hypertensive disorders in pregnancy-kabera rene
TRANSCRIPT
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
1/35
National University of Rwanda
Family and Community Medicine
Hypertensive Disorders in Pregnancy
KABERA Ren,MD
PGY IV Resident
Family and Community MedicineNational University of Rwanda
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
2/35
Introduction
Hypertensive disorders complicating pregnancy are common
and form one of the deadly triad, along with hemorrhageand infection, that contribute greatly to maternal morbidity
and mortality.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
3/35
Classification
Gestational hypertension
Preeclampsia.
Eclampsia.
Preeclampsia superimposed on chronic hypertension.
Chronic hypertension.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
4/35
Gestational hypertension
BP 140/90 mm Hg for first time during pregnancy
No proteinuria
BP returns to normal < 12 weeks' postpartum
Final diagnosis made only postpartum
May have other signs or symptoms of preeclampsia, forexample, epigastric discomfort or thrombocytopenia
Gestational hypertension has replaced the term pregnancy-
induced hypertension to describe women who develop
hypertension without proteinuria after 20 weeks of gestation.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
5/35
Gestational hypertension
Gestational hypertension is a provisional diagnosis that
includes women eventually diagnosed with preeclampsia orchronic hypertension, as well as women retrospectively
diagnosed with transient hypertension of pregnancy.
Fifty percent of women diagnosed with gestational
hypertension between 24 and 35 weeks develop
preeclampsia
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
6/35
Preeclampsia Minimum criteria
BP 140/90 mm Hg after 20 weeks' gestation
Proteinuria 300 mg/24 hours or 1+ dipstick
Increased certainty of preeclampsia
BP 160/110 mg Hg
Proteinuria 2.0 g/24 hours or 2+ dipstick
Serum creatinine > 1.2 mg/dL unless known to be previously elevated
Platelets < 100,000/mm3
Microangiopathic hemolysis (increased LDH)
Elevated ALT or AST
Persistent headache or other cerebral or visual disturbance
Persistent epigastric pain
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
7/35
Preeclampsia
Described as a pregnancy-specific syndrome of reduced organ
perfusion secondary to vasospasm and endothelial activation. Proteinuria is an important sign of preeclampsia
Significant proteinuria is defined by 24-hour urinary protein
exceeding 300 mg per 24 hours, or persistent 30 mg/dL (1+dipstick) in random urine samples.
Renal biopsy specimens: glomerular lesion.
The minimum criteria for the diagnosis of preeclampsia are
hypertension plus minimal proteinuria.
The more severe the hypertension or proteinuria, the more
certain is the diagnosis of preeclampsia
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
8/35
Preeclampsia
Epigastric or right upper quadrant pain is thought to result from
hepatocellular necrosis, ischemia, and edema that stretchesthe Glisson capsule.
This characteristic pain is frequently accompanied by
elevated serum hepatic transaminase levels and usually is a
sign to terminate the pregnancy.
The pain presages hepatic infarction and hemorrhage or
catastrophic rupture of a subcapsular hematoma. Fortunately,
hepatic rupture is rare.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
9/35
Preeclampsia
Thrombocytopenia is characteristic of worsening preeclampsia
Thrombocytopenia is due platelet activation and aggregationas well as microangiopathic hemolysis induced by severe
vasospasm.
Evidence of gross hemolysis such as hemoglobinemia,hemoglobinuria, or hyperbilirubinemia is indicative of severe
disease.
Other factors indicative of severe hypertension include
cardiac dysfunction with pulmonary edema as well as obviousfetal growth restriction.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
10/35
Preeclampsia
Exact mechanism not known
Immunologic
Genetic
Placental ischemia
Endothelial cell dysfunction Vasospasm
Hyper-responsive response to vasoactive hormones (e.g.
angiotensin II & epinephrine)
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
11/35
Preeclampsia
Abnormality Mild Severe
1. Diastolic blood pressure < 100 mg Hg 110 mm Hg or higher
2. Proteinuria Trace to 1+ Persistent 2+ or more
3. Headache Absent Present
4. Visual disturbances Absent Present
5. Upper abdominal pain Absent Present6. Oliguria Absent Present
7. Convulsion Absent Present
8. (eclampsia)
9. Serum creatinine Normal Elevated
10. Thrombocytopenia Absent Present
11. Liver enzyme elevation Minimal Marked
12. Fetal growth restriction Absent Obvious
13. Pulmonary edema Absent Present
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
12/35
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
13/35
Eclampsia
Seizures that cannot be attributed to other causes in a woman
with preeclampsia The seizures are generalized and may appear before,
during, or after labor.
Recent study reported that a fourth of eclamptic seizuresdeveloped beyond 48 hours postpartum
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
14/35
Superimposed Preeclampsia
New-onset proteinuria 300 mg/24 hours in hypertensive women
but no proteinuria before 20 weeks' gestation A sudden increase in proteinuria or blood pressure or platelet
count < 100,000/mm3 in women with hypertension and proteinuriabefore 20 weeks' gestation
All chronic hypertensive disorders, regardless of their cause,predispose to development of superimposed preeclampsia andeclampsia.
The diagnosis of chronic underlying hypertension is made when:
Hypertension (140/90 mm Hg or greater) is documentedantecedent to pregnancy.
Hypertension (140/90 mm Hg or greater) is detected before 20weeks, unless there is gestational trophoblastic disease.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
15/35
Chronic Hypertension
BP 140/90 mm Hg before pregnancy or diagnosed before
20 weeks' gestation not attributable to gestationaltrophoblastic disease
Hypertension first diagnosed after 20 weeks' gestation andpersistent after 12 weeks' postpartum.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
16/35
Etiology
Chorionic villi for the first time.
Superabundance of chorionic villi, as with twins or hydatidiformmole.
Preexisting vascular disease.
Genetically predisposed to hypertension developing duringpregnancy.
Abnormal trophoblastic invasion of uterine vessels. Immunological intolerance between maternal and fetoplacental
tissues.
Maternal maladaptation to cardiovascular or inflammatory
changes of normal pregnancy. Dietary deficiencies.
Genetic influences.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
17/35
Diagnosis
Hypertension is diagnosed when the resting blood pressure is
140/90 mm Hg or greater. Edema has been abandoned as a diagnostic criterion
because it occurs in too many normal pregnant women to be
discriminant.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
18/35
Pathophysiology
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
19/35
Pathophysiology Prostacyclinis produced by endothelial cells and
thromboxane A2 by platelets from their common precursor
arachidonic acid via the cyclooxygenase pathway.
Thromboxane A2 promotes platelet aggregation and
vasoconstriction, whereas prostacyclininhibits platelet
aggregation and promotes vasodilation. The balance between platelet thromboxane A2 and
prostacyclinfosters localized platelet aggregation and
consequent clot formation while preventing excessive
extension of the clot and maintaining blood flow around it.
The thromboxane A2-prostacyclin balance can be shifted
toward prostacyclin by administration of low doses of aspirin.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
20/35
Pathophysiology Aspirin produces irreversible inhibition of cyclooxygenase by
acetylating serine residue in its active site.
Obviously, this reduces production of both thromboxane A2 andprostacyclin.
Endothelial cells produce new cyclooxygenase in a matter of hourswhereas platelets cannot manufacture the enzyme, and the level
rises only as new platelets enter the circulation. This is a slow process because platelets have a half-life of about 4
days.
Administration of small amounts of aspirin for prolonged periodsreduces clot formation and has been shown to be of value in
preventing myocardial infarctions, unstable angina, transientischemic attacks, and stroke.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
21/35
PathophysiologyBrain
There are two distinct but related types of cerebralpathology.
The first is gross hemorrhage due to ruptured arteries caused
by severe hypertension
The second type of cerebral lesion is variably demonstrated
with preeclampsia but probably is universal with eclampsia.
These are more widespread, focal, and seldom fatal.
The principal postmortem lesions are edema, hyperemia,
ischemias, thrombosis, and hemorrhage
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
22/35
Pathophysiology
Cardiac/Pulmonary Increased CO & SVR
CVP normal or slightly increased
Plasma volume reduced
Pulmonary edema Decrease oncotic/collid pressure
Capillary/endothelial damage leak
Vasoconstriction
increase PWP and CVP
Occurs 3 % of preeclamptic patients
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
23/35
Pathophysiology
Liver Usually mild
Severe PIH or preeclampsia complicated by HELLP
periportal hemorrhages
ischemic lesion
generalized swelling
hepatic swelling epigastric pain
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
24/35
Pathophysiology
Kidney Adversely affected proteinuria
GFR and CrCl decrease
BUN increase, may correlate w/ severity
RBF compromised
ARF w/ oliguria PIH, esp. w/ abruption, DIC, HELLP
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
25/35
Pathophysiology
Uterus
Activity increased
Hyperactive/hypersensitive to oxytocin
Preterm labor frequent
Uterine/placental blood flow decreased by 50-70%
Abruption incidence increased
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
26/35
Management
Basic management objectives for any pregnancy complicated
by preeclampsia are: 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.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
27/35
Antepartum Hospital Management
Hospitalization is considered at least initially for women with
new-onset hypertension, especially if there is persistent orworsening hypertension or development of proteinuria.
A systematic evaluation is instituted to include the following:
Detailed examination followed by daily scrutiny for clinical
findings such as headache, visual disturbances, epigastric
pain, and rapid weight gain.
Weight on admittance and every day thereafter.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
28/35
Management Analysis for proteinuria on admittance and at least every 2
days thereafter. Blood pressure readings in the sitting position with an
appropriate-size cuff every 4 hours, except between midnight
and morning.
Measurements of plasma or serum creatinine, hematocrit,
platelets, and serum liver enzymes, the frequency to be
determined by the severity of hypertension.
Frequent evaluation of fetal size and amnionic fluid volumeeither clinically or with sonography.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
29/35
Management of chronic hypertension
Methyldopa (Aldomet),labetalol, and nifedipine (Procardia)
are oral agents commonly used to treat chronic hypertensionin pregnancy.
The beta blocker atenolol (Tenormin) has been associated with
IUGR,
Women in active labor with uncontrolled severe chronic
hypertension require treatment with intravenous labetalol or
hydralazine.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
30/35
Management of Severe Preeclampsia
Magnesium sulfate: Loading dose of 4 to 6 g diluted in 100
mL of normal saline, given IV over 15 to 20 minutes, followedby a continuous infusion of 2 g per hour
Assess serum magnesium level if urine output is < 30 mL perhour or there is a loss of deep tendon reflexes, decreased
respiratory rate, or altered mental status Therapeutic range for serum magnesium is 4 to 7 mg per dL
Corticosteroids (if between 24 and 34 weeks of gestationand not previously administered)
Betamethasone (Celestone), 12 mg IM initially, then repeat in24 hours or Dexamethasone, 6 mg IM initially, then repeatevery 12 hours for three additional doses
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
31/35
Management of Severe Preeclampsia For systolic blood pressure > 160 mm Hg or diastolic >
110 mm Hg, one of the following should be given toachieve a systolic measurement of 140 to 155 mm Hgand/or a diastolic measurement of 90 to 105 mm Hg:
Hydralazine, 5 to 10 mg IV every 15 to 30 minutes(maximal dose: 30 mg)
Labetalol, 20 mg IV initially; if the initial dose is noteffective, double the dose to 40 mg and then 80 mg at 10-minute intervals until target blood pressure is reached or atotal of 220 mg has been administered; the maximal dose
of IV labetalol is 220 mg in a 24-hour period Calcium gluconate, 1 g IV; keep at bedside in case of
respiratory depression from magnesium sulfate use
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
32/35
Management Eclampsia Protecting the airway and minimizing the risk of aspiration by
placing the woman on her left side, suctioning her mouth, and
administering oxygen. intubations should be immediately available.
Close observation, soft padding, and use of side rails on the
bed may help prevent trauma from falls or violent seizureactivity.
After the convulsion has ended and the patient is stabilized,
plans should be made for prompt delivery.
In rural or remote areas, physicians need to consider the risk
of transfer versus the benefits of tertiary maternal and
neonatal care.
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
33/35
Management of eclampsia Magnesium sulfate is the drug of choice because it is more
effective in preventing recurrent seizures than phenytoin(Dilantin) or diazepam (Valium).
If a patient has already received a prophylactic loading
dose of magnesium sulfate and is receiving a continuous
infusion, an additional 2 g should be given intravenously.
Otherwise, a 6-g loading dose is given intravenously over 15
to 20 minutes, followed by maintenance infusion of 2 g per
hour. A total of 8 g of magnesium sulfate should not be exceeded
over a short period of time
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
34/35
References American Academy of Family Physician : www.aafp.org
Williams obstetrics Review of Medical Physiology
-
8/3/2019 Hypertensive Disorders in Pregnancy-Kabera Rene
35/35
End
Thank you