Transcript Hypertensive Disorders with Pregnancy

Hypertensive Disorders With
Pregnancy
Amr Nadim, MD
Professor of Obstetrics & Gynecology
Ain Shams Maternity and Women’s Hospital
[[email protected]]
• C.G. is a 39 year old married white female gravida 2, para 0,
with one spontaneous abortion who presented for prenatal care
at 14 weeks gestation. Blood pressure at that time was 130/80.
The patient had no significant medical history and her
gynecologic history was significant only for oral contraceptive
use several years ago. The patient noted that her physician
stopped the birth control pills after only two cycles, but the
patient was not told why.
• The pregnancy had been unremarkable until approximately one
month ago when the patient noted increased swelling of her
hands and feet. A 6 Kg. weight gain in two weeks time was
noted. Blood pressure at that time was 124/78. There was no
urinary protein. On the day prior to admission, at 28 weeks, the
patient presented with a blood pressure of 160/98 and had
been sent home to bedrest with instructions to take a single
baby aspirin daily. On the day following, the patient was noted
at home to have a persistent blood pressure of 180/100.
Avant propos…
• Complicates 7-10% of pregnancies
– 70% Preeclampsia-eclampsia
– 30% Chronic hypertension
– Eclampsia 0.05% incidence
• 20% of Maternal Deaths
• Cause of 10% of Preterm birth
• Etiology unknown
• Young female 3 fold increased risk
• African American 2 fold increased risk
• Multifetal pregnancies
– Twins
– Triplets
• Hypertension
• Diabetes Mellitus
• Renal Disease
• Collagen Vascular Disease
Hypertension during Pregnancy: Classification
• Pregnancy-induced hypertension
– Hypertension without proteinuria/edema
– Preeclampsia
• mild
• severe
– Eclampsia
• Coincidental HTN: preexisting or persistent
• Pregnancy-aggravated HTN
– superimposed preeclampsia
– superimposed eclampsia
• Transient HTN: occurs in 3rd trimester, mild
Preeclampsia: Definition
• Hypertension
– > 140/90
– relative  no longer considered diagnostic
• Proteinuria
– > 300 mg/24 hours or  1or 2+ on urine
dipstick
– may occur late
• Edema (non-dependent)
– so common & difficult to quantify it is rarely
evoked to make or refute the diagnosis
Criteria for Severe Preeclampsia
• SBP > 160 mm Hg
• DBP > 110 mm Hg
• Proteinuria > 5 g/24 hr.
or 3-4+ on dipstick
• Oliguria < 500 cc/24 hr.
•  serum creatinine
• Pulmonary edema or
cyanosis
• CNS symptoms (HA, vision
changes)
• Abdominal (RUQ) pain
• Any feature of HELLP
– hemolysis
–  liver enzymes
– thrombocytopenia
• IUGR or oligohydramnios
Preeclampsia: Risk Factors
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Nulliparity (or, more correctly, primipaternity)
Chronic renal disease
Angiotensinogen gene T235
Chronic hypertension
Antiphospholipid antibody syndrome
Multiple gestation
Family or personal history of preeclampsia
Age > 40 years
African-American race
Diabetes mellitus
Etiology and Prevention
• Etiology is unknown.
• Many theories:
– genetic
– immunologic
– dietary deficiency (calcium, magnesium, zinc)
• supplementation has not proven effective
– placental source (ischemia)
Etiology and Prevention
• A major underlying defect is a relative
deficiency of prostacyclin vs. thromboxane
• Normally (non-preeclamptic) there is an 8-10
fold  in prostacyclin with a smaller  in
thromboxane
– prostacyclin salutatory effects dominate
• vasodilation,  platelet aggregation,  uterine tone
• In preeclampsia, thromboxane’s effects
dominate
–  thromboxane (from platelets, placenta)
–  prostacyclin (from endothelium, placenta)
Preeclampsia Prophylaxis: Aspirin
• Aspirin has been extensively studied as a
targeted therapy to  thromboxane
production
• CLASP study, A multicenter RCT
[CLASP Collaborative Group, Lancet 1994;343:619-29]
– 9364 women, risk factors for PIH or IUGR or who
had PIH or IUGR
– 60 mg ASA daily vs. placebo
– Small reduction (12%) in occurrence of PIH
– Small reduction in preterm deliveries: 20 vs 22%
– No difference in neonatal outcome
Preeclampsia Prophylaxis: Aspirin
• NIH study of high-risk patients, RCT, 60 mg
aspirin daily vs. placebo [Caritis, et al., N Engl J Med
1998;338:701-5]
– pre-gestational DM (471 patients)
– chronic hypertension (774 patients)
– multifetal gestations (688 patients)
– prior history of preeclampsia (606 patients)
• No reduction in development of preeclampsia
in any subgroup or groups in aggregate
• No difference in perinatal death, preterm
delivery, IUGR, maternal or fetal hemorrhagic
complications
Preeclampsia: Mechanism
• At this time the most widely accepted
proposed mechanism for preeclampsia is:
Global Endothelial Cell Dysfunction
• Endothelial cell dysfunction is just one
manifestation of a broader intravascular
inflammatory response
– present in normal pregnancy
– excessive in preeclampsia
– Proposed source of inflammatory stimulus:
placenta
Pathophysiology
Of importance, and distinguishing preeclampsia
from chronic or gestational hypertension, is
that preeclampsia is more than hypertension; it
is a systemic syndrome, and several of its
“non-hypertensive” complications can be lifethreatening when blood pressure elevations
are quite mild.
Pathophysiology: Cardiovascular
• In severe preeclampsia, typically
hyperdynamic with normal-high CO, normalmod. high SVR, and normal PCWP and CVP.
• Despite normal filling pressures,
intravascular fluid volume is reduced (3040% in severe PIH)
• Variations in presentation depending on
prior treatment and severity and duration of
disease
• Total body water is increased (generalized
edema)
Pathophysiology: Cardiovascular
• Preeclamptic patients are prone to develop
pulmonary edema due to reduced colloid
oncotic pressure (COP), which falls further
postpartum:
Colloid oncotic pressure:
Normal pregnancy:
Preeclampsia:
Antepartum
22 mm Hg
18 mm Hg
Postpartum
17 mm Hg
14 mm Hg
Pathophysiology
• Respiratory:
– Airway is edematous; use smaller ET tube (6.5)
–  risk of pulmonary edema; 70% postpartum
• Renal:
– Renal blood flow & GFR are decreased
– Renal failure due to  plasma volume or renal
artery vasospasm
– Proteinuria due to glomerulopathy
• glomerular capillary endothelial swelling w/subendothelial
protein deposits
– Renal function recovers quickly postpartum
Pathophysiology: Hepatic
• RUQ pain is a serious complaint
– warrants imaging, especially when
accompanied by  liver enzymes
– caused by liver swelling, periportal
hemorrhage, subcapsular hematoma, hepatic
rupture (30% mortality)
• HELLP syndrome occurs in ~ 20% of
severe preeclamptics.
Pathophysiology
• Coagulation:
– Generally hypercoagulable with evidence of
platelet activation and increased fibrinolysis
– Thrombocytopenia is common, but fewer than
10% have platelet count < 100,000
– DIC may occur,
• Acutely esp. with placental abruption
• Neurologic:
– Symptoms: headache, visual changes, seizures
– Hyperreflexia is usually present
– Eclamptic seizures may occur even w/out BP
• Possible causes: hypertensive encephalopathy, cerebral edema,
thrombosis, hemorrhage, vasospasm
Hypertension during Pregnancy: Classification
• Pregnancy-induced hypertension
– Hypertension without proteinuria/edema
– Preeclampsia
• mild
• severe
– Eclampsia
• Coincidental HTN: preexisting or persistent
• Pregnancy-aggravated HTN
– superimposed preeclampsia
– superimposed eclampsia
• Transient HTN: occurs in 3rd trimester, mild
Classification
• Chronic hypertension
• Preeclampsia-eclampsia
• Preeclampsia Superimposed upon
chronic hypertension or Renal Disease
• Gestational hypertension (only during pregnancy)
• Transient hypertension (only after pregnancy)
Chronic Hypertension
Defined as hypertension diagnosed
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Before pregnancy
Before the 20th week of gestation
During pregnancy and not resolved
postpartum
Gestational Hypertension
• Gestational Hypertension:
–Systolic >140
–Diastolic>90
–No Proteinurea
–25% Develop Pre-eclampsia
Gestational Hypertension
Diagnosis of gestational hypertension:
• Detected for first time after midpregnancy
• No proteinuria
• Only until a more specific diagnosis can be
assigned postpartum
If:
• BP returns to normal by 12 weeks postpartum,
diagnosis is transient hypertension.
• BP remains high postpartum, diagnosis is
chronic hypertension.
• Proteinurea develops Superimposed
Preeclampsia is diagnosed (25% incidence)
Preeclampsia-Eclampsia
• Occurs after 20th week (earlier with
trophoblastic disease)
• Increased BP (gestational BP elevation)
with proteinuria
• ‘LL’ Edema is NOT part of this definition
Diagnosis of Preeclampsia-Eclampsia
• Gestational Hypertension:
–Systolic >140
–Diastolic>90
• Proteinuria is defined as urinary
excretion
– 0.3 g protein or greater in a 24-hour
– +2 or greater on urine dip specimen
Blood Pressure Measurement
How would you measure the Blood Pressure
for a pregnant lady?
Preeclampsia-Eclampsia
• Blood pressure
• Measure blood pressure
– in the sitting position,
– with the cuff at the level of the heart.
– Inferior vena caval compression by the gravid
uterus while the patient is supine can alter
readings substantially, leading to an
underestimation of the blood pressure.
– Blood pressures measured in the left lateral
position similarly may yield falsely low values if
the blood pressure is measured in the higher arm
and the cuff is not maintained at heart level.
• Allow women to sit quietly for 5-10 minutes
before measuring the blood pressure.
Blood Pressure Assessment:
Patient preparation and posture
Standardized technique:
Patient
1. No caffeine in the preceding hour.
2. No smoking or nicotine in the preceding 15-30 minutes.
3. No use of substances containing adrenergic stimulants such as
phenylephrine or pseudoephedrine (may be present in nasal
decongestants or ophthalmic drops).
4. Bladder and bowel comfortable.
5. Quiet environment. Comfortable room temperature.
6. No tight clothing on arm or forearm.
7. No acute anxiety, stress or pain.
8. Patient should stay silent prior and during the procedure.
Blood Pressure Assessment:
Patient preparation and posture
Standardized technique:
Posture
• The patient should be calmly seated for at least 5
minutes, with his or her back well supported and arm
supported at the level of the heart. His or her feet
should touch the floor and legs should not be
crossed.
• The patient should be instructed not to talk prior and
during the procedure.
Recommended Technique
for Measuring Blood
Pressure
• Standardized technique:
– Use a mercury
manometer or a recently
calibrated aneroid or a
validated electronic
device.
– Aneroid devices should
only be used if there is
an established
calibration check every 612 months.
Recommended Technique
for Measuring Blood Pressure
• Electronic
oscillometric devices:
– Use a validated electronic
device according to BHS,
AAMI or IP standards.
– For self blood pressure
measurement devices, a
logo on the packaging
ensures that this type of
device and model meets
the international standards
for accurate blood
pressure measurement.
AAMI=Association for the Advancement of Medical Instrumentation;
BHS=British Hypertension Society; IP: International Protocol.
Office
Home / Self
Recommended Technique
for Measuring Blood Pressure
(cont.)
–Select a
–cuff with the
appropriate size
Cuff size
Arm circumference (cm)
Size of Cuff (cm)
From 18 to 26
9 x 18 (child)
From 26 to 33
12 x 23 (standard adult
model)
From 33 to 41
15 x 33 (large, obese)
More than 41
18 x 36 (extra large,
obese)
Recommended Technique
for Measuring Blood Pressure (cont.)
– Locate brachial and
radial pulse
– Position cuff at the
heart level
– Arm should be
supported
Recommended Technique
for Measuring Blood Pressure (cont.)
– To exclude possibility
of auscultatory gap,
increase cuff
pressure rapidly to
20-30 mmHg above
level of
disappearance of
radial pulse
– Place stethoscope
over the brachial
artery
Recommended Technique
for Measuring Blood Pressure (cont.)
– Drop pressure by 2 mmHg / sec
•
Appearance of sound (phase I
Korotkoff) = systolic pressure
– Record measurement
– Drop pressure by 2 mmHg / beat
•
Disappearance of sound (phase V
Korotkoff) = diastolic pressure
– Record measurement
– Take 2 blood pressure
measurements, 1 minute apart
Recommended Technique
for Measuring Blood Pressure
(cont.)
Korotkoff sounds
200
180
160
No sound
Clear sound
Phase 1
Muffling
140
No sound
Phase 2
Auscultato
ry gap
120
Muffled sound
Phase 3
Muffled sound
Phase 4
No sound
Phase 5
100
80
Systolic BP
Diastolic BP
60
40
20
0
mm Hg
Possible readings:
184 / 100
136 / 100
184 / 86 = correct
136 / 86
Preeclampsia-Eclampsia
• Blood pressure
– Record Korotkoff sounds I (the first sound) and V
(the disappearance of sound) to denote the systolic
blood pressure (SPB) and DPB, respectively.
– In about 5% of women, an exaggerated gap exists
between the fourth (muffling) and fifth
(disappearance) Korotkoff sounds, with the fifth
sound approaching zero. In this setting, record both
the fourth and fifth sounds (eg, 120/80/40 with
sound I = 120, sound IV = 80, sound V = 40).
Recommended Technique
for Measuring Blood Pressure
Standardized technique:
• For initial readings, take
the blood pressure in both
arms and subsequently
measure it in the arm with
the highest reading.
• Thereafter, take two
measurements on the side
where BP is highest.
Recommended Technique
for Measuring Blood Pressure (cont.)
Record the blood pressure
to the closest 2 mmHg on
the manometer
as well as the arm used
and whether the patient
was supine, sitting or
standing.
Recommended Technique
for Measuring Blood Pressure (cont.)
• Avoid digit
preference for
five (5) or zeros
(0) by not
rounding up or
down.
• Record the heart
rate.
Recommended Technique
for Measuring Blood Pressure (cont.)
• The seated blood pressure is used to
determine and monitor treatment
decisions.
• The standing blood pressure is used
to test for postural hypotension, if
present, which may modify the
treatment.
Blood Pressure Assessment:
Patient preparation and posture
Standing position
For patients over age 65, diabetics and patients being treated
with antihypertensives, check if there are postural changes
while taking blood pressure reading, i.e. after one to five
minutes in the standing position and under circumstances
when the patients complains of symptoms suggestive of
hypotension.
Classification of PreeclampsiaEclampsia
• Mild Pre-eclampsia
• Severe Pre-eclampsia
Classification of Preeclampsia-Eclampsia
• Criteria for Severe Preeclampsia (one or
more)
– Blood Pressure: >160 systolic, >110
diastolic
– Proteinurea: >5gm in 24 hours, over 3+
urine dip
– Oligurea: less than 400ml in 24 hours
– CNS: Visual changes, headache, scotomata,
mental status change
– Pulmonary Edema
– Epigastric or RUQ Pain: Usually indicates
liver involvement
Classification of PreeclampsiaEclampsia
• Criteria for Severe Preeclampsia (one or
more)
– Impaired Liver Function tests
– Thrombocytopenia: <100,000
– Intrauterine Growth Restriction: With or
without abnormal doppler assessment
– Oligohydramnios
Classification of Preeclampsia
Superimposed Upon Chronic Hypertension
• Hypertension and no proteinuria < 20 weeks:
New-onset proteinuria after 20 weeks
• Hypertension and proteinuria < 20 weeks:
– Sudden increase in proteinuria
– Sudden increase in BP in women whose
hypertension was well controlled
– Thrombocytopenia (platelet count <100,000
cells/mm3)
– Increase in ALT or AST to abnormal levels
Clinical Implications of
Preeclampsia
• Preeclampsia ranges from mild to severe.
• Progression may be slow or rapid – hours to
days to weeks.
For clinical management, preeclampsia should
be over diagnosed to prevent maternal and
perinatal morbidity and mortality – primarily
through timing of delivery.
Symptoms of Preeclampsia
• Visual disturbances typical of preeclampsia are
scintillations and scotomata. These disturbances are
presumed to be due to cerebral vasospasm.
• Headache is of new onset and may be described as
frontal, throbbing, or similar to a migraine
headache. However, no classic headache of
preeclampsia exists.
• Epigastric pain is due to hepatic swelling and
inflammation, with stretch of the liver capsule. Pain
may be of sudden onset, it may be constant, and it
may be moderate-to-severe in intensity.
Symptoms of preeclampsia
• While mild lower extremity edema is common in
normal pregnancy, rapidly increasing or
nondependent edema may be a signal of
developing preeclampsia. However, this signal
theory remains controversial and recently has
been removed from most criteria for the
diagnosis of preeclampsia.
• Rapid weight gain is a result of edema due to
capillary leak as well as renal sodium and fluid
retention.
Physical Findings in Preeclampsia
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Blood Pressure
Proteinurea
Retinal vasospasm or Retinal edema
Right upper quadrant (RUQ) abdominal
tenderness stems from liver swelling
and capsular stretch
Physical findings in Preeclampsia
– Brisk, or hyperactive, reflexes are common
during pregnancy, but clonus is a sign of
neuromuscular irritability that raises concern.
– Among pregnant women, 30% have some lower
extremity edema as part of their normal
pregnancy. However, a sudden change in
dependent edema, edema in nondependent
areas such as the face and hands, or rapid
weight gain suggests a pathologic process and
warrants further evaluation
Differential Diagnosis
• Documentation of HBP before conception
or before gestational week 20 favors a
diagnosis of chronic hypertension
(essential or secondary).
• HBP presenting at midpregnancy (weeks
20 to 28) may be due to early
preeclampsia, transient hypertension, or
unrecognized chronic hypertension.
Laboratory Tests
High-risk patients presenting with normal
BP:
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Hematocrit
Hemoglobin
Serum uric acid
If 1+ protein by routine urinalysis (clean catch)
present obtain a timed collection for protein and
creatinine
• Accurate dating and assessment of fetal growth
• Baseline sonogram at 25 to 28 weeks
Laboratory Tests
Patients presenting with hypertension
before gestation week 20:
• Same tests as described for high-risk
patients presenting with normal BP
• Early baseline sonography for dating
and fetal size
Laboratory Tests
Patients presenting with hypertension
after midpregnancy:
• Quantification of protein excretion
• Hemoglobin and hematocrit and platelet
count
• Serum creatinine, uric acid, and
transaminase level
• Serum albumin, LDH, blood smear, and
coagulation profile
Preeclampsia: Treatment
• Goal is to prevent eclampsia and other severe
complications.
• Attempts to treat preeclampsia by natriuresis
or by lowering BP may exacerbate pathologic
changes.
• Palliate maternal condition to allow fetal
maturation and cervical ripening.
Preeclampsia: Treatment
Maternal Evaluation
• Goals:
– Early recognition of preeclampsia
– Observe progression, both to prevent
maternal complications and protect wellbeing of fetus.
• Early signs:
– BP rises in late second and early third trimesters.
– Initial appearance of proteinuria is important.
Fetal Monitoring
Preeclampsia: Treatment
• Maternal Evaluation…When To Hospitalize?
– Often, hospitalization recommended with new-onset
preeclampsia to assess maternal and fetal conditions.
– Hospitalization for duration of pregnancy indicated for
preterm onset of severe gestational hypertension or
preeclampsia.
– Ambulatory management at home or at day-care unit
may be considered with mild gestational hypertension
or preeclampsia remote from term
Preeclampsia
Indication of Delivery
Preeclampsia
• Antepartum Management of Preeclampsia
– Little to suggest therapy alters the underlying
pathophysiology of preeclampsia.
– Restricted activity may be reasonable.
– Sodium restriction and diuretic therapy appear
to have no positive effect.
Obstetric Management
• Classically “stabilize and deliver”
Obstetric Management
• Medical management while awaiting
delivery:
– use of steroids X 48 hours if fetus < 34 wks
– antihypertensives to maintain DBP < 105-110
– magnesium sulfate for seizure prophylaxis
– monitor fluid balance, I/O, daily weights,
symptoms, reflexes, HCT, plts, LFT’s, proteinuria
Obstetric Management
• Indications for expedited delivery:
– fetal distress
–  BP despite aggressive Rx
– worsening end-organ function
– development or worsening of HELLP syndrome
– development of eclampsia
Antihypertensive Therapy
• Most commonly, for acute control: hydralazine,
labetolol
• Nifedipine may be used, but unexpected
hypotension may occur when given with MgSO4
• For refractory hypertension: nitroglycerin or
nitroprusside may be used
– Nitroprusside dose and duration should be limited
to avoid fetal cyanide toxicity
– Usually require invasive arterial pressure mon
• Angiotensin-converting enzyme (ACE) inhibitors
contraindicated due to severe adverse fetal
effects
Seizure Prophylaxis & Treatment
• Magnesium sulfate vs. phenytoin for seizure
prophylaxis in preeclampsia
Lucas, et al., N Engl J Med 1995;333:201-5.
– 2138 patients (75% had mild PIH)
– Maternal & fetal outcomes similar except 10
seizures in the phenytoin group (0 in MgSO4)
• Mg vs. diazepam & Mg vs. phenytoin for
preventing recurrent seizures in eclamptics
Eclampsia Trial Collaborative Group, Lancet 1995;345:1455
– Mg pts were 52% or 67% less likely to have a
recurrent seizure than diazepam or phenytoin pts
Seizure Prophylaxis
• Evidence is strong that magnesium
sulfate is indicated for
– seizure treatment in eclamptics
– seizure prophylaxis in severe preeclamptics
• Role of magnesium prophylaxis in mild
preeclamptics is less clear
– awaits large, prospective, randomized,
placebo-controlled trial
Magnesium Sulfate
• Magnesium sulfate has many effects; its
mechanism in seizure control is not clear.
– NMDA (N-methyl-D-aspartate) antagonist
– vasodilator
• Brain parenchymal vasodilation demonstrated in
preeclamptics by Doppler ultrasonography
– increases release of prostacyclin
• Potential adverse effects:
– toxicity from overdose (respiratory, cardiac)
–  bleeding
–  hypotension with hemorrhage
–  uterine contractility
Magnesium Sulfate
• Renally excreted
• Preeclamptics prone to renal failure
• Magnesium levels must be monitored frequently
either clinically (patellar reflexes, urinary output) or
by checking serum levels q 6-8 hours
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Therapeutic level:
Patellar reflexes lost:
Respiratory depression:
Respiratory paralysis:
Cardiac arrest:
4-7 meq/L
8-10 meq/L
10-15 meq/L
12-15 meq/L
25-30 meq/L
• Treatment of magnesium toxicity:
– stop MgSO4, IV calcium, manage airway
Treatment of Eclampsia
• Seizures are usually short-lived.
• If necessary, small doses of barbiturate or
benzodiazepine (STP, 50 mg, or midazolam, 1-2 mg)
and supplemental oxygen by mask.
• If seizure persists or patient is not breathing, rapid
sequence induction with cricoid pressure and
intubation should be performed.
• Patient may be extubated once she is completely
awake, recovered from neuromuscular blockade, and
magnesium sulfate has been administered.
Anesthetic Goals of Labor Analgesia in
Preeclampsia
• To establish & maintain hemodynamic
stability (control hypertension & avoid
hypotension)
• To provide excellent labor analgesia
• To prevent complications of preeclampsia
– intracerebral hemorrhage
– renal failure
– pulmonary edema
– eclampsia
• To be able to rapidly provide anesthesia for
C/S
Regional vs. General Anesthesia
in Preeclampsia
• Epidural anesthesia would probably be
preferred by many anesthesiologists in a
severely preeclamptic pt in a non-urgent
setting
• For urgent cases it is reassuring to know
that spinal is also safe
• This allows us to avoid general anesthesia
with the potential for encountering a
swollen, difficult airway and/or labile
hypertension
Regional vs. General
Anesthesia in Preeclampsia
• General anesthesia is a well-known
hazard in obstetric anesthesia:
– 16X more likely to result in anestheticrelated maternal mortality
– Mostly due to airway/respiratory
complications, which would only be
exaggerated in preeclampsia
Hawkins, Anesthesiology 1997;86:273
Platelets & Regional Anesthesia
in Preeclampsia
• Prior to placing regional block in a preeclamptic it is
recommended to check the platelet count.
• No concrete evidence at to the lowest safe platelet
count for regional anesthesia in preeclampsia
• Any clinical evidence of DIC would contraindicate
regional anesthesia.
Hazards of General Anesthesia
in Preeclampsia
• Airway edema is common
– Mandatory to reexamine the airway soon before
induction
– Edema may appear or worsen at any time during the
course of disease
• tongue & facial, as well as laryngeal
• Laryngoscopy and intubation may  severe BP
– Labetolol & NTG are commonly used acutely
– Fentanyl (2.5 mcg/kg), alfentanil (10 mcg/kg), lidocaine
may be given to blunt response
Hazards of General Anesthesia
in Preeclampsia
• Magnesium sulfate potentiates depolarizing &
non-depolarizing muscle relaxants
– Pre-curarization is not indicated.
– Initial dose of succinylcholine is not reduced.
– Neuromuscular blockade should be monitored &
reversal confirmed.
Invasive Central Hemodynamic
Monitoring in Preeclampsia
• Usually reserved for patients with
complications
– oliguria unresponsive to modest fluid challenge
(500 cc LR X 2)
– pulmonary edema
– refractory hypertension
• may have increased CO or increased SVR
• Poor correlation between CVP and PCWP in
PIH
– However, at most centers anesthesiologists
would begin with CVP & follow trend
• not arbitrarily hydrate to a certain number
– If poor response, change to PA catheter
Conclusions
• Preeclampsia is a serious multi-organ system
disorder of pregnancy that continues to defy
our complete understanding.
• It is characterized by global endothelial cell
dysfunction.
• The cause remains unknown.
• There is no effective prophylaxis.
Conclusions
• Delivery is the only effective cure.
• Magnesium sulfate is now proven as the
best medication to prevent and treat
eclampsia.
• Epidural analgesia for labor pain
management & regional anesthesia for C/S
have many beneficial effects & are
preferred.
Antihypertensive Therapy
• Patients with chronic hypertension should continue
on their pre-pregnancy medication if NOT
contraindicated with pregnancy.
• The usual cut off to prescribe Antihypertensives
with pregnancy is 150/100.
• Care should be taken NOT to compromise the fetal
circulation by bringing the blood pression down to
normal.
Alpha-methyl Dopa
• The most commonly used and
presumably the safest with pregnancy.
• The usual dose starts with 250mg tds to
be increased up to 2 grams per day.
• It blocks the adrenaline release at post
synaptic sites.
Hydralazine
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Dose: 5-10 mg every 20 minutes
Onset: 10-20 minutes
Duration: 3-8 hours
Side effects: headache, flushing,
tachycardia, lupus like symptoms
• Mechanism: peripheral vasodilator
Labetalol
• Dose:
– IV:20mg, then 40, then 80 every 20 minutes, for a
total of 220mg
– Oral 100 mg bid to be increased up to 200 mg qid.
( maximum 2400mg daily)
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•
•
•
Onset: 1-2 minutes
Duration: 6-16 hours
Side effects: hypotension
Mechanism: Alpha and Beta block
Nifedipine
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•
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Dose: 10 mg po, not sublingual
Onset: 5-10 minutes
Duration: 4-8 hours
Side effects: chest pain, headache,
tachycardia
• Mechanism: CA channel block
Clonidine
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•
•
Dose: 1 mg po
Onset: 10-20 minutes
Duration: 4-6 hours
Side effects: unpredictable, avoid rapid
withdrawal
• Mechanism: Alpha agonist, works
centrally
Nitroprusside
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•
•
•
Dose: 0.2 – 0.8 mg/min IV
Onset: 1-2 minutes
Duration: 3-5 minutes
Side effects: cyanide accumulation,
hypotension
• Mechanism: direct vasodilator
Preeclampsia
• Indications for Delivery in Preeclampsia
• Maternal
– Gestational age 38 weeks
– Platelet count < 100,000 cells/mm3
– Progressive deterioration in liver and renal function
– Suspected abruptio placentae
– Persistent severe headaches, visual changes, nausea,
epigastric pain, or vomiting
Delivery should be based on maternal and fetal
conditions as well as gestational age.
Preeclampsia
• Indications for Delivery in Preeclampsia
• Fetal
– Severe fetal growth restriction
– Nonreassuring fetal testing results
– Oligohydramnios
Preeclampsia
• The “cure” for preeclampsia is
delivery
– The “cure” is always beneficial for the
mother, although c-section might be
needed
– The “cure” may be deleterious for the
fetus
Preeclampsia
• Route of Delivery
– Vaginal delivery is preferable.
– Aggressive labor induction (within 24 hours).
– Neuraxial (epidural, spinal, and combined
spinal-epidural) techniques offer advantages.
– Hydralazine, nitroglycerin, or labetalol may be
used as pretreatment to reduce significant
hypertension during delivery.
Preeclampsia
• Anticonvulsive Therapy
– Indicated to prevent recurrent
convulsions in women with eclampsia
or to prevent convulsions in women
with preeclampsia.
– Parenteral magnesium sulfate
reduces the frequency of eclampsia
and maternal death. (Caution in renal
failure.)
Treatment of Acute Severe
Hypertension in Pregnancy
• SBP > 160 mm Hg and/or DBP > 105
mm Hg
– Parenteral hydralazine is most commonly
used.
– Parenteral labetalol is second-line drug
(avoid in women with asthma and CHF.)
– Oral nifedipine used with caution. (Shortacting nifedipine is not approved by FDA for
managing hypertension.)
– Sodium nitroprusside may be used in rare
cases.
Postpartum Counseling and
Followup
• Counseling for Future Pregnancies
• Risk of recurrent preeclampsia
increases with
– Preeclampsia before 30 weeks (40%)
– Multiparas as compared with nulliparas or
new father
– Risk of recurrent preeclampsia may be
substantially greater in African Americans.
Remote Prognosis
• Preeclampsia-Eclampsia
– The more certain the diagnosis of
preeclampsia, the lower the prevalence of
remote cardiovascular disorders.
– Preeclampsia-eclampsia in subsequent
pregnancies helps define future risk.
– Gestational hypertension in any pregnancy
increases remote cardiovascular risk.
Eclampsia
• Women older than 40 years with preeclampsia
have 4 times the incidence of seizures compared to
women in their third decade of life.
– Twenty-five percent of eclampsia cases occur before
labor (ie, antepartum).
– Fifty percent of eclampsia cases occur during labor (ie,
intrapartum).
– Twenty-five percent of eclampsia cases occur after
delivery (ie, postpartum).
– Patients with severe preeclampsia are at greater risk to
develop seizures.
– Twenty-five percent of patients with eclampsia have only
mild preeclampsia prior to the seizures
Causes:
The cause of the seizures is not clear,
although several processes have been
implicated in their development.
– Areas of cerebral vasospasm may be severe
enough to cause focal ischemia, which may in
turn lead to seizures.
– Pathologic alterations in cerebral blood flow and
tissue edema induced by vasospasm may result
in headaches, visual disturbances, and
hypertensive encephalopathy, resulting in a
seizure.
• Prior to the seizures,
Symptoms include the
following:
–
–
–
–
–
–
Headache (82.5%)
Hyperactive reflexes (80%)
Marked proteinuria (52%)
Generalized edema (49%)
Visual disturbances (44.4%)
Right upper quadrant pain or
epigastric pain (19%)
• Sometimes, there is:
– Lack of edema (39%)
– Absence of proteinuria
(21%)
– Normal reflexes (20%)
Eclamptic seizure
– The patient may have 1 or more seizures.
– Seizures generally last 60-75 seconds.
– The patient's face initially may become
distorted, with protrusion of the eyes.
– The patient may begin foaming at the
mouth.
– Respiration ceases for the duration of the
seizure.
• The seizure may be divided into 2 phases:
– Phase 1 lasts 15-20 seconds and begins with facial twitching. The
body becomes rigid, leading to generalized muscular
contractions.
– Phase 2 lasts approximately 60 seconds. It starts in the jaw,
moves to the muscles of the face and eyelids, and then spreads
throughout the body. The muscles begin alternating between
contracting and relaxing in rapid sequence.
• A coma or a period of unconsciousness follows phase 2.
– Unconsciousness lasts for a variable period.
– Following the coma phase, the patient may regain some
consciousness.
– The patient may become combative and very agitated.
– The patient has no recollection of the seizure.
• A period of hyperventilation occurs after the tonic-clonic
seizure. This compensates for the respiratory and lactic
acidosis that develops during the apneic phase.
• Seizure-induced complications may include tongue biting,
head trauma, broken bones, or aspiration.