Hypertensive Disorders of

Pregnancy
By: 03 Karpoor Mohammed Ibraheem
04 Kasinathan Saravanan
 OUTLINE

 Types of Hypertensive Disorders in Pregnancy

 Diagnosis of Hypertension

 To Know The Risk Factors of Hypertension in Pregnancy

 Etiopathogenesis of Pregnancy

 Prevention Strategies of Preeclampsia

 Treatment of Hypertension
 Types of Hypertension

 Preeclampsia and Eclampsia syndrome

 Chronic hypertension of any etiology
 Preeclampsia superimposed on chronic hypertension
 Gestational Hypertension
 Diagnosis of Hypertension

 Hypertension is diagnosed empirically when systolic and diastolic blood

pressure exceeds 140 mm Hg and 90 mm Hg.

 Korotkoff phase V is used to define diastolic pressure.

 A sudden rise in MAP but still in a normal range-"delta hypertension"-may

signify preeclampsia even if BP <140/90 mm Hg.
 Gestational Hypertension

 BP ≥140/90 mm Hg for the first time after mid-pregnancy, but with NO

proteinuria. Almost half of these women subsequently develop preeclampsia
syndrome

 “Transient hypertension" if evidence for preeclampsia does not develop and

the blood pressure returns to normal by 12 weeks postpartum.
 Preeclampsia Syndrome
 Described as a pregnancy-specific syndrome that can affect virtually every organ
system  
 Hypertension + proteinuria  
 Proteinuria is a primary diagnostic criterion and an objective marker and reflects the
system-wide endothelial leak  
 Multiorgan involvement may by reflected in thrombocytopenia, renal dysfunction,
hepatocellular necrosis (“liver dysfunction”), central nervous system perturbations, or
pulmonary edema.
Preeclampsia can be divided into 4 types

 Early onset: < 34 weeks

 Late onset: > or equal to 34 weeks
 Preterm onset: < 37 weeks
 Term onset: > or equal to 37 weeks
Reference: Williams Obstetrics 26th edition chapter 40 pg. 689
Reference: Williams Obstetrics 26th edition chapter 40 pg. 690
 Eclampsia

 Convulsions in a woman with preeclampsia that is not attributable to

other cause
 Eclampsia is most common in the last trimester
 Headache and visual disturbance can precede Eclampsia
 Preeclampsia Superimposed on
Chronic Hypertension
 Chronic underlying hypertension is diagnosed in women with documented BP ≥ 140/90
mm Hg before pregnancy or before 20 weeks' gestation, or both.

 If new-onset or worsening baseline hypertension is accompanied by new-onset

proteinuria or other findings, then 'superimposed preeclampsia' is diagnosed.

 Compared with "pure" preeclampsia, superimposed preeclampsia commonly develops

earlier in pregnancy.
 Risk Factors
 Preeclampsia is seen in young and nulliparous women.
 Older women are at greater risk for chronic hypertension with
superimposed preeclampsia.
 History of Preeclampsia
 Incidence markedly influenced by
 Race
 Ethnicity
 Genetic predisposition.

Smoking lowers the risk of hypertension during pregnancy

Reference: Williams Obstetrics 26th
edition chapter 40 pg. 691
 Etiopathogenesis
Satisfactory theory concerning the origins of preeclampsia and gestational
hypertensive disorders are more likely to develop in women with the following
characteristics:

 Exposure to chorionic villi for the first time

 Exposure to a superabundance of chorionic villi, as with twins or hydatidiform

mole

 Preexisting conditions associated with endothelial cell activation or

inflammation

 Genetic predisposition to hypertension developing during pregnancy.

 Etiology
1. Placental implantation with abnormal trophoblastic invasion of uterine vessels

2. Dysfunctional immunological tolerance between maternal, paternal (placental),

and fetal tissues

3. Maternal maladaptation to cardiovascular or inflammatory changes of

normal pregnancy

4. Genetic factors including inherited predisposing genes and epigenetic

influences
Reference: Williams Obstetrics 2
edition chapter 40 pg. 692
 Stage 1: Placental Syndrome
Immunological Factors

 Maternal immune tolerance to paternally derived placental and fetal

antigens

 In women destined to have preeclampsia, extra villous trophoblasts

early in pregnancy express reduced amounts of immunosuppressive
non classic human leukocyte antigen G (HLA-G).

 women previously exposed to paternal antigens, such as a prior

pregnancy with the same partner, may be "immunized" against
preeclampsia. Conversely, multiparas impregnated by a new partner
have a greater risk of preeclampsia
 Stage 1: Placental Syndrome
Genetic Factors

 Preeclampsia appears to be a multifactorial, polygenic disorder

 The hereditary predisposition for preeclampsia likely stems from interactions

of literally hundreds of inherited genes-both maternal and paternal-that
control many enzymatic and metabolic functions throughout every organ
system

 Plasma-derived factors may induce some of these genes in preeclampsia

 Stage 11: Maternal Syndrome
Endothelial cell activation

 In response to ischemia or other inciting causes, placental factors are

released and initiate a series of events

 Thus, antiangiogenic and metabolic factors and other inflammatory

leukocyte mediators are thought to provoke systemic endotheliopathy,
which is used synonymously here with endothelial cell activation or
dysfunction.

 Injury to systemic endothelial cells is seen as a centerpiece of

preeclampsia pathogenesis
 Stage 11: Maternal Syndrome
Vasospasm and hypertension

 Systemic endothelial activation causes vasospasm, which elevates

resistance to produce hypertension. Concurrently, systemic endothelial cell
injury promotes interstitial leakage, and platelets and fibrinogen are
deposited in the subendothelial space.

 With diminished blood flow because of maldistribution from vasospasm

and interstitial leakage, ischemia of the sur rounding tissues can cause
necrosis, hemorrhage, and other end-organ disturbances.
 Stage 11: Maternal Syndrome
Increased pressors response

 Women with early preeclampsia, however, have enhanced vascular reactivity to

infused norepinephrine and angiotensin II

 Moreover, increased sensitivity to angiotensin II clearly precedes the onset of

gestational hypertension
 Pathophysiology
Cardiovascular System
 Disturbances in the cardiovascular system are common with
preeclampsia syndrome. These are related to:

(1) Greater cardiac afterload imposed by hypertension;

(2) Cardiac preload, which is reduced by a pathologically diminished

volume expansion during pregnancy and which is increased by
administration of intravenous crystalloid or oncotic solutions;

(3) Endothelial activation leading to leakage of intravascular fluid into

the extra cellular space
 Pathophysiology
Cardiovascular System

 Pulmonary edema may develop despite normal ventricular function

because of an alveolar endothelial-epithelial leak

 Hemoconcentration is the hallmark feature in those with eclampsia

 Pathophysiology
Hematological Changes
 Thrombocytopenia

 Hemolysis which manifests as elevated serum LDH levels and reduced haptoglobin
levels. RDW is higher in preeclamptic women

 Hemolysis and thrombocytopenia with severe preeclampsia, abnormally elevated

serum liver transaminase levels that indicated hepato-cellular necrosis referred to this
combination of events as the HELLP syndrome
 Pathophysiology
Coagulation Changes

 Increased factor VIII consumption

 Increased levels of fibrinopeptides and D-Dimers

 Decreased levels of antithrombin III, protein C and protein S

 Increased fibronectin levels

 Pathophysiology

Fluid and Electrolyte alterations

 In women with severe preeclampsia, the volume of extracellular fluid, which

manifests as edema, is usually much greater than that in normal pregnant
women.

 In women with preeclampsia, electrolyte concentrations do not differ

appreciably from those of normal pregnant women.
 Pathophysiology
Kidney

 In preeclampsia, morphological changes are characterized by

glomerular endotheliosis, which blocks filtrations

 Of clinical importance, renal perfusion and GFR are slightly reduced

 Plamsa uric acid concentration is typically elevated

 Detection of proteinuria helps to establish the diagnosis of

preeclampsia
Reference: Williams Obstetrics 2
edition chapter 40 pg. 698
 Pathophysiology
Liver

 Gross and microscopic anatomical derangements lead to elevated hepatic

transaminase levels, this transaminitis indicates hepatocellular injury and is a
marker of severe preeclampsia

 It manifests with moderate to a severe right-upper quadrant or mid epigastric pain

and tenderness

 Periportal hemorrhage and infarction may extend to develop a hepatic hematoma

 Pathophysiology
Central Nervous System
 Headaches and visual symptoms are common with severe
preeclampsia, and associated convulsions define eclampsia

 Headache and scotoma arise from cerebrovascular

hyperperfusion that has predilection to occipital lobes

 Convulsions are caused by release of excitatory

neurotransmitters and burst of action potentials
 Pathophysiology
Central Nervous System
 Blindness is rare with preeclampsia alone, but it complicates
with eclamptic convulsions

 Occipital blindness is called amaurosis

 Blindness from retinal lesions is caused either by serous retinal

detachment or rarely by retinal infarction which is termed
purtscher retinopathy
Prevention

Reference: Williams Obstetrics 26

edition chapter 40 pg. 704
 Prevention
 Low doses of 50 to 150 mg daily, aspirin effectively inhibits platelet
thromboxane A, biosynthesis. It has minimal effects on vascular prostacyclin
production. Still, several clinical trials have shown benefits in prevention of
preeclampsia

 ACOG recommends low dose aspirin be given between 12 and 28 weeks of

gestation to help prevent preeclampsia in high risk women
 Evaluation
With hospitalization, a systematic evaluation begins:

 Detailed examination, which is coupled with daily scrutiny for

headache, visual changes, or epigastric pain

 Daily weight measurement to identify rapid weight gain

Quantification of proteinuria or a urine protein: creatinine ratio

 Blood pressure readings with an appropriate-size cuff every 4 hours,

unless previously elevated, which would mandate more frequent
readings
 Evaluation
With hospitalization, a systematic evaluation begins:

 Measurements of serum creatinine and hepatic transaminase levels and a

hemogram that includes a platelet count. The frequency of testing is
determined by hypertension severity.

 Although some recommend assessment of serum uric acid and lactate

dehydrogenase levels and coagulation, their value has been questioned

 Evaluation of fetal size and well-being and amnionic fluid volume

 Reduced physical activity may have benefits, although evidence is not

robust.
 Management
GOALS

 Termination of pregnancy with the least possible trauma to mother

and fetus

 Birth of an infant who subsequently thrives

 Complete restoration of health to the mother

 Consideration for
delivery
 Termination of pregnancy is the only known cure for pre-eclampsia.

 Headache, visual changes, or epigastric pain are indicative that convulsions may
be imminent, and oliguria is another ominous sign

 With a preterm fetus the tendency is to delay delivery to help reduce the risk of
neonatal death or serious morbidity

 For patients with non severe preeclampsia, induction of labor is done at 38

weeks AOG
 Corticosteroid for lung
maturation

 To enhance fetal lung maturation, glucocorticoids have been administered in

women with severe hypertension who are remote from term
Clinical Management
algorithm for severe
preeclampsia at <34 weeks
 Management of severe preeclampsia
and eclampsia

 This parenterally administered agent is an effective anticonvulsant and avoids

producing central nervous system depression. It may be given intravenously by
continuous infusion or intramuscularly by intermittent injection

 Because labor and delivery is a more likely time for seizures to develop, women
with severe preeclampsia or eclampsia usually are given magnesium sulfate during
labor and for 24 hours postpartum

 Magnesium sulfate is not given to treat hypertension.

Management of severe preeclampsia
and eclampsia
 Toxicology
 Eclamptic convulsions are almost always prevented or arrested by plasma
magnesium levels maintained at 4 to 7 mEq/L (4.8 to 8.4 mg/ dL, or 2.0 to 3.5
mmol/L )

 Patellar reflexes disappear when the plasma magnesium level reaches 10 Eq/L—
about 12 mg/dL—presumably because of a curariform action. This sign serves to
warn of impending magnesium toxicity.

 When plasma levels rise above 10 mEq/L, breathing becomes weakened. At 12

mEq/L or higher levels, respiratory paralysis and respiratory arrest follow.

 Treatment with calcium gluconate or calcium chloride, 1 g intravenously, along with

withholding further magnesium sulfate, usually reverses mild to moderate
respiratory depression.
Antihypertensives
Complications