do not
respond to the autonomic stimulation of blood
vessels; this ensures that there is a constant
uninterrupted blood flow to the intervillous space

21. According to the immunological theory, there is sufficient
similarity between paternal and maternal HLA antigens,
which prevents early fetal antigens from detection by the
maternal immune system
This leads to failure of production of blocking antibodies
early in gestation
As fetal antigens increase in amount later in gestation, the
maternal immune system responds by producing antibodies
that destroy placental trophoblasts

22. SYSTEMIC ENDOTHELIAL
DYSFUNCTION
All of the clinical features of preeclampsia can be
explained as maternal responses to generalized
endothelial dysfunction
Disturbed endothelial control of vascular tone causes
hypertension, increased vascular permeability results
in edema and proteinuria, and abnormal endothelial
expression of procoagulants leads to coagulopathy.
These changes also cause ischemia of target organs,
such as the brain, liver, kidney, and placenta.

23. Laboratory evidence supporting generalized
endothelial dysfunction in preeclamptic women
- Decreased production of endothelial-derived
vasodilators -nitric oxide and prostacyclin
- increased production of vasoconstrictors -endothelins
and thromboxanes.
- Enhanced vascular reactivity to angiotensin II

24. Organ
system
Pathology complication
CVS Generalized vasospasm; increased
afterload; left ventricular strain and
failure; microvascular endothelial
damage and fluid and protein leakage
•Hypertension
•Congestive heart failure
•Generalized edema
•Pulmonary edema
Hematolog
ic
Excessive consumption of platelets to
repair endothelial damage; RBC
damage as they pass through the
spastic arterioles
•Thrombocytopenia
•Microangiopathic
hemolytic anemia
Renal Decreased glomerular filtration rate
due to spasm; renal glomerulo
endotheliosis; renal tubular necrosis;
renal cortical necrosis in advanced
•Acute renal failure
•Proteinuria
•Hyperuricemia
Respirator
y
Pulmonary capillary endothelial
damage and leakage ( in addition to
hypoproteinemia due to proteinuria
and left ventricular failure)
Pulmonary edema

25. Organ
system
pathology complication
Gastrointes
tinal
Hepatocellular injury distal to vascular
spasm site; focal hemorrhages distal to
spasm site; coalescing focal
hemorrhages leading to large hematoma
collection under the Glisson’s capsule
•Hepatic failure
•Sub capsular hematoma
•Acute liver rupture
CNS Cerebral hypoxia due to vasospasm;
focal hemorrhages distal to the
vasospasm; secondary cerebral edema;
intracranial hemorrhages
•Eclampsia
•Hemorrhagic stroke
•Cerebral edema and
death due to coning
•Transient blindness –
retinal or cortical
HELLP
syndrome
Concomitant occurrence of
microangiopathic hemolysis;
thrombocytopenia and liver damage
features in a woman with preeclampsia

26. system pathology complication
Blood volume Due to generalized vasospasm,
there is contracture of the total
vascular space. The normal
increase in blood volume that
occurs during normal pregnancy
fails in preeclampsia. They tend
to have a contracted and overall
reduced blood volume
•Less tolerant to blood
loss at delivery with an
easy propensity to post
partum hemmorhage
with small amount of
blood loss
•Less tolerant to fluid
administration with a
propensity to develop
pulmonary edema

27. symptoms sign Diagnostic study
•Non severe preeclampsia
is asymptomatic
•Symptoms are late
features indicating severe
disease or imminent risk of
convulsions
•These symptoms include
headache, blurring of
vision, epigastric pain,
oliguria and generalized
body swelling
•Hypertension
•Generalized
edema/anasarca
•Excessive weight gain
•Exaggerated deep
tendon reflexes
•Proteinuria
•24 hour urine for
proteinuria
•Liver and renal function
tests
•Hematocrit
•Peripheral blood smear
for shistocytes
(fragmented RBC)
•Platelet count
•Serum uric acid
measurement
•Fetal well being studies
As preeclampsia is asymptomatic until it progresses to severe stages, detection
and diagnosis requires active screening of all pregnant women during antenatal
care. Routine blood pressure measurements, weight gain surveillance and check
for symptoms and proteinuria are performed to detect preeclampsia early.

28. Management
Objective
Preserve health of mother & fetus
Prevent progression to eclampsia
Delivery of alive, mature fetus
* Once Dx is made definitive Rx is delivery
* Precise Knowledge G.A Important for Mx.
Mx of Non severe PE
Hospitalization  at time of Dx
Purpose Evaluate maternal & fetal condition

29. Hospital Mx
Maternal follow up
 Weight on admn. & every other day
 B/P  Q 4 hrly
 Daily clinical Hx premonitory Sx
 Urine protein every 48 hrs
Hct, Plc, RFT, LFT, uric Acid, coagulation profile
weekly or 2x/week.

30. Fetal evaluation
Daily FHR Auscultation & fetal mov’t count
Fetal growth: clinical & U/Sound
Well being NST/BPP (2x/week)
**Non sevre PE remote from term delivery at term
but pregnancy should not pass 40 weeks.
** no need of antihypertensive or seizure prophylaxix

31. Mx of severe PE
characterized by progressive deterioration of both
maternal & fetal condition
 All should be delivered if disease develope >34 week
G.A or prior to 34 weeks if there is
- Maternal (Fetal) distress
- Labor or PROM
- Severe IUGR
**Delivery should be based on maternal and fetal
conditions as well as GA

32. Mx of severe PE includes
Maternal & fetal evaluation same Non PE but more
frequent.
Anticonvulsant to prevent convulsion
Antihypertensive To control B/P in safe range
Induction of labor Delivery
 Admit to labor & delivery area.
 Then Maternal & fetal evaluation 1st 24 hr
 Anti-convulsant  parenteral route To prevent seizure

34. Indication
Anti- convulsant drugs
 Mg so4
 Diazepam

Phenytoin

35. Antepartum mg't of severe PE
Magnesium Sulfate (Mg So4)
Mg so4
Agent of choice for seizure prophylaxis
Dose: loading dose 4gm 20%soln  over 10-15min
followed by 10 g of 50% solution half on each buttock
maintenance dose: 5gmI.M/4 hr
Make sure the following before giving next dose
1. Patellar reflex is present
2.RR at least 16 breaths/min
3. UOP of previous 4 hr exceeded 100 ml
Side effect: Weakness, paralysis, cardiac toxicity
Monitor: RR, DTR,Level of consciousness, UOP
Antidote: Calcium gluconate 10 ml of 10% I.V

36. MgSO4 level (mg/dl)
4.8- 8.4
8- 10
12 -17
13- 17
19 -20
Effects
Therapeutic level
Loss of DTR
Respiratory depression
CNS depression, coma
Cardiac arrest
Clinical effects are related directly to plasma
levels

37. Antihypertensive
 If DBP > 110 mmHg
Acute Rx
Arteriolar dilators – Hydralazine 5mg iv then 5-10mg
Q 20min.
B- Blocker – labetalol
Ca channel blocker – nifedipine

38. Maintenance Rx
Centrally acting  Methyl dopa
B- Blockers- labetalol
Ca channel Blocker -nefidipine
ACE inhibitors C/I in pregnancy

39. Delivery
PE progressive disease
Timely delivery  decreases maternal and fetal
morbidity& mortality
Stabilize maternal status before Delivery
Route of delivery…vaginal delivery is
preferable

40. Indication to Delivery in PE
>37 wks with mild PE
> 34 wks with severe PE
< 34 wks with any of
 maternal or fetal Distress
 Severe IUGR
 HELLP syndrome
 Pulm. Edema
 Deranged LFT/RFT
 Uncontrolled B/P despite Appropriate drugs
 Imminent eclampsia

41. Steroid
All pts with severe PE < 34 wks
prevent RDS, treatment of thrombocytopenia
Intrapartum care
• Maternal – V/S Q 30min
Avoid fluid overload
 input/output every 1 hr
FHR monitor Q 15min or EFM
Shorten 2nd stage labor – Instrumental delivery
Fluid –125ml/hr, U.O.P > 30ml/hr
Active Mx of 3rd Stage

42. Postpartum
Close follow up & monitor B/P
Anticonvulsant for 24-48 hrs

43. Eclampsia
Definitionn: Occurrence of seizure or coma in
woman with PE that cannot be attributed to other
cause
Preventable complication of preeclampsia
50% intrapartum
25% antepartum
25% postpartum
Atypical eclampsia
Occurrence of eclampsia before 24 week of GA or
after 7th
postpartal day

44. Most common last trimester & wide spectrum of Sn
& Sign and symptom ranging from:
Extremely B/P <-- --> minimal B/P
proteinuria 4+ <-- --> No proteinuria (14%)
Generalized edema <-- -->No edema (26%)
Patellar reflex 4+ <-- --> normal reflex
##1st warning sign may be excessive Wt gain

45. Diagnosis
Features of preeclmpsia
+
Generalized tonic-clonic seizure
Aura
Tonic phase
Clonic phase
Post-ictal comavery brief or even not present

46. Complications of eclampsia
Known complications of PE
+
• Aspiration and asphyxia
• Trauma
• Preterm seizure
• Fetal distress and asphyxia
• Crebral edema in prolonged or repititive seizure

47. Managem
ent
Description
General •Airway and oxygenation- put in left lateral position; suction airway, insert airway to
depress tongue and prevent injury, administer oxygen via face mask or endotracheal tube
if in respiratory failure
•Prevent trauma – tongue depressor ; fall accident etc
•Fluid resuscitation if in hemodynamic instability- IV line and fluids
Control
convulsion
Administer anticonvulsants – Magnesium sulphate (first line drug); diazepam ( if
magnesium is not available); phenobarbitone; phenytoin… can also be used if the two are
not available
Control
severe HTN
If BP >160/110 mmHg, use fast acting antihypertensives (hydralazine; labetalol;
diazoxide; sodium nitroprusside) to maintain BP between 140/90-160/110.
Fluid mx Restrict fluid administration to 125ml/hr and monitor input-output including urine
output
Organ
support
If any evidence of organ failure; requires critical care and organ support to maintain
homeostasis
Delivery After the above measures are taken and patient is stabilized; pregnancy should be
terminated by the most appropriate route. No conservative Mx !

48. Prognosis
Reading assignment
effect of preeclampsia-eclampsia syndrome for
future pregnancy

49. DDX All pregnant women & convulsion should be
considered Eclampsia till other cause R/O
 Epilepsy - encephalitis, meningitis
Cerebral malaria - cerebral tumor
Hypertensive encephalopathy

50. References
1. Williams obstetrics, 24th
edition
2. Normal and problematic pregnancy, Gabbe, 6th
edition
3. Uptodate 21.6
4. Management protocol on sstetric case, FMOH,
january, 2010

51. Quize
1. Define severe preeclampsia(2 points)
2. Mention at least four risk factors for preeclampsia.
(2 points)
3. List the two common theories incriminated in
preeclampsia(2 points)
4. How do you define proteinuria in preeclampsia(2
points)
5. What is the preferred drug for seizure
prophylaxis(1 point)
6. What is the definative mx for preeclampsia(1 point)

52.  THANK YOU