2. INTRODUCTION
Hypertension is one of the most common
complication during pregnancy
Increased maternal and perinatal morbidity
and mortality.
It is a sign of an underlying pathology that
may be pre-existing or appears for the first
time during pregnancy that is why it is also
called as TOXEMIA OF PREGNANCY.
4. HISTORY:
Fits occurring during pregnancy were recognized as early
as in 4th century B.C. by Hippocrates
Eclampsia is a Greek word that means SHINE FORTH
implies sudden development
1903 Chesley- Preeclampsia word included in books
1976 Pritchard and Mc Donald- Hypertensive disorders of
pregnancy & Diagnostic criteria of preeclampsia:
hypertension, proteinuria, edema after 20 weeks
5. DEFINITION:
Hypertension is defined as systolic pressure of
at least 140 mm of Hg and diastolic pressure of
at least 90 mm of Hg.
Proteinuria is defined as more than 300 mg /24
hrs. Or two clean catch midstream or catheter
specimens of urine collected at least more than
four hours apart.
6. CLASSIFICATION OF PIH ACCORDING TO
AMERICAN SOCIETY OF HYPERTENSION
1.Preeclampsia-eclampsia
2.Chronic hypertension of any cause
3.Preeclampsia superimposed on chronic
hypertension
4.Gestational hypertension
7. PREECLAMPSIA-ECLAMPSIA
It is a multi-system disorder of unknown
etiology.
New onset of hypertension & proteinuria in a
previously normotensive woman
After 20 weeks of gestation
Returning to normal after 12 weeks of
pregnancy.
Oedema not a part of diagnosis now.
A retrospective diagnosis
8. Eclampsia : new onset of seizures or
unexplained coma during pregnancy or
postpartum period in patients with pre-
existing preeclampsia and without pre-
existing neurological disorder.
9. SEVERE ECLAMPSIA HAS FOLLOWING CRITERIA:
• Systolic BP of 160 mm of Hg or Diastolic BP of 110 mm of Hg
Or
Higher on two occasions at least 4 hours apart while the patient is
on bed unless antihypertensive therapy is initiated before this time
• Thrombocytopenia i.e. platelet count less than 100,000/microliter
• Impaired liver functions indicated by abnormally elevated blood
concentrations of liver enzymes, severe persistent right upper
quadrant or epigastric pain unresponsive to medication and not
accounted for by alternative diagnoses, or both
10. Progressive renal insufficiency in serum
creatinine level greater than 1.1 mg/dl or a
doubling of serum creatinine concentration in
the absence of other renal disease
• Pulmonary oedema
• New onset of cerebral or visual disturbances
11. NOTE: In view of recent studies that indicate
minimal relationship between the quantity of
urinary protein and pregnancy outcome in these
patients, massive proteinuria i.e. greater than 5
mg has been eliminated and also foetal growth
restriction as it is managed similarly in pregnant
women with or without preeclampsia.
12. RISK FACTORS:
Maternal factors
Obesity
Nulliparity
Maternal age more than 40 yr.
Previous preeclampsia
Chronic hypertension
Diabetes
Renal disease
Multiple gestation
Genetic
Thrombophilias- anti-phospholipid syndrome, protein c,s
deficiency, factor v Leiden
15. ETIOLOGY AND PATHOGENESIS
Exact cause is unknown that’s why it is
called as “the disease of theories.”
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
16.
17.
18. Other causes are:
a. Inflammatory mediators: imbalance between
Prostaglandins and I2 and thromboxane
causing Vasoconstriction, Platelet
aggregation, increased Vasopressor response
and increased uterine activity.
b. Genetic: Family history of pre eclampsia:
genetic origin
Mutations in Complement Regulatory Protein
gene
Genes assoc.: MTHFR, F5
Leiden, AGT, HLA, NOS3, F2(prothrombin), AC
E
19. c. Immunologic: Exposure to sperms of
different partner long term exposure to paternal
antigen in sperms of same partner- protective
activated auto antibodies to angiotensin
receptor-1 AA-AT1 that activates AT1
receptors causing increased sensitivity to
angiotensins and finally leading to
hypertension.
23. A. Maternal:
a) Cardiovasular System:
-Reduction in total blood volume is proportional
to severity of the disease
-Decreased colloid oncotic pressure coupled
with increase vascular permeability, loss of
intra vascular fluids and proteins into the
interstitial tissues that increases risk of
pulmonary oedema.
24. • Increased peripheral vascular resistance and
sympathetic over activity leads to elevated BP
• Cardiac output is variable i.e. it could be either
increased, decreased or unchanged
• Pulomary capillary wedge pressure also vary
with severity of systemic vascular resistance. If
systemic vascular resistance is high then PAWP is
low.
• In the end it is a low volume, high pressure and
high resistance state.
25. b)Respiratory System: it’s a state of
generalised oedema involving face, neck upper
airway specifically larynx, pharyngeal oedema
that may hamper in visualisation of vocal cord
making it a case of difficult intubation.
26. c) Central Nervous System: Signs of hyper-
irritability such as headache, visual
disturbances,hyperexcitability, hyperreflexia, c
oma,seizures all due to cerebral edema and
hypoperfusion
27. d) Renal: Renal functions are grossly affected.
Arteriolar spasm leads to proteinuria,
decreased GFR, decreased urea clearance,
elevated uric acid and creatinine level. Out of
these hyperuricemia is an early sign of
deteriorating renal function resulting in
decreased urine output and may progress to
anuria.
28. e) Hepatic: there is distention of liver capsule
due to edema, periportal necrosis, fibrin
deposition in hepatic sinusoids occurs leading
to HELLP syndrome, Periportal haemorrhage
, subcapsular bleeding,hepatic rupture: 32%
maternal mortality
29. f) Coagulation abnormalities:
Hemoconcentration (pts with anemia may
appear to have normal hematocrit)
Thombocytopaenia is most common. Despite
of normal platelet count, platelet function is
impaired. Platelet count correlates with disease
severity and incidence of abruptio placenta.
DIC due to activation of coagulation cascade
causes overconsumption of coagulants and
platelets leading to spontaneous haemorrhage.
30.
31. B. Uteroplacental circulation: Uterine and
intervillous blood flow is diminished by 50-70%
due to hemoconcentration, increased blood
viscosity and vasoconstriction leading to hypo
perfusion causing foetal hypoxia and IUGR.
Placental abruption is more common in
patients with preeclampsia.
32. HELLP SYNDROME:
Consists of Haemolysis, elevated liver enzymes and
low platelets. Incidence rate is 4-12% in preeclamptics
and associated with high mortality and morbidity.
Diagnostic criteria:
Haemolysis defined as abnormal peripheral smear
and increased bilirubin >1.2 mg/dl
Elevated liver enzymes i.e. increased serum glutamic
oxaloacetic transaminase >70IU and increased
serum Lactate dehydrogenase >600 U/L
Low platelet count <1,00,000 mm3
34. PREDICTION OF PREECLAMPSIA
No screening test is really helpful
Various screening methods are:
- Diastolic notch at 24weeks by Doppler
ultrasonography
- Absence or reversal of end diastolic flow
- Average mean arterial pressure ≥ 90 mmHg in
second trimester
- Infusion test: angiotensin infusion required to
raise the blood pressure >20 mm Hg from
baseline
35. Roll over test: Rise in blood pressure >20
mmHg from baseline on turning supine at 28-
32 weeks gestation is positive.
36. 2. ECLAMPSIA
Is the new onset of seizures or unexplained coma
during pregnancy or postpartum period in patients
with pre-existing PE and without pre-existing
neurological disorder.
Epidemiology:
• 0.1- 5.5 per 10,000 pregnancies
• Decreasing incidence with time
• Antepartum(50%): mostly in third trimester
• Intrapartum (30%):
• Postpartum(20%): usually within 48hours, fits
beyond 7days generally rules out Eclampsia
37. RISK FACTORS:
• Maternal age less than 20 years
• Multigravida
• Molar pregnancy
• Triploidy
• Pre-existing hypertension or renal disease
• Previous severe Preeclampsia or Eclampsia
• Nonimmune hydrops fetalis
• Systemic Lupus Erythematosus
38. CLINICAL FEATURES
Eclamptic convulsions are epileptiform and consist
of four stages
• Premonitory stage: twitching of muscles of
face, tongue, limbs and eye. Eyeballs rolled or
turned to one side
• Tonic stage: opisthotonus, limbs flexed, hands
clenched
• Clonic stage: 1-4 min, frothing, tongue
bite, stertorous breathing
• Stage of coma: variable period.
39.
40. Pathogenesis: Loss of normal cerebral auto
regulatory mechanisms cerebral
hyperperfusion leading to Edema & ↓cerebral
blood flow.
41. DIAGNOSIS:
Lab Investigations:
• Complete Blood Count
• Platelet count
• LFT
• RFT
• Urine analysis
• Serum electrolytes
• Peripheral blood smear
• Prothrombin time
• Type and screen antibody if present
• Angiotensin II test: a dose of 8mk/kg/body weight to
increase Diastolic Blood pressure by 20 mm of Hg is taken
as positive
43. 1. Control Hypertension: Most commonly, for acute
control: hydralazine, labetalol
• 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 effect
47. 2. Improve intravascular volume: Main aim is to
increase CVP & PCWP range 4-6 cm H2O &
5-10 mm HG and to increase urine output to 1
ml/kg/hr.
There is a controversy between colloid and
crytalloid as both complicates the condition
causing low colloid oncotic pressure and
leaky capillary predisposing them to risk of
non-carcinogenic pulmonary oedema
Fluid recommendation: crystalloids to be
administered at the rate of 1-2 ml/kg/hr. and
alternating according to CVP, PCWP and
Urine Output.
48. 3. Seizure Prophylaxis & Treatment:
Magnesium sulphate therapy. Magnesium
sulfate has many effects; its mechanism in
seizure control is not clear. It is an NMDA
(N-methyl-D-aspartate) antagonist
vasodilator
Brain parenchymal vasodilation
demonstrated in preeclamptics by Doppler
ultrasonography increases release of
prostacyclin
49. Potential adverse effects:
• Toxicity from overdose (respiratory, cardiac)
• Bleeding
• Hypotension with haemorrhage
• Uterine contractility
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
51. Treatment of magnesium toxicity:
- stop MgSO4
- IV 1 g 10% calcium gluconate slow
- Administer Oxygen
- Secure airway
- Ventilation
52. Anaesthetic Implication: MgSo4 potentiate
and prolongs both actions of depolarizing
and non-depolarizing Muscle relaxants.
Intubating dose of succinylcholine should not
be decreased as onset and duration of action
of single dose does not alter in preeclamptic
patients. NDMR when used neuromuscular
monitoring with peripheral nerve stimulation
and dose titration should be done
accordingly.
53. VARIOUS REGIME OF MAGNESIUM THERAPY
• Pritchard Regime:
- Loading dos: 4g (20 ml of 20%) MgSo4 IV over 4 min.
immediately followed by 10g (20 ml of 50%) IM i.e. 5
gm in each buttocks
- If convulsion persists after 15 min 2 g IV over 2 min
- Maintenance dose: 5g IM every 4 hours alternate side
• Zuspan or Sibai regime:
- Loading dose: 6 g IV over 20 min
- Maintenance dose: 2-3 g/hr. IV every 6 hr
54. 4. 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.
55.
56.
57. WHEN TO DELIVER??
Maternal Indication:
- Recurrent Severe Hypertension
- Recurrent symptoms of severe preeclampsia
- Progressive renal insufficiency i.e. serum
creatinine concentration greater than 1.1 mg/dL or a
doubling of the serum creatinine concentration in the
absence of other renal disease
- Persistent thrombocytopenia or HELLP
syndrome
- Pulmonary oedema
- Suspected abruption placenta
- Progressive labour or rupture of membranes
58. Fetal Indication:
- Gestational age of 34 0/7 weeks
- Severe fetal growth restriction
- Persistent Oligohydramnios
- BPP of 4/10 or less on at least two
occasions 6 hours apart
- Reversed end-diastolic flow on
umbilical artery Doppler studies
- Recurrent variable or late
deceleration during NTS
Fetal death
59. PAE:
What all to be evaluated before inducing??
- Condition of mother: stabilization is required
before inducing
- Severity of condition
- Associated organ involvement
- Airway assessment
- BP
- Fluid status
- Evidence of coagulation
- Medication
- Fetal status
64. 1. Normal Vaginal Delivery: Main aim is
- To establish & maintain hemodynamic stability
(control hypertension & avoid hypotension)
- To provide excellent labor analgesia
- To prevent complications of preeclampsia
Intracerebral haemorrhage
Renal failure
Pulmonary Edema
Eclampsia
- To be able to rapidly provide anaesthesia for C/S
65. a) Controlled IV analgesia: Fentanyl
- Loading dose: 1 mcg/kg
- Maintenance dose: 25-50 mcg every 20 min
b) Regional Anaesthesia: Epidural Block-
Guidelines-
- CBC and Coagulation profile
- Baseline BP
- Continue anticonvulsive therapy
- Crytalloid and albumin to increase CVP
- Segmental Epidural block with dilute increments
66. Advantage of Epidural Block:
- Hypertensive response to pain is attenuated
by epidural block
- Decreased levels of catecholamine which
facilitates BP control
- May improve intervillous blood flow and
stable cardiac output
- Can also be used in Caesarean section
67. a) Regional Anaesthesia:
Give aspiration prophylaxis
Availability of blood and blood products
Pre-hydration
Oxygen administration: 6lt/min
Epidural Block: 8-10 ml of 1.5-2% lignocaine or
0.5% Bupivacaine with 25-50 mcg of Fentanyl
and the block should be raised to a minimum
level of T4
68. Sub-arachnoid Block: 5-10mg of 0.5%
bupivacaine with 20 mcg of Fentanyl
If hypotension occurs treat with Inj Ephedrine
Avoid ergot alkaloids once baby is extracted
Pot-op pain relief with epidural Fentanyl
infusion of 10-25 mcg or Morphine 4 mg
69. Platelet count and regional anaesthesia:
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 anaesthesia in
preeclampsia
Any clinical evidence of DIC would
contraindicate regional anaesthesia.
70. Platelets <1 lakh/mm3
-clinical evidence of bleeding
-Platelet trend-Every 6hourly if
stable, every 1-3hrly if declining
-coagulation profile: PT/PTTK/INR
-quality of platelets
-risk vs benefit
Platelets <50,000: contraindication
71. Bleeding time has been discredited as an indicator of
epidural bleeding risk and is not indicated.
Remove epidural catheter only when platelet count
returns normal (at least 75000-80000/mm3)
Emergency imaging studies and neurologic
evaluation if epidural hematoma suspected
In various studies, it has been found that low dose
aspirin doesn’t significantly affect bleeding time;
neuraxial analgesia can be given safely without any
complication
Low-dose aspirin is not a contraindication to regional
anaesthesia in preeclampsia
72. b) General Anaesthesia: When to Induce???
- Coagulopathy
- Fetal distress requiring emergency LSCS
- Patient refusal
73. Hazards of GA:
- Upper airway oedema: careful airway
assessment is required.
- Difficulty in cord visualisation
- Worsening of mallampatti grading
- Difficulty in laryngoscopy and intubation:
Maternal BP should be stabilized and seizure
prophylaxis should be given in view of response to
laryngoscopy and intubation. Labetalol & NTG are
commonly used acutely
74. - Fentanyl (2.5 mcg/kg), alfentanil (10
mcg/kg), lidocaine may be given to blunt
response
- MgSo4 therapy interfering with DMR and
NDMR
- Impaired hepatic/renal blood flow affecting
drug metabolism and clearance
- High risk of Aspiration
75. How to Induce??
• Prior to induction aspiration prophylaxis is
administered: 30 ml of 0.3 M of Sodium Citrate 30
min before induction
• IV lines
• Monitors
• Failed intubation kit
• Working suctions
•All drugs- GA, anti-hypertensives, anti-convulsive
76. Pre-oxygenate the patient
Pre-medicate
Induction: Rapid sequence induction using
Thiopentone 4-5mg/kg and Succinylcholine 1-
1.5 mg/kg
Intubation: sellicks manuever is maintained till
the cuff of endotracheal tube is inflated. Small
size cuffed endotracheal tube is used 6.0-6.5 ID
Maintained With: N2O:O2 (50:50) and a volatile
agent preferably Isoflurane.
77. •If the patient is on MgSo4 therapy then
neuromuscular blocked must be monitored
with peripheral nerve stimulator and dose
should be titrated accordingly
•Avoid ergot alkaloids
•Extubtion response to be pre-treated with
lignocaine or beta blockers like esmolol
•Continue anti-convulsive therapy in post op
period.
•Semiconscious patient with cerebral lesions
should be ventilated electively.
78. Regional Vs General Anaesthesia:
Epidural anaesthesia would probably be
preferred by many anaesthesiologists 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 anaesthesia with
the potential for encountering a swollen, difficult
airway and/or labile hypertension
79. General anaesthesia is a well-known hazard
in obstetric anaesthesia:
16X more likely to result in aesthetic-related
maternal mortality
Mostly due to airway/respiratory
complications
81. Preeclampsia is a multisystem disorder.
Management is supportive, delivery is the
only definitive.
Preeclampsia patients: High risk for difficult
intubation.
Hypertensive response to laryngoscopy may
lead to intracranial haemorrhage.
82. Spinal Anaesthesia not contraindicated in
severe Preeclampsia.
Eclampsia can be prevented by prophylactic
MgSO4 therapy.
Eclamptic patients should be monitored for at
least 24 hrs. Post-partum.
Magnesium sulfate is now proven as the best
medication to prevent and treat eclampsia.
Epidural analgesia for labour pain
management & regional anaesthesia for C/S
have many beneficial effects & are preferred.
83. REFERENCE:
Miller’s Anaesthesia 7th Edition
Stoelting’s anaesthesia and co-existing
disease 5th edition
Barash 6th editon
Hypertesion in Pregnancy; the american
college of OBGNY
