1. Dr.SREEJITH.H

2.  Hypertensive disease is the 4th
leading cause of
maternal death
 Preeclampsia complicates about upto 8% of
pregnancies
 In U.S preeclampsia complicates approx 7-10%
of pregnancies
 Eclampsia 1 in 10000-150000 pregnancies
 Severe PIH contributes to 20-40% of maternal
deaths & 20% of perinatal deaths

3.  Pregnancy Induced Hypertension
 Preeclampsia
 Eclampsia
 Chronic hypertension
 Chronic hypertension with superimposed
preeclampsia

4.  Defined as a systolic BP >140 mm Hg or
diastolic BP >90 mm Hg
OR
 a constant increase in systolic or diastolic BP
by 30 mmHg & 15 mm Hg respectively above
patient’s baseline

5.  Classic Triad of Preeclampsia - Hypertension
Proteinuria, Edema
 Defined as hypertension occuring after 20
wks gestation or in early postpartum period
& returned to normal within 3 months after
delivery
OR
 Onset after 20wks gestation & atleast one of
the following

6.  Proteinuria >300 mg/24 hr
 Oliguria /serum plasma creatinine ratio >0.09mmol/L
 Headaches with hyperreflexia,eclampsia,clonus,or visual
disturbances
 Increased liver enzymes , plasma glutathione S-transferase –
alpha 1-1, or serum alanine aminotransferase or right
quadrant pain
 Thrombocytopenia,increased LDH, haemolysis, DIC
 Intrauterine growth retardation

7.  SBP > 160 mm Hg
 DBP > 110 mm Hg
 Proteinuria > 5 g/24° or
3-4+ on dipstick
 Oliguria < 500 cc/24°
 ↑ 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

9.  Nulliparity(Elderly & young primigravida)
 Chronic renal disease(Nephritis)
 Angiotensin gene T235
 Chronic hypertension
 Antiphospholipid antibody syndrome
 Multiple gestation
 Family or personal history of preeclampsia
 Age > 40 years
 African-American race
 Diabetes mellitus

10.  DISEASE OF THEORIES
 Etiology is unknown.
 Many theories:
 Abnormal Placentation
 Endothelial cell dysfunction
 Imbalance b/w TXA2 & PGI2
 dietary deficiency (calcium, magnesium, zinc)
▪ supplementation has not proven effective

11.  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)

12.  Aspirin has been extensively studied as a targeted
therapy to ↓ thromboxane production
 CLASP study, 1994, multicenter, randomized
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

13.  NIH study of high-risk patients, randomized, 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

14.  At this time the most widely accepted proposed
mechanism for preeclampsia is:
▪ global endothelial cell dysfunction
 Redman: endothelial cell dysfunction is just one
manifestation of a broader intravascular
inflammatory response
Redman, et al., Am J Obstet Gynecol 1999;180:499-506
 present in normal pregnancy
 excessive in preeclampsia
 Proposed source of inflammatory stimulus: placenta

15.  In severe preeclampsia, typically hyperdynamic
with normal-high CO, normal-mod. high SVR,
and normal PCWP and CVP.
 Despite normal filling pressures, intravascular
fluid volume is reduced (30-40% in severe PIH)
 Variations in presentation depending on prior
treatment and severity and duration of disease
 Total body water is increased (generalized
edema)

16.  Preeclamptic patients are prone to develop
pulmonary edema due to reduced colloid oncotic
pressure (COP), which falls further postpartum:
Colloid oncotic pressure:
Antepartum
Postpartum
Normal pregnancy: 22 mm Hg 17 mm Hg
Preeclampsia: 18 mm Hg 14 mm Hg

17.  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

18.  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.

19.  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, 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

20.  Hemolysis – abnormal peripheral smear
Increased bilirubin level
 Elevated liver enzymes- SGOT>70U/L
LDH>600U/L
 Low platelet count<100000/mm3
 Clinical features –Malaise(90%) , Epigastric pain(90%),
Nausea & vomitting(50%), Flu like syndrome
 Usually before 36 weeks
 70% antepartum & 30% postpartum
 Rapidly progress to DIC
 Associated with high maternal & fetal mortality

21.  LIKE A FLASH OF LIGHTENING
 Preeclampsia complicated by convulsion /coma
 Most common in primi & multiple pregnancy
Cause of convulsion
 Hypertensive encephalopathy
 Vasospasm- ischemia
 Infarction
 Haemorrhage
 Oedema

22.  Antepartum – 50%,intrapartum-30%
postpartum-20%
3 stages
 Premonitory stage- unconsciousness,
twitching of facial muscles
 Tonic stage(30s) – tonic spasm, opisthotonm
 Clonic stage (1-4 min)– frank convulsions

23.  Differential Diagnosis
Epilepsy,ICSOL,Meningitis,Hysteria
Management
 MgSO4 is the DOC for seizure control & prevention of recurrent
eclamptic seizures
 Reduces seizures by >50%
 4g MgSO4 iv over 10 min followed by a maintanence infusion of 1g/hr
 Mg also causes vasodilataion & increase in CO by reducing SVR
 Narrow Therapeutic Index ,with serum Mg level b/w 2 & 3.5 mmol/L .
Therapeutic level 4-6 mEq/L
 If toxicity present 10 ml 10 % Ca gluconate given slow iv

24. MATERNAL
Eclampsia, Renal Failure, Pulmonary edema,
CVA, Blindness, PPH, Sepsis, Residual HTN
FETAL
IUGR, IUD, RDS, Prematurity, Intracranial
Haemorrhage
CAUSES OF MATERNAL DEATH
Eclampsia, Intracranial haemorrhage, ARF,
Pulmonary edema, DIC, HELLP

25. CS
Fetal Distress
Worsening of Biophysical Profile
RAPID DELIVERY
Eclampsia
Severe HTN not responding to treatment
Renal & Hepatic Dysfunction
coagulopathy

26.  Hospitilistaion & Bed Rest(Lt lateral position)
 Adequate Hydration & Diet (avoid excess Na)
 Antihypertensives
 Anticonvulsants
GENERAL PRINCIPLES
 Minimise vasospasm
 Improve circulation
 Improve intravascular volume
 Correct acid base & electrolyte imbalance
 Decrease CNS irritability

27.  Classically “stabilize and deliver”
 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
 Indications for expedited delivery:
 fetal distress
 ↑ BP despite aggressive Rx
 worsening end-organ function
 development or worsening of HELLP syndrome
 development of eclampsia

28.  Most commonly, for acute control:
1.)Hydralazine
Arterial dilator, dose 5-10mg iv ,slow onset 20-30mtsDOA: 2-3 hrs
2) Labetolol
10-20mg iv, Improves placental blood flow ,Rapid onset of action 1-2mts
DOA-2-3hrs
CI- Bronchial asthma,CCF
 Most common for chronic control:
Alpha methyl dopa.
Central alpha 2 agonist
Dose – 250 mg bd
DOC for chronic treatment

29.  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 monitoring
 Angiotensin-converting enzyme (ACE) inhibitors
contraindicated due to severe adverse fetal effects

30.  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

31.  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

32.  Renally excreted
 Preeclamptics prone to renal failure
 Magnesium levels must be monitored frequently
either clinically (patellar reflexes) or by checking
serum levels q 6-8 hours
▪ Therapeutic level: 4-7 meq/L
▪ Patellar reflexes lost: 8-10 meq/L
▪ Respiratory depression: 10-15 meq/L
▪ Respiratory paralysis: 12-15 meq/L
▪ Cardiac arrest: 25-30 meq/L
 Treatment of magnesium toxicity:
 stop MgSO4, IV calcium, manage airway

33.  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.

34.  Labor analgesia
 Anaesthesia for CS & Obstertic complication
 Neonatal resuscitation
 To prevent complications of preeclampsia
 intracerebral hemorrhage/convulsions
 renal failure
 pulmonary edema
 Eclampsia

35.  To establish & maintain hemodynamic
stability (control hypertension & avoid
hypotension)
 To provide excellent labor analgesia
 To prevent complications of preeclampsia
 To be able to rapidly provide anesthesia for
C/S
 To avoid drug induced depression

36.  Newer studies shows that degree of hypotension in spinal & epidural
block is same in PIH pt
 So we can use either spinal / epidural
 Graded epidural in a preeclampsia patient
 5ml (0.5% bupivacaine)loading dose to attain T10 level
 Then 5 ml increment at 5 mt interval to attain T4 level
 Fentanyl(50-100mcg) can be added to increase speed of onset , duration
quality
Advantages of epidural
 Gradual onset of sympathetic blockade
 Cardiovascular stability
 Avoids neonatal depression

37.  Hood, et al., Anesthesiology 1999;90:1276-82
 Retrospective study
 Lowest intraoperative blood pressures not different
 Total ephedrine use was small & not different
 Spinal group received 400 cc more IV fluid
 No pulmonary edema attributable to intraop fluid
 Maternal & infant outcomes were similar

38.  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
 In the absence of such signs, most
anesthesiologists would proceed at plt count
>100000, many would proceed at 80000-100000,
<80000 some would proceed (esp. spinal)

39.  When placing a regional block in a patient with a
platelet count < 100000, the most important thing
is to monitor resolution of block closely
 Bleeding time has been discredited as an indicator
of epidural bleeding risk and is not indicated.
Channing-Rogers, Semin Thromb Hemost 1990;16:;1-30
 Low-dose aspirin is not a contraindication to
regional anesthesia in preeclampsia
 CLASP study: 1422 women on aspirin received epidurals
without any bleeding complications

40.  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

41.  General anesthesia is a well-known hazard in
obstetric anesthesia:
 16X more likely to result in anesthetic-related
maternal mortality
 Mostly due to airway/respiratory complications,
which would only be exaggerated in preeclampsia
Hawkins, Anesthesiology 1997;86:273

42.  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

43.  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.

44.  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

45.  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.

46.  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.