Obestetrics Gynecology

2011
Dr Azam's Notes in Anesthesiology

– Second Edition
Obstetrics and Gynecology
Dr. Mohammed Azam Danish

Consultant Anesthesiologist & Critical Care Specialist
www.DrAzam.com
Dr Azam's Notes In Anesthesiology 2011
-Second Edition
Dr Azam’s Notes in Anesthesiology

2nd Edition
Obstetrics and Gynecology

By
Dr. Azam
Consultant Anesthesiologist & Critical Care
www.DrAzam.com Obstetrics &Gynecology

-Second Edition
PREFACE
This book grew from notes first written in 2003 - 2004 for the students at the J J M
Medical College in Davangere.
There are many textbooks to choose from when preparing for the “Anesthesiology
examination”. The candidate suffers not from the lack of information but rather from
being inundated with it. The candidate then has the task of information sorting and data
compression to memorize and utilize all this information.
Graphic representation of data is an excellent form of data compression; figures or

drawings are frequently asked about at the viva examination, particularly since the
candidate’s understanding of a problem comes across most clearly when drawing a
figure or a using a picture. Figures are also a good way of approaching a topic.
I constructed parts of Dr Azam’s Notes in Anesthesiology for Postgraduate students

when preparing for the Anesthesiology examination and later when preparing for
tutorials.
Dr Azam’s Notes is aimed primarily at trainees in Anesthesia though more experienced

practitioners may find it useful as a refresher in recent concepts and advances
Dr Azam’s Notes is not a substitute for the major anesthesiology text books but
concentrates on principles of management of the most challenging anesthetic cases.
The format is designed to provide easy access to information presented in a concise

manner. I have tried to eliminate all superfluous material. Selected important or
controversial references are presented as well as suggestions for further reading. Some
relate more to basic principles, physiology, pharmacology, etc. – bookwork. Others are
more practical in nature, discussing the principles of anesthetic techniques for certain
high-risk situations.
Dr Azam’s Notes have been created keeping the Postgraduate needs while preparing
for the exams, and also help in his day to day practice. I am sure that Dr Azam’s Notes
will not only help him to secure highest marks but also help him to gain knowledge to
its full.

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A NOTE TO THE READER
Anesthesiology is an ever-changing field. Standard safety precautions must be followed,

but as new research and clinical experience broaden our knowledge, changes in
treatment and drug therapy may become necessary or appropriate. Readers are advised
to check the most current product information provided by the manufacturer of each
drug to be administered to verify the recommended dose, the method and duration of
administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences,

neither the author nor the publisher nor any other party who has been involved in the
preparation or publication of this work warrants that the information contained herein
is in every respect accurate or complete, and they disclaim all responsibility for any
errors or omissions or for the results obtained from use of the information contained in
this work. Readers are encouraged to confirm the information contained herein with
other sources. It is the responsibility of the licensed prescriber, relying on experience
and knowledge of the patient, to determine dosages and the best treatment for each
individual patient. Neither the publisher nor the editor assumes any liability for any injury
and/or damage to persons or property arising from this publication.

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DEDICATION
To Mohammed Shafiulla, my father, my oxygen,

companion, and best friend; for being my major pillar of
support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless
gratitude, for the sake of your children. I owe you a debt I can
never repay.
I also would like to thank my mom (Naaz Shafi), my wife

(Roohi Azam), my two lovely kids (Falaq Zohaa &
Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book.
I also thank my Colleagues Dr Rajshekar Reddy & Dr Sachin for

their support.
Finally, I would like to thank my teachers. The dream begins

with a teacher who believes in you, who tugs and pushes and
leads you to the next plateau, sometimes poking you with a
sharp stick called "truth."

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Contributions
01. Dr. Rajshekar Reddy – UAE
02. Dr. Surendra – UAE
03. Dr. Nagaraj Chandy – Hubli
04. Dr.Kusuma – Bangalore
05. Dr Sachin Doijode – London
06. Dr Chandrashekar – Bangalore
07. Dr Sidhu – Bangalore
08. Dr Ravindra B K – Bangalore
09. Dr Harshavardhan – Mangalore
10. Dr Anil Kumar – Tamil Nadu
11. Dr Mashooda – Kerla
12. Dr Anusuya – Bangalore
13. Dr Sudhir – Bangalore
14. Dr Uma – Davangere
15. Dr Rajeev – UAE
16. Dr Surendra – UAE
17. Dr Shivananda – Shimoga
18. Dr Soujanya – Bangalore
19. Dr Aslam Faris – Kerla
20. Dr Nandakumar – Tamil Nadu
21. Dr Anuradha – Bangalore
22. Dr Arun G Pai – Kerla
23. Dr Geetha – Bangalore

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Table of Contents
PREFACE .......................................................................................................................................................... 3
DEDICATION .................................................................................................................................................... 5
CHAPTER 1 - PHYSIOLOGICAL CHANGES OF PREGNANCY ............................................................................... 11
WEIGHT GAIN AND WATER METABOLISM: .................................................................................................................. 11

PLASMA PROTEIN CHANGES DURING PREGNANCY: ....................................................................................................... 12
CARDIOVASCULAR SYSTEM: ............................................................................................................................. 19
INFERIOR VENACAVAL COMPRESSION: ...................................................................................................................... 21
Compensatory Mechanism:......................................................................................................................... 21
Types of caval compression: ........................................................................................................................ 22
Incidence: .................................................................................................................................................... 22
Risk women: ................................................................................................................................................ 22
Clinical features: Maternal effects ............................................................................................................ 22
Fetal effects ................................................................................................................................................. 22
Prevention: .................................................................................................................................................. 23
HAEMATOLOGICAL EFFECTS: ........................................................................................................................... 25
Anesthetic implication: Acid aspiration syndrome: .................................................................................... 28
CHAPTER 2 - PLACENTAL CIRCULATION .......................................................................................................... 39
DEFINITION:......................................................................................................................................................... 39
CHAPTER 3 - ANESTHESIA FOR PET................................................................................................................. 46
CLASSIFICATION OF HYPERTENSIVE DISEASES IN REGNANCY: ......................................................................... 46

DEFINITION ...................................................................................................................................................... 47
DEFINITION OF PREECLAMPSIA: ................................................................................................................................ 47
DEFINITION OF SEVERE PREECLAMPSIA ........................................................................................................... 48
FACTORS CONTRIBUTING TO HYPERTENSION .................................................................................................. 51
NORMAL PREGNANCY ...................................................................................................................................... 52
PATHOPHYSIOLOGICAL CONSIDERATIONS IN PREECLAMPSIA ......................................................................... 54
OBSTETRIC MANAGEMENT .............................................................................................................................. 59
Obstetric management includes; ................................................................................................................ 59
TREATMENT OF MILD PREECLAMPSIA ............................................................................................................. 61
TREATMENT OF SEVERE PREECLAMPSIA: ......................................................................................................... 62
HELLP SYNDROME: ........................................................................................................................................... 62
MAGNESIUM SULPHATE .................................................................................................................................. 64
Mechanism of action; .................................................................................................................................. 64
Maintenance dose: ...................................................................................................................................... 65
Magnesium toxicity is prevented by maintaining; ...................................................................................... 65
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ANESTHETIC MANAGEMENT: ...................................................................................................................... 67
MONITORING ................................................................................................................................................... 68
OPTIMIZATION OF INTRA VASCULAR VOLUME STATUS: .................................................................................. 68
CHAPTER 4 - PLACENTA AND ITS CIRCULATION .............................................................................................. 78
PLACENTA AND ITS CIRCULATION: ................................................................................................................... 78

PLACENTAL CIRCULATION: ............................................................................................................................... 78
FETO PLACENTAL CIRCULATION .................................................................................................................. 79
UMBILICAL CORD OR FUNIS; ....................................................................................................................... 79
Fetal circulation;.......................................................................................................................................... 80
PLACENTAL TRANSFER OF DRUGS: ................................................................................................................... 82
Protective mechanisms to protect the fetus from drugs administered to the mother: ............................... 82
PLACENTAL BARRIER/ MEMBRANE: ................................................................................................................. 82
MECHANISM OF TRANSFER ACROSS PLACENTA ......................................................................................... 83
FACTORS AFFECTING PLACENTAL TRANSFER OF DRUGS; ................................................................................. 83
CHAPTER 5 ANESTHESIA FOR PREGNANT PATIENTS WITH CO-EXISTING DISEASES – VHD, DIABETES MELLITUS
AND BRONCHIAL ASTHMA ............................................................................................................................. 94
PATHOPHYSIOLOGY: .............................................................................................................................................. 99
PRESSURE VOLUME LOOP: .................................................................................................................................... 100
SYMPTOMS:....................................................................................................................................................... 100
MEDICAL MANGEMENT OF MS IN PREGNANCY: ............................................................................................ 102
ANESTHETIC TECHNIQUE FOR DELIVERY AND LSCS: ....................................................................................... 102
MODIFIED WHITE’S CLASSIFICATION OF DIABETES IN PREGNANCY: .............................................................. 106
Diagnosis of DM in pregnancy: ................................................................................................................. 111
CHAPTER 6 - ASTHMA IN PREGNANCY ......................................................................................................... 120
PATHOPHYSIOLOGY: ............................................................................................................................................ 120

PHYSIOLOGIC EFFECTS: ......................................................................................................................................... 120
FACTORS THAT CAN PRECIPITATE BRONCHOSPASM INCLUDE – ...................................................................................... 120
THEORIES ATTEMPT TO EXPLAIN THE PATHOPHYSIOLOGY ............................................................................ 120
CLINICAL SYMPTOMS AND SIGNS: ........................................................................................................................... 121
EFFECT OF PREGNANCY ON ASTHAMA: .................................................................................................... 121
EFFECT OF ASTHMA ON PREGNANCY ....................................................................................................... 122
PHARMACOTHERAPY: ............................................................................................................................... 122
Bronchodilator agents:.............................................................................................................................. 123
CHAPTER 7 - EMERGENCY CAESAREAN SECTION: BEST PRACTICE ................................................................ 130
TABLE: CATEGORIZATION OF URGENCY OF CAESAREAN SECTION ................................................................................... 130

Placenta praevia and accreta .................................................................................................................... 135
CHAPTER 8 - ANESTHESIA FOR CAESAREAN SECTION AND NEONATAL ACID BASE STATUS; A META –
ANALYSIS ..................................................................................................................................................... 137
DISCUSSION: ...................................................................................................................................................... 137

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FACTORS CONSIDERED IN THIS STUDY: ..................................................................................................................... 137
2. Significance of Base Excess; ............................................................................................................. 137
Other factors influencing neonatal Acid – Base balance........................................................................... 138
CHAPTER 9 - INCIDENTAL SURGERIES DURING PREGNANCY AND ITS ANESTHETIC IMPLICATIONS ............... 141
CHAPTER 10 - OBSTETRIC HAEMORRHAGE .................................................................................................. 158
Physiological anemia:................................................................................................................................ 158

MANAGEMENT OF MAJOR OBSTETRIC HAEMORRHAGE:............................................................................................... 159
CHAPTER 11 - ANTE PARTUM HAEMORRHAGE (APH) .................................................................................. 161
CAUSES:............................................................................................................................................................ 161
ABRUPTIO PLACENTAE ................................................................................................................................... 161
DEFINITION:....................................................................................................................................................... 161
MECHANISM OF COAGULATION FAILURE: ................................................................................................................. 162
Anesthetic management: .......................................................................................................................... 162
PLACENTA PRAEVIA ........................................................................................................................................ 163
DEFINITION:....................................................................................................................................................... 163
CLASSIFICATION: ................................................................................................................................................. 163
CLINICAL PURPOSE: ............................................................................................................................................. 164
Pre-disposing factors: ................................................................................................................................ 164
CHAPTER 12 - UTERINE RUPTURE ................................................................................................................. 167
TREATMENT ....................................................................................................................................................... 167

Anesthetic management: .......................................................................................................................... 167
CHAPTER 13 -ANESTHESIA FOR CAESAREAN SECTION IN APH (EMERGENCY) ............................................... 168
REGIONAL ANESTHESIA IN ANTIPARTUM HAEMORRHAGE ............................................................................................. 168

POST PARTUM HAEMORRHAGE ..................................................................................................................... 169
Causes: ...................................................................................................................................................... 169
UTERINE ATONY ............................................................................................................................................. 169
Risk factors for uterine atony: ................................................................................................................... 169
CHAPTER 14 - RETAINED PLACENTA ............................................................................................................. 171
Treatment: ................................................................................................................................................ 171
CHAPTER 15 - PLACENTA ACCRETA, INCRETA & PERCRETA .......................................................................... 173
CLINICAL FEATURES: ............................................................................................................................................ 173

Versions: .................................................................................................................................................... 173
CHAPTER 16 - ANESTHETIC MANAGEMENT OF OBSTETRIC PATIENTS FOR NON-OBSTETRIC SURGERY ......... 174
FACTORS INFLUENCING ANESTHETIC CONSIDERATIONS: .............................................................................. 174
CHAPTER 17 - LAPAROSCOPY DURING PREGNANCY..................................................................................... 182
RECOMMENDATIONS FOR SAFE LAPAROSCOPY: ......................................................................................................... 182

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LAPAROSCOPIC TUBAL LIGATION: .................................................................................................................. 183
CHAPTER 18 - AMNIOTIC FLUID EMBOLISM ................................................................................................. 187
SIGNS AND SYMPTOMS:........................................................................................................................................ 187

Pathophysiology: ....................................................................................................................................... 188
Diagnosis: Signs of symptoms. .................................................................................................................. 188
CHAPTER 19 - LABOUR ANALGESIA .............................................................................................................. 190
NERVE SUPPLY OF THE UTERUS AND THE BIRTH CANAL ................................................................................ 190
Physiological changes secondary to pain in labor. .................................................................................... 191
PAIN RELIEF IN LABOR - NON REGIONAL................................................................................................... 197
Psychological methods: ............................................................................................................................. 197
Physical methods:...................................................................................................................................... 197
CHAPTER 20 - WALKING EPIDURALS IN LABOUR .......................................................................................... 202
ADVANTAGES: .................................................................................................................................................... 202

Advantages: .............................................................................................................................................. 202
SIDE EFFECTS:..................................................................................................................................................... 202
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Chapter 1 - PHYSIOLOGICAL CHANGES OF PREGNANCY
INTRODUCTION:
The challenges presented by a parturient requiring anesthesia / analgesia or
both make the role of the obstetric anesthesiologist both challenging and rewarding.
Pregnancy is physiologic state. The reproductive age of a women begins at
menarche and ends in menopause. During pregnancy there is progressive anatomical
and physiological changes not only confined to the genital organs but also to all systems
of the body. This is principally a phenomenon of maternal adaptation to the increasing
demands of the growing fetus.
Weight gain and water metabolism:

In a normal pregnancy, there is a variable amount of weight gain. The total weight gain
averages 12 kg. it is distributed as
First trimester – 1 kg.
Second trimester – 5 kg
Third trimester – 6 kg
The total weight gain at term is distributed as
1) Reproduction weight gain =6 kg
Fetus – 3.3 kg
Placenta – 0.6 kg
Liquor – 0.8 kg
Breasts – 0.4 kg
Uterus – 0.9 kg
2) Net maternal weight gain = 6 kg
Increase in blood volume – 1.3 kg
Increase in extracellular fluid – 1.2 kg
Accumulation of fat and protein – 3.5 kg
During pregnancy, there is variable amount of retention of electrolytes-sodium,
potassium and chloride. The sodium is osmotically active and partially controls the
distribution of water. The amount of water retained during pregnancy at term is
estimated to be 6.5 liters.
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Sodium retention –
A) Is due to increased renal plasma flow and increased GFR. These both should
actually increase sodium excretion. But their action is counter acted by
increased Aldosterone secondary to Renin – Angiotensin → increased ADH.
B) Posture also affects sodium retention – upright and supine positions are both
anti natriuretic. Both these postures increase intra-neural luminal pressure and
they also causes decrease venous return to right side of the heart and this is
sensed by atrial volume receptors and further stimulates sodium retention.
Plasma protein changes during pregnancy:

Non – Pregnancy Change
Pregnant near term
Plasma protein concentration (gm/100 7 6 Decreased
ml)
Albumin (gm/100 ml) 4.3 3 Decreased (30%)
Globulin (gm/100 ml) 2.7 3 Slight increase
Albumin: globulin 1.7:1 1:1 Decreased
Total serum protein concentration decreases from 7.3 to 6.5 g/100ml
Change is primarily due to decrease in albumin concentration (from 4.3 to 3.4
g/100ml).
Globulin concentration though fall in first trimester, level rises subsequently 5-
10% above the non pregnant values.
These changes result in progressive decrease in albumin – globulin ratio that
1.7:1 to 1:1 to term.
Maternal colloidal osmotic pressure decreases in parallel with decline in serum
albumin concentration from non pregnant values of 25-26 mm Hg to 22 mm Hg
at term.
Anesthetic implication:
Transportation of patient becomes difficult.
Positioning the patient for regional procedures becomes difficult.
Location of spinous process processes become difficult.
Enlarged breast makes intubation difficult – use of stubby handle.
Single weight checking is of little value except to identify the overweight or
underweight patient. Regular weight checking should be done.
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Rapid gain in weight of more than 0.5 kg a week or more than 2kg in a month in
later months of pregnancy may be early manifestation of pre-eclampsia.
Excessive weight gain in pregnancy result in deposition of fat in anatomical
locations around airway both in pharyngeal structures and in shoulder and neck
makes access to the airway difficult from both without and within.
RESPIRATORY SYSTEM:
The functional respiratory changes of normal pregnancy are produced by interaction of
endocrinological factors with anatomical alteration in airway, thoracic cage, respiratory
muscles and cardiovascular system.
Mother must provide respiratory exchange in both in her own lungs and at placental
site.
What are the anatomical changes seen?

Diaphragm is pushed up by gravid uterus – 4 cm and hence breathing becomes
more diaphragmatic than abdominal.
Because of enlarging uterus and partly through relaxation of ligamentous
attachment of ribs results in
- Compensatory increase in A-P and transverse diameters of chest.
- Thoracic cage circumference increased by 5-7 cm.
Increased sub-sternal angle from acute to obtuse angle is seen and this change
never returns to normal.
Flaring of ribs is seen.
Chain to chest distance is decreased.
Reduction in length from apex to base of lungs reduces the negative pressure
that can be generated, especially at the base. This lead to atelectasis and closure
of small airway.
What are the physiological changes seen?

Upper airway:
Capillary dilatation occurs throughout the respiratory tract which is most severe in
third trimester.
Engorgement of nasal / oral / pharynx/ larynx mucosa.
10 fold increased difficulty in intubation is observed.
o Nasal breathing becomes difficult.
o Voice change seen due to oedema of false cords
o Small ET tube should be used.
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Repeated attempts at intubation cause further airway oedema / bleeding
Mechanism: Proposed mechanism for these changes is that increased estrogen
stimulate hyaluronic acid component of interstitial tissue and thus increase tissue
hydration and oedema. Capillaries become congested, hyperplastic and mucus gland
hypersecretes. These changes are worsened in presence of allergies, URTI and pre-
eclampsia.
Lower airway:
Maternal respiratory changes at term:
Variable Average change
Mechanics
Tidal volume → + 40%
Respiratory rate → + 15%
Minute ventilation → + 50%
Alveolar ventilation → + 70%
Dead space → No change
Airway resistance → - 36%
Total pulmonary resistance → - 50%
Lung compliance (alone) → No change
Total compliance → - 30%
Chest-wall compliance (alone) → 45%
FEV1 → No change ,
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Volumes and Capacities
Functional residual capacity → - 20%
Residual volume → - 20%
Expiratory reserve volume → - 20%
Vital capacity → No change
Closing volume → No change
Inspiratory lung capacity → + 5%
total lung capacity → 0 to – 5%
diffusing capacity → - 5%
Blood gases
Arterial pCO2 → - 10 to 20mm Hg
Arterial PO2 → + 10 mm Hg
Arterial pH → No change
S. Bicarbonate → - 4 mEq/L
Oxygen consumption → + 20%
Anesthetic Implication:
1) Elevation of diaphragm acts as restrictive effect on residual volume and

expiratory reserve volume, reducing both, so that the functional residual
capacity is decreased by 10-25% at 3`d trimester.
Decrease in FRC
Great importance to
RV by - 20%
OBG anesthetist
ERV
2) Importance - unchanged closing volume with decreased FRC leads to early small
airway closure.
This is further aggravated in supine position. Therefore reduced FRC with increased O 2
consumption in pregnancy lead to more rapid decline in oxygenation during periods of
apnea.
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(To conclude pregnant patients desaturation more quickly than non-pregnant following
apnea due to decreased FRC / increased O2 consumption / unchanged closing volume).
Decreased FRC with increased tidal volume
This result in relatively large volume of inspired air mixing with smaller volume of air in
lung. Therefore alveolar gas mixture can be altered with unusual rapidity and thereby
induction is faster.
4) Decreased FRC with increased MV during pregnancy speeds N? washout and
oxygenation while breathing with 100% O2.
Two methods of oxygenation and N2 washout have been evaluated. i.e. 3 min tidal
volume breathing (elective surgery) and 4 vital capacity breaths hyperventilation
(emergency setting).
Both have shown similar levels of arterial oxygenation during rapid sequence
intubation.
5) O2 consumption increased because of
Maternal metabolism
Fetal metabolism
o Work of breathing
6) Decreased airway resistance - progesterone induced relaxation of bronchial
muscle.
7) Blood gases - increased MV and with change in shape of thorax cause increased
alveolar ventilation.
Acid base balance:

The hyperventilation causes changes in the acid base balance. Arterial PCO2 falls from
38 to 32mmHg and pO2 raises from 94mm Hg to 105mmHg.
This facilitates transfer of CO2 from fetus to mother and O2 from mother to the fetus.
Acid base changes:

Non Pregnant Pregnancy near Change
term
Arterial PCO2 38mm Hg 32 mm Hg Diminished
PH 7.40 7.42 Slight increase
Arterial pO2 95mm Hg 105 mm Hg Increased
Plasma HCO3 26 mmol/L 22 mmol/L Decreased
O2, dissociation curve shift to right-more O2delivery to fetus.
P50 shift from 26.7 to 30.4mm Hg
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2-3 DPG concentration within maternal erythrocytes is increased.
8) Minute ventilation - In early pregnancy it is increased due to effect of progesterone
on respiratory center. In 2nd and third trimester minute ventilation is increased due
to increase in tidal volume without any change in respiratory rate.
9) Dead space - there is no change in dead space because of anatomical change in
thoracic cage shorten the airway length while at the same time there is increase, is
cross sectional area because of progesterone; induced bronchial smooth muscle
relaxation.
CARDIOVASCULAR SYSTEM:
Pregnancy converts normal female cardiovascular system into a hyperdynamic /
vasodilated / hypervolemic / hypercoagulable and hypo osmolar state.
Hypercoagulability provides reserve capacity for compensate minimize the effect of
acute blood loss that occurs at delivery.
What are differences seen on cardiac examination between pregnant and non-
pregnant women?
On X-ray - Elevated diaphragm and anatomical changes in bony thoracic cage
with lordosis shift heart anterior and to left.
Apical impulse heard in 4th intercostal space lateral to mid clavicular line.
o Loud S1, and S2
Increased splitting of mitral and tricuspid components of S1
o No change in S2.
o S3 may be heard in about 84% of parturient.
Grade I and II early to mid systolic murmur heard at left sternal border
secondary to cardiac enlargement with dilation of tricuspid annulus leading to
regurgitation (96% of patients).
10% of patients develop continuous hissing murmur due to increased mammary
blood flow. (mammary murmur) - Murmur disappears on firmly pressing
stethoscope to the chest.
o 9% of parturient show pericardial effusion.
o ECG may show left axis deviation. Maternal cardiovascular changes at
term
Maternal cardiovascular changes at term:

Variable Average change
Cardiac output → + 40%
Heart Rate → + 15-30%
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Stroke volume → + 30%
Myocardial thickness → + 4%
Systemic vascular resistance → - 21%
Blood volume → + 35%
Plasma volume → + 45%
R.B.C. volume → + 30%
Total Blood volume:

Starts to increase from 10th wk and expands rapidly to maximum of about 45%
above non-pregnant level at 3rd trim.
Total blood volume
Plasma volume (50%) RBC volume (30%)

Plasma volume increase seems to correlate with fetal size and number. Normal
singleton pregnancy is associated with an increase in plasma volume of 40-50%
but increase of nearly 100% have been recorded with triplet or quadruplet
pregnancy
o Increase in RBC volume is secondary to increase erythropoietin and
erythropoeisis secondary to stimulatory effects of prolactin, progesterone
and placental lactogen.
Since there is more increased in plasma volume than RBC volume, hematocrit
falls. This results in dilutional anemia of pregnancy. Increased plasma volume is
secondary to 100 fold rise in estrogen and progesterone which stimulate renin -
angiotensin - aldosterone system resulting in Na and water retention.
Though there is anemia -seen, O2 transport capacity is not impaired because of
Increased cardiac output
Increased PaO2
Right ward shift of O2 curve
Cardiac output:
Increased by about 40% of pre-pregnant value. Increase in CO is primarily due to
increase in stroke volume. Elevation in stroke volume is accounted by increase of
left ventricular end diastolic volume which occurs without a change of end
systolic volume, thus ejection fraction increases. this occurs without a change in
myocardial contractility.
CO = stroke volume (10-20m1 increased) and heart rate (10-15/min)
Cardiac output increases from 1e week of pregnancy: reaches peak at 24-30
weeks. Cardiac output in non-pregnant state is 4.5L/min which increase to 6.1,
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6.1, 6.26 L/min in 1st, 2nd and 3rd trimester respectively. It returns to normal
level by 6 weeks post-partum.
Principal changes during pregnancy;

Non – Pregnancy Total Change
Pregnant near term increment
Blood volume (ml) 4000 5500 1500 + 30 – 40%
Plasma volume (ml) 2500 3750 1250 + 40-50%
Red cell volume (ml) 1400 1750 350 + 20-30%
Hematocrit (whole body) 38% 32% Diminished
Anesthetic implications:
Supine hypotension syndrome:
Introduction: enlarging utero-fetal mass occupies a position anterior to the abdominal
aorta and venacava. If a parturient adopts the supine position, this mass will press on
these vessels.
Pressure of utero-fetal mass has 2 effects.
Inferior venacaval compression Aortic compression

↓ ↓
Occur earlier in pregnancy Later around 28-30 wks
around 13-16 wks gestation Gestation
Inferior Venacaval Compression:

When pregnant women assume supine position there results reduction in cardiac
output without reduction in arterial BP. This is because of venacaval compression by
gravid uterus before presenting part is fixed.
Compensatory Mechanism:
1. Venous return to the heart now occurs via vertebral venous plexus and Para-
spinal veins which empty into azygous vein and through ovarian plexus which drain
utero-placental vascular bed and enter inferior vena cava proximal to site of venacaval
compression.
2) Reflex peripheral vasoconstriction.
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Types of caval compression:
1) Concealed caval occlusion - Mother seldom experiences any symptoms because
of arterial BP is maintained by compensatory mechanism.
2) Revealed caval occlusion - In 8-15% of patients when compensatory mechanism
fails, the experience symptoms of caval compression. This is termed as overt
caval compression or supine hypertension syndrome.
Incidence:
8-15% of patients.
Risk women:
Primi gravida with strong abdominal muscles or tightly drawn abdominal skin
(Billiard ball appearance).
Gravida with large uterus - multiple pregnancies, hydraminos, PIH, obesity.
Reduced intravascular volume - Hypovolemia, dehydration, bleeding.
Inhibition of maternal compensatory mechanisms – Vasodilatory effects of
narcotics, sedatives and general anesthesia.
- Sympathetic blockade due to regional anesthesia.
Clinical features:
Maternal effects
Cardiac output may fall by 50%
Nausea / vomiting / sweating / pallor / giddiness / bradycardia / hypotension /
shock (hypotension usually does not occur 5-10 minutes of assuming supine
position).
Fetal effects
Marked decrease in uterine blood flow results in fetal hypoxia and acidosis
which change rate and rhythm of fetal heart.
Intervillous blood flow decreases by 20%
o Fetal PO2 decreases.
(Aortic compression in later pregnancy (28-30 wks) there is also associated
aortic compression at level of lumbar lordosis (L3,-L5).
Mild aortic compression seen in around 40% of parturient - narrowing of pulse
pressure, slight lowering of systemic pressure in lower limbs.
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Severe aortic compression seen in 8% of parturient - this worsens during uterine
contractions and increased risk is associated with occipital posterior position of
fetus.
Prevention:
1) Avoid supine position in later pregnancy
2) Transport the patient in complete left lateral position
3) Lateral tilt of 15°- prevents venacaval compression
4) Lateral tilt of 34° - prevents aortic compression.
5) Left lateral uterine displacement
6) Care must be taken to detect aortocaval compression during epidural insertion.
Flexing the patient may result in pressure from thighs pushing the uterus
posteriorly on the vessels of posterior abdominal wall.
7) Administer oxygen as high FIO2 as possible to reduce fetal hypoxia.
8) Fluid therapy.
Tests: Aortic compression detection
- Fall in BP in lower limbs

- Fetal distress - fast sign
- all in femoral artery pressure during uterine contraction - "Posterio effect".
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HAEMATOLOGICAL EFFECTS:
Pregnancy is associated with a hypercoagulable state
Increase in concentration of Decreased fibrinolytic activity

Coagulation factors
Fibrinogen and actors I, VII,
VIII, IX, X, XII increase
Factors XI and XIII decrease
Factors II, V remain
Unchanged
o There are fibrin split products indicating increase fibrinolytic activity.
o PT and PTT shortened by 20%.
Increased level estrogen during pregnancy cause inhibition of antithrombin-III
(antithrombin- III is a naturally occurring anticoagulant which along with
protein C and S inhibit formation of thrombin factor Xa, IXa, XIa and XIIa:
Platelets:
A study shows significant decrease in platelet counts during last S weeks of
pregnancy; however count was within normal non pregnant range. Platelet size
was increased indicating preponderance of younger platelets. This shift in profile
of platelet size supported the hypothesis of chronic intravascular coagulation
process during normal pregnancy.
Changes in blood coagulation factors:

Non pregnant Pregnancy near Change
term
Platelets (cu.mm) 18,00,000 Controversial Static or 15% reduction
observation of the count
Fibrinogen (mg%) 200-400 300-600 + 50%
Fibrinolytic activity - Depressed -
Clotting time - Unaffected -
5-6 fold. increase in risk of pulmonary embolism because
Venous stasis
Hypercoagulability
Vascular wall changes in pregnancy
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Increased coagulation factors renders pregnancy a hypercoagulable state with
an increased incidence of DVT and pulmonary embolism.
GASTRO INTESTINAL SYSTEM:

Changes occur throughout gastrointestinal tract during pregnancy i.e., there is change
in-
1) Gastric motility,
2) Gastric secretion and
3) Together with changes in oesophagus and gastro-esophageal junction
What are the change seen pregnant patient?

I) Effect of enlarging uterus
Stomach and intestine are displaced cephalad into left dome of diaphragm
Axis of stomach is rotated to right approximately by 45°
Stomach is shifted from vertical to -horizontal position and this changes the
angle of gastro-oesophageal junction causing pocketing of gastric contents and
hindering gastric emptying.
Gastric pressure is increased
II. Hormones
Progesterone - Gastric emptying is delayed because of smooth muscle relaxation
(Also because of decreased motility, which usually has stimulatory effect on GIT)
Lower oesophageal sphincter tone is reduced
Gastrin - Secreted from placenta and pyloric plants stimulate acid secretion
resulting in increased gastric volume.
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Anesthetic implication: Acid aspiration syndrome:
Introduction:
Perioperative risk of aspiration of gastric contents is not only restricted to pregnant
women but however pregnancy related changes of gastric and lower oesophageal
sphincter function increases the risk especially during labour.
Hard dictum for anesthetists:

It is always wise for an anesthetist to assume that any parturient presenting for
anesthesia will be suffering from oesophageal reflux, whether or not she has symptoms
and whether or not she has fasted. (Always consider pregnant patient - full stomach!!)
History:
Acid aspiration pneumonitis developing in pregnant patient is referred to as
MENDELSON syndrome.
First described by Hall in 1940 and later by Mendelson in 1946.
Incidence: Aspiration accounts for 1-20% of-all anesthetic deaths. Anesthesia
accounts for 10% of maternal deaths and with aspiration for 52% of maternal
deaths.
Pathophysiology: Pregnancy affects 2 sphincters
Lower oesophageal sphincter Upper oesophageal sphincter

Present between oesophagus and stomach Present between oesophagus and pharynx
This prevents regurgitation of gastric This prevents regurgitation of gastric
contents into oesophagus (Oesophageal contents from oesophagus to pharynx
reflex or pyloric or heart burn) (water brash)
Controlled by vagus nerve Controlled by voluntary in involuntary
Pressure at LOS is 15-25 mm Hg more than Pressure around 40 mm Hg
gastric pressure
What happens to these sphincters in pregnancy?

Increased intra-gastric pressure to about 30-35 mmHg by enlarging uterus
↓
Push gastric contents into oesophagus
But this is not aspirated into pharynx or lungs as the patient is conscious and UOS pressure
is 40mm Hg.
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In patients under general anesthesia or unconscious patient, UOS pressure falls to as
low as 8 mm Hg resulting in aspiration of gastric contents (Mendelson's syndrome).
Risk factors
Unconscious patient- Under GA
Lighter planes of anesthesia
During emergence of anesthesia.
Factors which delay gastric emptying time.
Pain / trauma
Narcotics / Increased ICP / Intestinal obstruction
Factors contributing to incompetence of gastro-oesophageal sphincter
Coughing and straining
Hiatus hernia
Alkaline pH.
Factors determining extend of injury:

Gastric volume > 25 ml
Gastric pH < 2.5
Particulate matter - Cause more injury than non particulate matter.
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Clinical stages:
Stage I: Profound dyspnoea / Tachypnea Bronchospasm X-ray may be normal.
Stage II: Increasing cyanosis and hypoxemia Minor X-ray finding seen.
Stage III: Profound hypoxemia with wide alveolar - arterial O2 gradient / Reduced
compliance. X-ray diffused bilateral infiltration seen.
Stage IV: ARDS
Prevention:
I) Drugs used for reduction of gastric acidity and volume of gastric contends.
Antacids - Neutralizing existing acid

Non particulate antacid - sodium citrate 0.3M of 30m] less than 30 min before
induction.
o Prokinetic drugs - Metoclopramide - 10 mg IV before induction or orally 2
hours pre operatively.
Direct inhibition of gastric secretion - Hz blockers like ranitidine. 150 mg orally
evening before or 2 hour prior to surgery.
II) Physical methods to reduce gastric volume.
Restriction of oral intake

Wide bore oral tube
III) Prevention of aspiration
Sellick's technique (cricoid pressure of 30 N)
Management:
Urgent removal of all contents from upper airway by through suctioning
Fiber optic bronchoscopy and suction should be carved out as early as possible
to remove remaining debris (no lavage - further disseminate the effects of
original aspiration).
Emergency intubation with O2 therapy
Correction of blood and fluid volume and acid base imbalance
Bronchodilator
Antibiotics/ steroids
Early shift to ICU for further management.
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RENAL:
What are the anatomical changes seen ?
Kidney becomes larger and heavier by approximately by approximately 20%
because of increased vascularization / blood volume / blood flow / water
content.
Glomerular size increases without increase in cell number.
Dilatation of calyces, renal pelvis and ureter begins in 1st trimester and well
established in 90% at third trimester. This is because of obstruction and
hormonal effects.
Mechanical obstruction seen to occur at pelvic brim
Over distention syndrome - Gross dilatation of ureter and renal pelvis may give
rise to this syndrome. Sufferers may have loin pain, radiating to groan
(Treatment - Placing patient in-'left lateral may be helpful)
What are the physiological changes?

o Renal plasma flow increases by 75% during 1" half of the pregnancy and
decreases until at term, it is approximately 50% above nom pregnant
value.
GFR controlled by:
a. Glomerular plasma flow
b. Glomerular blood pressure
c. Hydrostatic extravascular pressure in bowman’s capsule.
d. Plasma oncotic pressure
e. Glomerular capillary ultra filtration coefficient.
(Increased GFR in pregnancy to about 50% is mainly due to increase in renal plasma
flow).
Anesthetic implication
Laboratory determinants of renal function are so altered that care should be
taken when `normal; non-pregnant values are applied to pregnant women.
ENDOCRINE:
Anterior pituitary gland is slightly enlarged. It is due to hyperplasia of prolactin
secreting cells.
Hyperplasia of thyroid gland occurs. The enlargement starts at 4th month of
pregnancy and continuous till labour. It regresses in 2-3 weeks after delivery.
o There is increased thyroxine binding globulin (TBG) level.
o Total T4 and T3 level increase, free T4, and T3 level remain
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CNS:
There is a decrease in the volume of local anesthetic necessary for spinal and epidural
an aesthesia. Dose reduction should be done by 30%. Following four mechanisms are
proposed.
1) Reduced volume in epidural space facilities/ spread of giver. Dose of local
anesthetic over a wider area - cephalic spread of solution may be enhanced
because of body contour (increased pelvic width).
2) Increased pressure within the epidural space facilitates dural diffusion and
higher CSF level of local anesthetics.
3) Venous congestion of lateral foramina decreases leak of local anesthetics via
dural root sleeve.
4) Increased progesterone level causes the peripheral nerve to be more sensitive to
conduction block of local anesthetics.
ENDOCRINE
Thyroid: Hyperplasia
↓ TSH
↑ Free T4, T3
↑ Urinary Iodide Excretion
↑ TBG
Parathyroid: Hyperplasia
↓ S. Calcium
↑ Urinary Calcium
↑ PTH
↓ Calcitonin
Pituitary:↑ Hyperplasia
↑ Prolactin / GH / ACTH
↑ Oxytocin
Adrenal: Hyperplasia of Zona fasciculata
↑ Cortisol
↑ Aldosterone
MAC is decreased by upto 40% at term. Reduced requirement are seen as early
as 10-12 weeks gestation and in immediate post-partum period. It returns to
normal by 3`d day after delivery.
o Reduced enzymatic degradation of opioids at term leads to elevated pain
threshold.
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Baseline pressures in epidural space are often positive at term in contrast to
negative pressure in non pregnant state.
CSF pressure can reach 70 cm of water during bearing down efforts.
Decrease the dose of local anesthetic by 30%.
Decrease the MAC by about 40%.
Engorged epidural veins increase the possibility of placing epidural catheter in
the vein, resulting in unintentional intravascular injection.
o There is higher incidence of dural puncture with epidural anesthesia.
HEPATIC:
The hepatic function and blood flow are unchanged. Minor elevation of serum
transaminases and lactic dehydrogenase level are seen in third trimester.
o Serum albumin level is decreased, resulting in decreased colloid oncotic
pressure.
Plasma cholinesterase activity is slightly decreased, but moderate doses of
succinylcholine are metabolized easily.
Decreased release of cholecystokinin result in incomplete emptying of gall
bladder, predisposing to the formation of cholesterol gallstones.
METABOLISM:
The basal metabolic rate is raised by 25% to meet the metabolic demands of
mother, placenta and fetus.
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Oxygen consumption is 35% above the non-pregnant state. This increase is mainly in
response to metabolic needs of the fetus, the uterus and the placenta.
Oxygen consumption increases to 40% and 70% above resting level during first
and second stage of labour.
Energy is delivered in the form of ATP and these are generated form
carbohydrates and fats predominantly.
Daily energy requirements:

During last trimester 200 kcal/day extra calories are required.
This can be met by - Carbohydrates 200 g/day

Proteins 1g/kg/day
Iron 15mg
Folic acid 100 µg
Calcium 800 mg
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Glucose:
Glucose is basic substance for energy production
Hexokinase
Glucose Glucose 6-P
Glucokinase in liver
Insulin stimulates Diabetes inhibits
Pregnancy is a diabetogenic state because of following reasons

HPL / progesterone / prolactin/ cortisol – act as insulin antagonist.
Reduced activity of liver glycokinase.
Peripheral insulin resistance increased to 3 fold because of cellular and post
insulin receptor changes (after placenta is delivered insulin resistance decreases
very rapidly).
Blood glucose increased by growth hormone / glucagon / catecholamine /
thyroid hormones.
How is glucose lost?

1) Placental metabolism accounts for 60% of glucose uptake
2) Transplacental transfer of glucose depends on maternal plasma concentration
and so high glucose levels are seen after heavy meals.
3) Glucose loss from kidney is because of increased filtration and decreased
absorption secondary to increased GFR.
Placenta act as partial barrier to insulin but not to glucose.
Fetal glucose levels reflect maternal levels. If maternal hyperglycemia is present
throughout pregnancy, the fetus will be exposed to it and this result in cell
hyperplasia in fetus and hyperinsulinemia.
This may result in fetal hypoglycemia after delivery.
(therefore glucose containing fluids are not given till delivery of the fetus)
Patient with gestational diabetes do not have the capacity to increase insulin
secretion. This results in altered glycogen metabolism in fetal lungs and in turn
decreases surfactant synthesis resulting in increased incidence of RESPIRATORY
DISTRESS SYNDROME.
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Protein metabolism:
There is a positive nitrogenous balance throughout pregnancy.
The conversion of amino acid to urea is suppressed, the blood urea levels fall to
15-20mg%.
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Chapter 2 - PLACENTAL CIRCULATION
Definition:
It is a tissue at any stage of gestation which mediates the transfer- of substances to and
from fetus.
Placental circulation consists of independent circulation of blood in two systems.
1) Utero-placental circulation
2) Feto-placental circulation
Placenta: It is composed of projections of fetal tissue (villi) that lie in maternal vascular
spaces (inter villous space).
Placental membrane / Barrier consists of

1) Syncytiotrophoblast
2) Cytotrophoblast
3) Extra-embryonic mesoderm
4) Capillary endothelium.
1) Utero-placental circulation: circulation of blood through intervillous space
Total amount of blood in mature placenta = 500q

Total amount of blood in intervillous space = 150m1
Blood flow in inter villous space ,= 500-600 ml/min
Blood replaced from intervillous space = 3-4 times / min
Pressure within intervillous space
- During uterine contraction - 30-50mm hg
- During uterine relaxation- 10-15mmHg
2) Feto-placental circulation
2 umbilical arteries carry impure blood from the fetus
Fetal blood flow through placenta - 400ml/min
Uterine blood flow - 650 - 750 ml/ min (10% of CO)
50ml/min (non-pregnant uterus)
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Uterine blood flow = Uterine arterial pressure- uterine venous pressure.
Uterine vascular resistance
Anesthetic importance
IV anesthetic agents - have variable effect on utero-placental blood flow
Thiopentone and propofol - ↓ uterine blood flow by decreasing maternal B.P.
Volatile anesthetics - B.P. and consequently utero placental blood flow.
Spinal and epidural anesthesia typically do not decrease uterine blood flow
provided B.P. is maintained.
Conclusion:
Appreciation of the roles of anesthesiologist, obstetrician, pediatrician and other
personnel who care for the mother and child will facilitate the highest level of
care.
Communication between the various members of the labour and delivery team is
paramount in preventing mortality and morbidity among pregnant and newborn.
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Chapter 3 - ANESTHESIA FOR PET
INTRODUCTION
Fits occurring in pregnant women was recognized and recorded as early as 4th century
B.C. When Hippocrates described the occurrence of seizures associated with pregnancy
and resolving wit!, delivery. Eclampsia - a Greek word that translates as `Shine Forth'
implying a sudden development. Because it was recognized that albuminuria and
hypertension could precede the onset of fits, the term pre-eclampsia was coined. Pre-
eclampsia is a multi system disorder of un-known etiology, but it is unique in pregnant
women after 20 weeks of gestation.
INCIDENCE:
Hypertensive disorders occur in 6% to 8% of all pregnancies.
Incidence of pre eclampsia is 0.04% Primi gravida -10%
Multi gravida - 5%
Mortality due to hypertensive disorders in US -.15%.
CLASSIFICATION OF HYPERTENSIVE DISEASES IN REGNANCY:

1) Preeclampsia:
Minimum criteria
BP ≥ 140/90 mm Hg after 20 weeks' gestation
Proteinuria ≥ 300 mg/24 hours or ≥ 1 + dipstick
Increased certainty of preeclampsia

o BP ≥ 160/110 mg Hg
o Proteinuria 2.0 g/24 hours or ≥ 2/1 + dipstick
o Serum creatinine ≥ 12 mg/dL unless known to be previously elevated
o Platelets < 100,000/mm3
o Microangiopathic hemolysis (increased LDH)
o Elected ALT or AST
Persistent headache or other cerebra. or visual disturbance
Resistant epigastric pain
2) Eclampsia
Seizures that cannot be attributed to other causes in a woman with preeclampsia.
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3) Superimposed preeclampsia (on chronic hypertension)
o New-onset Proteinuria ≥ 300 mg/24 hours in hypertension women but no
Proteinuria before 20 weeks gestation.
A sudden increase in Proteinuria or blood pressure or platelet count <
100,000/nuxr3 in women with hypertension and Proteinuria before 20 weeks'
gestation.
4) Chronic hypertension
o BP ≥ 140/90 nun Hg before pregnancy or diagnosed before 20 weeks'
gestation not attributable to gestational trophoblastic disease.
Or
o Hypertension first diagnosed after 20 weeks' gestation and persistent
after 12 weeks' postpartum.
5) Gestational hypertension
o BP ≥ 140/9o mm Hg for first time during pregnancy

o No Proteinuria
o BP returns to normal within 12 weeks' postpartum
o Final diagnosis is made only postpartum
o May have other signs or symptoms of preeclampsia, for example,
epigastric discomfort or thrombocytopenia.
DEFINITION
Pre eclampsia is a syndrome with the features of hypertension, Proteinuria edema
occurring after 20 weeks of gestation.
Definition of preeclampsia:
Gestation: > 20 weeks
Arterial pressure: Diastolic >110 mm Hg on any one occasion. Diastolic > 90 mm
Hg on 2 or more occasions at least 4 h apart.
Proteinuria: > 300 mg in 24 hours or 2 clean catch mid stream or, catheter
specimens of urine collected at least 4 hours apart with
a) I gram albumin / liter or ≥ 2 + on reagent strip
b) 0.3 gm albumin / liter, or I + on reagent strip if specific gravity is < 1.030 and
pH < 8.
Oedema: Not essential for diagnosis.
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MILD:
B.P. ≥ 140/90 mm Hg < 160/110 mm of Hg or an increase in > 30 nun Hg in systolic B.P.
or > 15 mm Hg in diastolic B.P.
Proteinuria > 300 mg/It for 24 hours or protein conc. Of 1 gram or more per liter in at
least 2 random specimens collected 6 hours or more apart.
Generalized oedema.
DEFINITION OF SEVERE PREECLAMPSIA

1) Arterial pressure > 160 mm Hg systolic or > 110 min Hg diastolic on two
occasions at least 6 hour apart.
2) Proteinuria > 5 g in 24 hours or > 3+ on dipstick
3) Oliguria < 400 ml in 24 hour
4) Cerebral signs-headache; blurred vision or altered consciousness.
5) Pulmonary oedema or cyanosis
6) Epigastric or right upper quadrant pain
7) Impaired liver function
8) Hepatic rupture
9) Thrombocytopenia
10) HELLP syndrome.
RISK FACTORS:
1. Maternal risk factors
First pregnancy
New partner/paternity
Age younger than 18 years or older than 35 years
Past history of preeclampsia
History of smoking.
Family history of preeclampsia in a first-degree relative
Black race
Obesity (BMI ≥35)
2. Maternal medical risk factors

Chronic hypertension secondary to Pheochromocytoma or renal artery stenosis
Preexisting type I diabetes mellitus
Renal disease
Systemic lupus erythematosus
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3. Placental/fetal risk factors
Multiple gestations
Hydrops fetalis
Gestational trophoblastic diseases
Genetic risk factors
Angiotensinogen gene T235
Circulating anticardiolipin antibody
Protein S deficiency; activated protein C resistance.
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FACTORS CONTRIBUTING TO HYPERTENSION
REDUCED UTERINE PERFUSION
PRESSURE
ENDOTHELIAL DYSFUNCTION
↑ ENDOTHELIN – 1 ↓ PROSTAGLANDIN I2
↑ THROMBOXANE ↓ NITRIC OXIDE (NO)
↑ ANGIOTENSIN – II
SENSITIVITY
↓ RPF AND GFR
↓ PRESSURE NATRIURESIS
HYPERTENSION
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NORMAL PREGNANCY
PROSTACYCLIN THROMBOXANE
↓ Vasoconstriction ↓ Vasoconstriction
↓ Platelet aggregation ↓ Platelet aggregation
↓ Uterine activity ↓ Uterine activity
↑Ultra placental ↑ Ultra placental
blood flow blood flow
Endoperoxide
Aracgudibuc Acid
PREECLAMPSIA
THROMBOXANE
PROSTACYCLIN
↓ Vasoconstriction
↓ Vasoconstriction ↓ Platelet aggregation
↓ Platelet aggregation ↓ Uterine activity
↓ Uterine activity ↑ Ultra placental
↑ Ultra placental blood flow
blood flow
Endoperoxide
Arachidonic Acid
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Comparison of the balance in the biologic actions of prostacyclin and thromboxane in
normal pregnancy with the imbalance of increase thrombaxane and decreased
prostacyclin in the pre-eclamptic patient
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PATHOPHYSIOLOGICAL CONSIDERATIONS IN PREECLAMPSIA
MATERNAL FACULTY EXCESSIVE
VASCULAR DISEASE PLACENTATION TROPHOBLAST
GENETIC, IMMUNOLOGIC OR
INFLAMMATORY FACTORS
REDUCED UTERO-PLACENTAL
PERFUSION
VASOACTIVE AGENTS NOXIOUS AGENTS

PROSTAGLANDINS, NITRIC CYTOKINES
OXIDE, ENDOTHELINS LIPID PEROXIDASES
ENDOTHELIAL
ACTIVATION
CAPILLARY LEAK
VASOSPASM EDEMA PROTEINURIA ACTIVATION OF

COAGULATION
→HYPERTENSION HEMOCONCENTRATION THROMBOCYTOPENIA

→SEIZURES
→OLIGURIA
→ABRUPTION
→ LIVER ISCHEMIA
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Genetic causes
Angiotensinogen gene t235
Decrease in calcitonin gene-related peptide
Mutations in mitochondrial transfer ribonucleic acid genes
Immunological causes
Digoxin – like immunoreactive substance
Metabolic causes
Nitric oxide regulation
Erythrocyte cation metabolism
Altered calcium metabolism
50hydroxytrypatamine metabolism
Xanthine oxidase activity
Prostaglandin 12 and thromboxane
Decreased prostaglandin 12 receptor affinity
Altered estrogen and progesterone metabolism.
SYSTEMIC MANIFESTATIONS
CVS
Blood Volume
Plasma volume is 30% to 40% lower in women with severe preeclampsia than in
normal parturient of similar gestational age.
Associated with decreased plasma volume, extravascular and interstitial volume
markedly increases.
Hematocrit rises due to hemo-concentration, which results in increased
frequency of placental infarction and low birth weight.
Hemodynamic Profile
Untreated pre-eclampsia women have lower cardiac output, stroke volume and
Pulmonary artery wedge pressure (PAWP) and higher Systemic vascular
resistance (SVR) compared to normotensive parturient with hyperdynamic. Left
ventricular function.
Women with severe preeclampsia who have received various forms of treatment.
Show an elevated cardiac output normal to high PAWP and normal to elevated
SVR associated with hyperdynamic Left ventricular
The changes in CVP often do not correlate the changes in PAWP.
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Cardiogenic Pulmonary Edema
Causes are:
a) Left ventricular dysfunction in the face of severe increase in SVR.

b) Chronic hypertension.
c) Peripartum cardiomyopathy and other condition.
In a subset of women who developed cardiogenic pulmonary edema associated with

severe hypertension, elevated cardiac output, elevated PAOP, normal SVR., pulmonary
edema resulted from intrinsic volume overload in the presence of impaired left
ventricular relaxation (diastolic dysfunction). These patients respond well to diuretic
therapy.
Non-cardiogenic Pulmonary Edema

a) Increased pulmonary capillary permeability
b) Iatrogenic fluid overload
c) A reduction in plasma oncotic pressure (POP - PAWP) gradient. POP is low in
preeclampsia patients due to renal loss and impaired synthesis of albumin
(hepatic dysfunction). This low POP along with Normal PAWP narrows the POP
– PAWP gradient and increases the risk of non cardiogenic edema.
RESPIRATORY SYSTEM
Upper airway edema associated with normal pregnancy is exaggerated in
preeclampsia which might pose problems for intubation. Multiple attempts at
intubation can lead to bleeding and further worsen the condition.
o Maternal ODC is shifted to left due to decreased 2, 3, diphosphoglycerate
concentration. This along with decreased utero-placental blood flow can
interfere with maternal fetal oxygen transfer
COAGULATION ABNORMALITIES
Preeclampsia is associated with microvascular endothelial damage (a marker of
vascular endothelial damage - fibronectin is raised) and reduced levels of
antithrombin III and α2 antiplasmin resulting in enhanced clotting.
Platelet activation, platelet consumption with shortened platelet lifespan are
characteristic.
o Thrombocytopenia is seen in 15-20% of women with preeclampsia and as
much as 50% of women with severe eclampsia
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Preeclampsia is also associated with altered function of platelets.
Thrombocytopenia is due to increased platelet destruction which is autoimmune
mediated.
Quantitative and qualitative assay of platelet (bleeding time) is important while
performing regional anesthesia.
RENAL FUNCTION
Both GFR and renal plasma flow are lowered.
Structural abnormalities like swelling of glomerular endothelial cells and,
deposition of fibrin along the basement membrane and narrowing of
glomerular capillary lumen.
The extent and severity of glomerular endotheliosis correlates with protein loss.
In addition, PIH impairs renal excretion of sodium, increases total body sodium.
Oliguria is common but progression to renal failure is rare.
In pregnant women creatinine level of > 1 mg/dl and urine output < 100 ml in 4
hours period indicate substantial renal involvement
HEPATIC FUNCTION
Damage ranges from mild hepatocellular necrosis to the ominous HELLP
syndrome with potential subcapsular bleeding and risk of hepatic rupture, which
is associated with a 60% mortality rate.
Pseudocholinesterase levels are lower compared to healthy parturient, the
duration of succinylcholine and ester type of local anesthetics may be prolonged.
CENTRAL NERVOUS SYSTEM

Neurological manifestations of preeclampsia include diffuse symptoms like severe
headache, confusion, excitability, nausea and vomiting, and focal signs like blurred
vision, blindness, hyperreflexia and hemiparesis.
o Seizures indicate the onset of eclampsia
Seizures may occur due to focal ischemia from widespread vasospasm of
intracranial arteries. They may also occur due to cerebral edema due to loss of
autoregulation and can occur during sudden and severe increases in MAP.
Visual disturbances are due to vasospasm of posterior cerebral arteries or cerebral
edema in the occipital regions.
o Other symptoms are due to cerebral irritation
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UTERUS AND PLACENTA
Utero-placental blood flow is reduced due to intense vasospasm, which results in
high cadence of IUGR, small for date babies fetal loss and perinatal mortality.
Uterus is hyperemic, sensitive to Oxytocin and the placenta is often small with
areas of infarction, calcification and fibrin deposition.
o Incidence of placental abruption is significantly higher.
PREDICTION: Investigators have attempted to identify early markers of faulty

placentation, reduced placental perfusion, endothelial cell dysfunction and activation of
coagulation. But all these attempts have resulted in testing strategies with low
sensitivity for the prediction of preeclampsia.
a) Any rise in Bp after 20 week of gestation.

b) Mean Arterial pressure greater than 90 mm of hg in 2nd trimester.
c) Angiotensin II infusion: Angiotensin II is infused in a stepwise fashion until there
is a 20 mm Hg rise in diastolic blood pressure. Women requiring less than 8 ng/
kg/min of angiotensin 11 had a positive predictive value of developing
preeclampsia of 20 - 40%.
d) Roll over test: women who developed hypertensive response increase of
diastolic pressure of 20 mm Hg induced by assuming the supine position.
After lying laterally recurs bent, later developed hypertension due to pregnancy.
Test is done between 28 and 32 weeks of pregnancy.
e) Raised serum uric acid levels: > 5.9 mg/dl (due to decreased renal orate
excretion) at 24 weeks of gestation might predict the subsequent development of
preeclampsia.
f) Reduced urinary calcium excretion in mid pregnancy might predict the
development of preeclampsia.
PREVENTION
a) Although in 1986, Waltenburg acid co-workers reported that, a low dose aspirin
(60 mg) given at 28 weeks of gestation reduced the incidence of preeclampsia
due to selective suppression of thromboxane synthesis by platelets and sparing
of epithelial prostacyclin production, the CLASP (Collaborative low dose aspirin
study) demonstrated that it is ineffective in preventing preeclampsia.
b) Fish oil supplementation (omega =3 fatty acid) which result in predominant
production of PG12 (vasodilation) which might lead to vasodilation.
c) Since, low dietary calcium is associated with pre-eclampsia, calcium
supplementation may result in moderate decrease in the risk of preeclampsia.
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d) Studies have shown that, antioxidant therapy with vitamin C and E has reduced
the incidence of preeclampsia.
Complications of PIH
Neurologic Hepatic
Headache Impaired function
Visual disturbances Elevated enzymes
Hyperexcitability Hematoma
Seizures Rupture
Intracranial hemorrhage Renal
Cerebral edema Proteinuria
Pulmonary Sodium retention
Upper airway edema Decreased glomerular filtration
Pulmonary edema Renal failure
Cardiovascular Hematologic
Decreased intravascular volume Coagulopathy
Increased arteriolar resistance Thrombocytopenia
Hypertension Platelet dysfunction
Heart failure Prolonged partial thromboplastin
time
Microangiopathic hemolysis
OBSTETRIC MANAGEMENT
Optimal management involves a team approach. Early involvement of the
anesthesiologist allows for proper pre-operative assessment, monitoring and decision
making regarding choice of analgesia and anesthesia.
Obstetric management includes;

1. Laboratory investigates on
2. Seizure prophylaxis
3. Treatment of hypertension
4. Decision regarding the mode and timing of delivery.
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LABORATORY INVESTIGATIONS
Test Rationale
Hemoglobin and hematocrit Haemoconcentration supports diagnosis of
preeclampsia and is an indicator of severity.
Values may be decreased, however, if
hemolysis accompanies the disease
Platelet count and bleeding time Thrombocytopenia suggests severe
preeclampsia
Quantification of protein excretion Pregnancy induced hypertension with
proteinuria should be considered
preeclampsia (pure or superimposed) until
it is proved otherwise.
Serum creatinine level Abnormal or rising serum creatinine levels,
especially in association with oliguria,
suggest severe preeclampsia.
Serum uric acid level Increased serum uric acid levels suggest the
diagnosis of preeclampsia
Serum transaminase levels Rising serum transaminase values suggest
severe preeclampsia with hepatic
involvement
Serum albumin, lactic acid dehydrogenase, For women with severe disease, these values
blood smear, and coagulation profile indicate the extent of endothelial leakage
(hypoalbuminemia), presence of hemolysis
(lactic acid dehydrogenase level increase,
schizocytosis, and spherocytosis), and
possible coagulopathy, including
thrombocytopenia.
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TREATMENT OF MILD PREECLAMPSIA
Mild Preeclampsia
Immediate
Hospitalization
> 37 weeks Maternal Evaluation < 37 weeks

Fetal Evaluation
Persistent hypertension
Persistent Proteinuria
Abnormal lab tests
Abnormal fetal growth
Unreliable patient
> 40 weeks Favorable

Yes No
cervix
Fetal jeopardy
Visual disturbances
Persistent headaches Keep in Ambulatory Management
Hospital Frequent evaluation
Magnesium Hospitalize if condition

Delivery changes
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TREATMENT OF SEVERE PREECLAMPSIA:
All women with this diagnosis are admitted to labour room.
a. Those women with gestational age beyond 35 weeks are delivered within 24
hours. Those women with 33-35 weeks gestation receive steroids to accelerate
fetal lung maturity and are then delivered.
b. Women with resistant hypertension or maternal and fetal deterioration are also
delivered within 24 hours regardless of gestational age and fetal lung maturity.
c. Seizure prophylaxis with magnesium sulfate and blood pressure control should
be done.
HELLP SYNDROME:
Variant presentation of severe PE/Eclampsia.
A combination associated with high maternal and perinatal morbidity and mortality.
Incidence - 2 to 12%
70% - Ante partum
30% - Post partum.
Diagnosis
o Usually near tern
o Patient may present with nonspecific symptoms such as malaise, nausea
and vomiting and right upper quadrant pain.
o Hypertension and Proteinuria may not be present in 20- 30% of cases.
Diagnostic Criteria Include
1. Hemolysis
o Abnormal peripheral smear
o Increased serum bilirubin (>1.2 mg/dl).
2. Elevated liver enzymes

o AST/SGOT > 70 IU/ltr
o LDH > 600 N /, Ltr
3. Low platelet count: <100000 / Cu.mm

Differential Diagnosis Include:
Viral hepatitis
o Gall bladder disease
o Acute fatty liver of pregnancy
o Kidney stones
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Gastroenteritis
o Peptic ulcer disease
o Thrombotic thrombocytopenic purpura.
Patients with a diagnosis of HELLP syndrome should be immediately transferred
to a tertiary care center for further evaluation and treatment.
Definitive treatment of the disease is - immediate delivery of the fetus.
Glucocorticoid therapy should be started in patients with ITELLP syndrome as it
increases maternal platelet count decreases ALT and LDH, increases maternal
urine output and decreases the potential risk of epidural hematoma in regional
anesthesia.
Patients with immature fetuses are also given glucocorticoids and are delivered
48 hours later.
Dosage of Dexamethasone
Ante partum Postpartum
In patients with platelet count > 1 lakh IV 10 mg IV/ 12hrly x 2 doses followed by 5mg
dexamethasone 6mg every 6 hrly for 4
th IV / 12 hrly x 2 doses.
doses. The above regimen is used to accelerate
In patients with platelet count < 1 lakh reversal of HELLP syndrome
In patients with platelet count 1-1.5 lakh
with eclampsia and epigastric pain
In patients with platelet count 1.5 lakh,
severe hyper tension and fulminant disease
High dose protocol is given IV
Dexamethasone 10 mg every 6th hrly for 2
doses and 6mg at 6 hr intervals for
additional 2-5 doses depending on maternal
laboratory values
II) Betamethazone 12mg IM every 12th hourly for 2 doses
Seizure prophylaxis:
Prophylaxis for convulsions should be-started with signs of cerebral irritability such as
headache, visual disturbances, epigastric pain or hyperreflexia. Following single
eclamptic convulsion, prophylaxis to prevent further convulsions with magnesium
sulphate should always be instituted, unless there are major contraindications.
Hypertension alone is not necessarily an indication for anticonvulsant therapy,
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convulsions may occur at moderately elevated blood pressures and blood pressure
alone is a poor predictor of the likelihood of occurrence of a convulsion.
MAGNESIUM SULPHATE
The evidence for the use of magnesium sulphate in eclampsia is strong and there is less
support for prophylactic or therapeutic role in preeclampsia as the proportion of
women with preeclampsia who progress to eclampsia is very small and side effects of
treatment must be born in mind.
Mechanism of action;
It is a cerebral vasodilator and prevents seizures by preventing cerebral ischemia. It
may prevent seizures by blocking the excitatory NMDA receptor. Magnesium depresses
both central and peripheral nervous systems. The cardiac conduction system and the,
contraction ability of myocardial, uterine and vascular smooth muscles are inhibited
due the direct action of magnesium ion on the cell membrane.
Dose Initial-: 2-6 g (20% solution) IV over 5-10 min
Maintenance: 1-3 g/h IV
Alternative: 5 g IM in each buttock (10 g total) initially. 5 g
IM q4h maintenance
Contraindications Documented hypersensitivity; heart block; Addison disease;
myocardial damage; severe hepatitis
Interactions Concurrent use with nifedipine may cause hypotension and
neuromuscular blockade; may increase neuromuscular blockade
with aminoglycosides and potentiate neuromuscular blockade
produced by tubocurarine, vecuronium, and succinylcholine (ACTS
SYNERGISTICALLY WITH MUSCLE RELAXANTS AND SO THE DOSES
OF muscle relaxants SHOULD BE DECREASED.); may increase
CNS effects and toxicity of CNS depressants, betamethasone; may
increase cardiotoxicity of ritodrine
Fetal effects It rapidly crosses placenta with both ionized and unionized cord
blood levels parallel those in maternal blood. It is found to decrease
short term fetal heart rate variability, FFIR acceleration, with high
maternal levels of this ion in newborn may exhibit decreased muscle
tone, respiratory depression and apnea.
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University of Tennessee guidelines for intravenous magnesium sulfate administration;
Give 30 ml of 20% magnesium sulfate (6g) in 100 ml of 5% dextrose over 10-15
minutes period.
Maintenance dose:
Add 20 g of magnesium sulfate in 1000 ml of D5 and give intravenously at a rate of 100
ml/hr (2gm/hr), obtain a serum magnesium level 4-6 hours later and adjust the rate of
infusion to keep serum magnesium level between 4.8 – 9.6 mg/dl. If serum magnesium
levels are not available, dose is adjusted according to the patellar reflex and the urine
output in previous 4 hours period.
Magnesium toxicity is prevented by maintaining;

Urine output of at least 30 ml/hr.
Deep tendon reflexes.
Respiratory rate of at least 14/min.
Pitchards guidelines for INTRAMUSCULAR Magnesium Sulfate Administration to

Patient with Pre-eclampsia
IV loading dose (only for patients with eclampsia)

Dilute 8 ml of 50% magnesium sulfate solution (4g) with 12 mil of sterile water or use
20 nil of a 20% solution (4g) and give intravenously in a 3-5 minute period.
IM loading dose: Administer 10 ml of 50% magnesium sulfate solution deeply in the
outer quadrant of each buttock. The IM dose should immediately follow IV dose in
patients with convulsions.
Maintenance dose: Give 5 g (10 ml of 50% solution) deep by IM injection in alternative
buttocks every 4 hours if (1) patellar reflex is present (2) urine output has been at least
100 ml during proceeding 4 hours (3) respiratory rate is normal (at least 14/min).
Continue maintenance dose until 24 hours postpartum.
CAUTION:
Anticonvulsants like diazepam or barbiturates produce significant maternal and
neonatal sedation and respiratory depression.
c) Phenytoin:
Although this drug was widely used in the past for the prevention and control of
eclamptic convulsions, recent evidence no longer supports its use. Phenytoin was used
with a loading dose of 15-25 mg/kg given slow IV never exceeding a rate of 25 mg/min
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followed by a second dose of 500 mg IV 12 hours after the end of initial infusion.
Currently available data suggest that magnesium is a more effective anticonvulsant in
women with preeclampsia.
Control of hypertension: Pregnant patients should be started on anti hypertensive
therapy if the systolic blood pressure is greater than 160mrn Hg or the diastolic blood
pressure is greater than 100mmHg. Hydralazine is the most widely accepted drug to
treat hypertension. The other drugs and their benefits are details in the following table.
Drug Mechanism Dose/route Onset/durati Advent ages Disadvantages
of action on of action
Methyldopa Alpha- 250 mg per oral Somnolence,
adrenergic bid/tid; not to dry mouth,
receptor exceed 3 g day caution in liver
blocker disease and
renal disease
Hydralazine Direct 5-10 mg bolus IV 20-30 minutes Easy to Slow onset
vasodilation 20mg in 500ml IV / 2 hours administer no tachycardia
of arterioles infusion equipment no decreased
special placental blood
monitors flow
maintains
cardiac output
Labetalol Beta-1 and 10-20 mg IV upto 1-2 minutes / Increased Large
alpha blocker 1-3mgkg 2-3 hours placental blood variations in
flow rapid effective dose
onset caution in
asthma and
COPD
Nitroprussid Arteriolar 0.05-10µgkg hr IV Less than 1 Rapid onset Unstable
e dilator infusion in 5% minute / few and offset solution
dextrose minutes potent no ill Increase ICP
effects on fetus cyanide toxicity
tachyphylaxis
invasive BP
monitoring is a
must
Sodium Venodilator 5-50 min IV Less than 2 Rapid onset IV pump to
nitroglycerin infusion minutes/ few and dissipation administer
minutes increase ICP
decrease
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cardiac index
Nifedipine Calcium 10-30 mg per oral 15 to 40 Uterine muscle Tachycardia
channel t.i.d not to exceed minute s/ 3 to relaxant headache
blocker 120-180 mg/day 6 hours increases renal
blood flow
Interaction of antihypertensive drugs with anesthetic drugs;
Beta blockers;
Compensatory baroreceptor reflex is blunted.

Compensatory response to acute hemorrhage are lost and hypotension and
myocardial depression can be pronounced.
Resting heart rate is low and bradycardia may become resistant to usual
treatment.
If the patient is also diabetic, warning signs of hypoglycemia are blunted.
Myocardial depression of inhaled and injected drugs becomes additive.
Calcium channel blockers;

Myocardial depression and peripheral vasodilation produced by inhalational
agents is exaggerated.
Antagonism of neuromuscular blockade may be impaired (decreased release of
presynaptic ach).
Administration of magnesium and calcium channel blocking agent can cause
severe hypotension and myocardial depression.
ANESTHETIC MANAGEMENT:
Pre-anesthetic preparation:
Anesthesiologist should be involved early in these patients because of their expertise in

pain management and hemodynamic manipulation. Pre-anesthetic evaluation includes
a. Assessment of the airway: The pharyngo laryngeal edema present in normal
pregnancy is exaggerated in preeclampsia. Supraglotic edema and swelling of the
tongue can make visualization of the vocal cords difficult or impossible. Airway
examination should also include; receding mandible, limited ability to extend the neck,
abnormal dentition, TM joint dysfunction, poor mouth opening and Mallampatti scoring
system.
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b. Hemodynamic status: The characteristic changes that occur in preeclampsia
pose an increased risk for abruption and maternal haemorrhage. Evaluation of
the blood pressure control and fluid status is essential.
c. Fetal condition: It is reflected by abnormal fetal surveillance and fetal heart rate
changes.
d. Evaluation of renal function, coagulation status, intravenous access and current
medications should be done.
MONITORING
Basic intrapartum monitoring of a parturient with preeclampsia include
1) HR
2) BP – NIBP
3) Pulse Oximetry
4) Temperature Monitoring
5) Urine output
6) Neuro muscular monitoring
7) Capnograph
8) Hourly examination of deep tendon reflexes.
9) Echocardiography.
OPTIMIZATION OF INTRA VASCULAR VOLUME STATUS:

Aim of fluid therapy is:
a) To increase CVP & PCWP to normal range 4-6 cm H2O & 5l mm of Hg

respectively.
b) To increase urine output to l ml kg hr
Controversy exists between colloid and crystalloid as the condition is
complicated by both low colloid oncotic pressure and capillary leak predisposing
them to risk of non cardiogenic-pulmonary edema.
The current recommendation is to administer crystalloids at the rate of 12ml/kg hr and
altering subsequently fluid therapy according to CVP, PCWP, and Urine. Output Pre-
hydration should be given in smaller volumes (200-300ml) boluses.
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LABOUR AND VAGINAL DELIVERY DECISION WHEN TO DELIVER
Severe hypertension unresponsive to antihypertensive
Renal dysfunction with progressive oliguria
Liver dysfunction
Development of coagulopathy
Onset of eclampsia
Evidence of severe fetal compromise
Rapidly deteriorating maternal health.
Invasive Hemodynamic Monitoring:

Central Venous Pressure versus Pulmonary Artery Catheter:
Controversy exists regarding the use of CVP catheter / PA catheter.
Correlation between CVP and pulmonary capillary wedge pressure is unreliable

when the CVP reading is greater than 6 cm of H2O.
Some favor PA monitoring because of the additional information it provides
regarding biventricular function, SVR and for the ability to measure Cardiac
output using the thermodilution technique.
Pulmonary Artery Catheter:

Indications
a. Severe hypertension unresponsive to conventional antihypertensive therapy.
b. Pulmonary edema.
c. Persistent oliguria unresponsive to fluid change.
Indication for arterial catheterization:
1. Poorly controlled blood pressure.

2. Need for frequent blood gas determinations.
3. Use of potent vasodilator such as nitroprusside /nitroglycerine.
4. Severe obesity making non-invasive monitoring difficult.
ANALGESIA FOR LABOR AND VAGINAL DELIVERY

Epidural Analgesia:
Advantages:
o Excellent pain relief and patient comfort.
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o Attenuation of hypertensive response to pain.
Reduces the maternal circulating catecholamine concentrations thereby
improving blood pressure control.
It improves utero-placental blood flow.
Once in place, it can provide effective anesthesia for labor/vaginal delivery/
cesarean section.
Epidural opioids provide excellent postoperative analgesia.
Patient Preparation:
1. Check a recent coagulation profile, at least a platelet count
A sequential testing is done to know whether or not a downward trend exists.

If the platelet count is between 70,000 to 1,00,000/Cu.mm, but stable and there
are no clinical signs of coagulopathy, one can proceed with epidural anesthesia.
If ultrasound examination suggests abruption or fetal death or if the patient has
liver dysfunction (HELLP syndrome), PT, PTT and fibrinogen concentration
should be checked.
2. Evaluation of volume status
A hematocrit >36% or U.O.P. < 0.5 ml/kg/hr suggests significant volume depletion.
In such patients, invasive hemodynamic monitoring should guide the fluid therapy.
Patients who are not severely volume depleted, need little crystalloid before the
induction of epidural block
Whatever may be the preloading, local anesthetic should be given slowly allowing
adequate time to respond if hypotension develops.
Controversy exists regarding the use of epinephrine containing local anesthetic
solutions in preeclampsia since these parturient have a exaggerated hypertensive
response to accidental intravascular injection or excessive systemic absorption
resulting in an exaggerated heart rate/blood pressure response. Epidural
epinephrine may also impair utero-placental blood flow. If a decision is taken to
include epinephrine in local anesthetic solution, lowest possible concentration
should be used and small incremental doses are given.
After the insertion of epidural catheter, patient is placed comfortably with good
uterine displacement.
o Induction is done with 3-5 ml increments of 0.125% Bupivacaine with
Fentanyl 1- 2 µg/ml or sufentanyl 0.5-lltg/ml. A total of 10-20 ml should be
sufficient.
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o Maintenance is done with continuous infusion/ PCEA with 0,0625% to
0.125% bupivacaine with fentanyll-2 µg/ml or sufentanyl 0.3-0.5 µg/ml at a
rate of 10-15 ml/hr.
Other Choices:
PCA with fentanyl / Nalbuphine / Meperidine can provide better labor analgesia than
intermittent bolus injection. But these techniques are associated with an increased use
of Naloxone during initial neonatal resuscitation.
ANESTHESIA FOR CAESARIAN SECTION - GENERAL CONSIDERATIONS

18 gauge line is a must.
iv fluid should not consist of dextrose and water alone because of danger of
water intoxication
Continuous infusion of o-4tocin has a marked antidiuretic effect.
Rapid infusion of dextrose containing solutions may cause neonatal
hypoglycemia and hyper blirubinemia.
Regional Anesthesia:
Advantages: Over general anesthesia
Smooth control of blood pressure (no hypertensive response due to intubation)

Maintenance of utero-placental perfusion while general anesthesia with thiopental
and succinylcholine reduces intervillous blood flow.
Ability to administer local anesthetics and IV fluids incrementally and thus
minimizing the possibility of fluid overload and pulmonary edema.
Patient will be awake and neurological status can be monitored.
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Comparison of the advantages and disadvantages of general vs. regional anesthesia
in pre-eclampsia.
Regional anesthesia
Advantages Disadvantages
Airway No intubation response. No risk of No control
failed intubation
Convulsions No active control risk of
convulsion
Drugs & No sedative drugs Risk of convulsions risk of
Technique high block
Speed Spinals: quick 5-10 mins Epidural: slow 20-30 mins
Blood pressure Less instability doe to lower Risk of hypotension (Less
control Catecholamines with epidural)
Coagulation No airway instrumentation & bleeding Risk of hematoma
Utero-placental Maintained improves utero-placental
circulation blood flow with epidural
General anesthesia
Advantages Disadvantages
Airway Control Exaggerated intubation response.
Increased risk of failed intubation
Convulsions Control
Drugs & technique Maternal awareness. Fetal depression
Speed Fast < 5 mins
Blood pressure control Less hypotension Increased catecholamines increases in
BP, PAWP, CVP with intubation
Coagulation No spinal hematoma Risk of airway haemorrhage
Utero-placental Impaired uterine and intervillous blood
circulation flow
Epidural anesthesia:
Before the insertion of epidural catheter, following should be assessed:

Coagulation status
Volume status and need for invasive hemodynamic monitoring.
Once the decision to insert an epidural catheter is taken, an additional 18 G IV cannula
should be inserted separate from medical infusions. Hydrate with 20ml/kg or until CVP
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is positive or PAOP is 5-10 mm Hg. If there is no invasive monitoring, U.O.P should
guide volume therapy.
After the insertion of epidural catheter, a test dose of 0J% bupivacaine 2-3 ml is injected
to detect subarachnoid catheter location and wait for 3-5 minutes. After confirming that,
it is in epidural space, 0.5% bupivacaine in 3-5 ml increments given carefully assessing
hemodynamic changes in between each increment of drug. Additional IV fluid or
vasopressor is given as needed. One can add 10 µg fentanyl to raise the level of sensory
blockade to Ta. Women who have been receiving local anesthetic opioid solution for
labor analgesia may need less drug at caesarian section.
The relationship between platelet count, platelet activity and the risk of epidural
hematoma following owing epidural puncture is not known. There is no evidence of
increased, epidural bleeding from low dose aspirin use in pregnancy.
Thrombocytopenia is common in PET, but bleeding time is probably not a useful test.
Since other coagulation defects (PT, P"IT) rarely occur in PET in the absence of
thrombocytopenia, platelet count alone has been proposed as a screening test.
Thromboelastography is currently being re-evaluated. For many women with PET the
very great benefits from regional analgesia far outweigh the small (but potentially
serious) risk of epidural hematoma formation.
RISKS AND BENFITS OF EPIDURAL ANALGESIA IN LABOUR IN WOMEN WITH SEVERE

PRE-ECLAMPSIA
Risk Benefits
Hypovolemia unmasked epidural Prevents aspiration syndrome reduced
hematoma revealed inferior vena caval stress response (catecholamines) maintains
occlusion / improves utero-placental blood flow
prevents administration of systemic opioids,
which may further depress the mother of
fetus available for operative delivery if
necessary
Spinal Anesthesia:
Although still very controversial, there is growing support for the use of spinal
anesthesia for abdominal delivery of the fetus. A small prospective randomized study of
pre-eclamptic women did not find significant blood pressure differences between spinal
and epidural anesthesia, Fluid requirements were however higher with spinal
anesthesia. When a patient does not have an epidural catheter in place or there is no
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sufficient time to place one because of non-reassuring fetal heart rate patterns, spinal
anesthesia may be preferable to general anesthesia.
VASOPRESSORS FOR TREATING INTRAOPERATIVE IIYPOTENSION:
Ephedrine increases B and has a positive inotropic effect. Because it does not have
determental effects on uterine blood flow, it is widely used in hypotensive parturient
patient. Its mixed alpha and beta adrenergic effects cause an increase in arterial BP
that is secondary to increased cardiac output and increased total peripheral
resistance.
Mephentermine is preferably avoided in these patients, as it severely increases the
SVR and also causes cerebral vasospasm and reduces placental blood flow.
o Phenylephrine is now becoming the drug of choice in spinal hypotension
especially if patient has tachycardia. It cause transient bradycardia. Large
doses should be avoided as large doses can cause overshoot hypertension.
GENERAL ANAESTIIESIA:
It is indicated in
a. Maternal haemorrhage
b. Sustained fetal bradycardia
c. severe thrombocytopenia
d. Patient refusal
Once the decision has been made to proceed with general anesthesia, the
anesthesiologist faces following challenges.
1. Potential difficulty of securing the pre-eclamptic airway

2. Potential aspirations of gastric contents
3. Hypertensive response to direct laryngoscopy and airway manipulation
4. Effect of MgSO4 on neuromuscular transmission and uterine tone.
The generalized edema in preeclampsia involving tongue, pharynx and larynx makes
landmark identification difficult resulting in difficult intubation. A knowledge of failed
intubation procedures and alternative techniques (light warm, fiberoptic
bronchoscope) is a must. When a difficult intubation is anticipated on initial
examination, it is better to proceed with awake oral fiberoptic intubation.
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The transient but severe hypertension that may accompany tracheal intubation can
result in cerebral haemorrhage or pulmonary edema which are the two most common
causes of maternal death in preeclampsia. The goal is to reduce the MAP by 20% or a
blood pressure of approximately 140/90. Following have been used with success
1. Labetalol: Upto 1 mg/kg
2. Nitroglycerine: IV bolus dose is given, but may not be effective in volume
expanded patients.
3. Short acting opioids like – fentanyl – 100 µg
4. Lidocaine – 1.5 mg/kg
5. Continuous infusion of SNP
6. Calcium channel blockers
7. Magnesium sulfate.
The anesthetic effects of magnesium are predictable and are usually managed without
difficulty.
Technique:
Before administering general anesthesia, aspiration prophylaxis with a non-particulate
antacid should be given. In operating room, patient should be placed in left uterine tilt
position and pre oxygenation with 100% oxygen for 3-5 minutes is done. Rapid
sequence intubation with cricoid pressure is done using thiopentone (4-5mg/kg) and
succinylcholine (1-1.5nmg/kg) and with a small size tube (6-6.5mm). Anesthesia is
maintained with oxygen + nitrous oxide + a volatile halogenated agent (isoflurane/
desflurane) before delivery. After delivery of the neonate, the volatile agent should be
decreased. Narcotic and benzodiazepines can be administered. During extubation,
emergence hypertension should be treated with agents used at induction.
POST PARTUM CONSIDERATIONS

Monitoring should continue for at least 24 hours after delivery or until diuresis
begins. Spontaneous diuresis should begin by 24 hours. If no diuresis and if
cardiac filling pressures are raising, small dose of diuretics.
In HELLP syndrome, he upward trend in platelet count should be apparent by 3 rd
postpartum day. Resolution to a count above 1,00,000/cu.mm may require 5-6
days.
o 14-27% of eclamptic seizures occur after delivery. MgS04 may have to be
continued for at least 240 hours or until diuresis.
Postoperative analgesia can be provided with epidural preservative free opioids,
patient controlled intravenous opioid analgesia or patient controlled epidural
opioids.
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A strict intake output chart should be maintained for at least 24 hours or until
diuresis develops. A total intake of 75 ng/lir should not be exceeded until the
patients begin to mobilize her extracellular water.
o Patients have to be changed from short term (parenteral) to long term
(oral) blood pressure medication. these patients may need treatment for
hypertension for upto 6 weeks after delivery.
POSTOPERATIVE ANALGESIA
o COX-2 Inhibitor
Conventional post cesarean analgesic management (IV/IM NARCOTIC AGENTS).
Epidural analgesia
Subarachnoid narcotic analgesia
Patient controlled analgesia
CSE Anesthesia.
CONCLUSIONS:
Although the specific etiologies of preeclampsia and eclampsia are not known,
investigations shed light on identifying certain patients at risk for this disease.
Preeclampsia affects multiple maternal organ systems including (especially) the
fetoplacental system. Drug interactions and altered maternal anesthetic responses must
be anticipated. Knowledge of the disease and its therapy is therefore crucial to the
anesthesiologist faced with the care of the pre-eclamptic or eclamptic patients. Optimal
anesthetic care should potentially include all the modalities of acute resuscitative and
critical care that would be applied to any critically ill patient.
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Chapter 4 - PLACENTA AND ITS CIRCULATION
Elizabeth Ramsey (1985), The preeminent researcher of past half century in
investigations of placental circulation, stated that "the modern era in the understanding
of the placenta would not have commenced while scientists still thought that maternal
and fetal vessels were anatomized end to end". The various significant physiological and
circulatory changes associated with pregnancy, child birth and the prenatal
pharmacology which involves the pharmacological process of drug absorption,
distribution, biotransformation and excretion, not in one individual but in two, the
mother and fetus, which are of fundamental importance to the anesthesiologist.
Ignorance of these changes has, in the past resulted in potentially serious errors in the
conduct of regional and general anesthesia and in misinterpretation of observations
made on the pregnant women.
PLACENTA AND ITS CIRCULATION:

Gross Anatomy (In Brief):
The placenta at term, is almost a circular disc with a diameter of 15-20cm and
thickness of about 2.5 cm at its centre. It thins off towards the edge.
It is spongy in consistency and weighs about 500 gms, the proportion to the
weight of baby being roughly 1:6 at term and occupies about 30% of the uterine
wall.
It presents two surfaces fetal and maternal and a peripheral margin.
PLACENTAL CIRCULATION:
Placental circulation consists of independent circulation of blood in two systems.
Utero-placental circulation.
Fetoplacental circulation
Utero-placental circulation:
It concern with the circulation of maternal blood through the intervillous space.
A mature placenta has a volume of 500ml of blood, 350ml is occupied in the villi
system (fetal capillary system) and 150 ml in intervillous space.
Blood flow in the intervillous space at term 500-600m1/min.
Maternal blood enters the intervillous space through spiral arteries, after
piercing the basal plate randomly at numerous sites.
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o These spiral arteries which are branches of uterine artery, are about 120-
200 in number, which run perpendicular to uterine wall and blood leaves
through spiral veins, which run parallel to uterine wall and drain into
uterine vein.
The arrangement of spiral arteries is such that there is gradual funneling of
spiral arteries which reduces the pressure of the blood before it reaches the
intervillous space. It thus increases the blood flow.
After bathing the external microvillus surface of chorionic villi, the maternal
blood drains back through venous orifices in the basal plate and enters the
uterine veins.
During uterine contraction, the veins are occluded but the arterial blood is forced
into the intervillous space. While relaxation facilitates venous drainage. This is
brought about by the fact that the spiral arteries are perpendicular and veins are
parallel to the uterine wall.
Thus during contraction, larger volume of blood is available for exchange even
though the- rate of flow is decreased. The blood in the intervillous space usually
does not clot due to presence of fibrinolytic enzyme activity of trophoblastic.
FETO PLACENTAL CIRCULATION

o The two umbilical arteries which carry the impure blood from fetus to
placenta. They enter the chorideal plexus, underneath the amnion, each
supplying one half of placenta.
The umbilical arteries break up into small branches which enter the stems of
chorionic villi. Each in turn divides into primary, secondary and tertiary vessels
of corresponding villi.
Maternal and fetal blood streams flow side by side, but in opposite direction.
This counter current flow facilitates material exchange, between mother and
fetus.
The fetal blood flow through placenta is about 4QOml/min. This is mainly
facilitated by pumping action of heart.
UMBILICAL CORD OR FUNIS;

This forms the connecting link between the fetus and the placenta through which
blood flows to and from the placenta.
Characteristics: It extends from the fetal umbilicus to the fetal surface of
placenta. About 50cm in length (30-100cm) diameter of about 1.5cm (1-2.5cm).
its thickness is not uniform due to presence of nodes or swellings at places
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known as false knots which are due to dilatation of umbilical veins or local
collection of wharton’s jelly.
Structure; the constituents of the umbilical cord when fully formed.
1. Covering epithelium
2. Wharton’s jelly-Protection to umbilical vessels.
3. Blood vessels – 2 arteries and 1 vein.
The arteries are derived from the internal iliac arteries of the fetus and carry the venous
blood from fetus to the placenta.
Initially there are two umbilical veins of which right disappears by 4th month. Carries
oxygenated blood from the placenta to the fetus.
Fetal circulation;
Fetal circulation differs from adult circulation in several ways. Almost all differences
are attributable to the fundamental difference in the site of gas exchange. In the adult,
gas exchange occurs in the lungs. Where in the fetus, exchange of gases and nutrition is
provided by the placenta.
The umbilical veins carrying the oxygenated and nutrient bearing blood from
placenta, (SaO2 80% and PaO2 40mrnHg) enters' the fetus at the umbilicus and
runs along the free margin of the falciform ligament to the liver.
In the liver, it gives of branches to left lobe of liver and receives deoxygenated
blood from portal vein.
The greater portion of oxygenated blood mixed with some portal venous blood;
bypass the liver through ductus venosus to enter inferior vena cava (IVC), which
carry deoxygenated blood from lower parts of the body.
o This mixture continues through the IVC to the right atrium.
In right atrium, most of the blood (Sa02 75%) from IVC is directed towards the
foramen ovale by the valve of IVC and crista dividens and passes into left atrium.
Here it is mixed with small amount of venous blood returning from lungs
through the pulmonary veins. The left atrial blood is passed on through the
mitral opening to the left ventricle.
o The, remaining amount of blood in right atrium i.e., from SVC and IVC
passes through the tricuspid opening into right ventricle (SaO2 25%).
During ventricular systole, the left ventricular blood is pumped into ascending
and arch of aorta and distributed by their branches to the heart, head, neck, brain
and arms. The right ventricular blood with low O2 content is discharged into the
pulmonary trunk.
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Since the resistance in the pulmonary arteries during the fetal life is very high,
the main portion of blood passes directly through the ductus arteriosus into the
descending aorta bypassing the lungs where it mixes with the blood from the
proximal aorta.
The mixed and deoxygenated blood via the descending aorta, leaves the body by
way of two umbilical arteries (SaO2 50 to 60%, Pao220 to 25mmHg) to reach, the
placenta, where it is oxygenated and gets ready for recirculation.
The mean C.0 in fetus is about 255ml/kg/min, which is about three times that of
an adult at rest. This high C.O helps to compensate for the low O2 content of fetal
blood i.e. by the high heart rate and low systemic vascular resistance.
The placenta receives the largest amount of combined ventricular output i.e.
about 55% and has the lowest vascular resistance in fetus.
CHANGES OF THE FETAL CIRCULATION AT BIRTH:

The hemodynamics of the fetal circulation undergoes profound changes soon after birth
due to –
o Cessation of placental blood flow and
o Initiation of respiration.
The following changes occur is the vascular system:

a. Closure of the umbilical arteries: Functional closure is almost immediate
preventing even slight amount of the fetal blood to drain out. Actual closure takes about
2-3 months. The distal parts form the lateral umbilical ligaments and the proximal
parts remain open as superior vesicle arteries.
b. Closure of umbilical veins: The obliteration occurs little later than the arteries,
allowing few extra volume of blood i.e. 80-100ml to be received by the fetus from
placenta. The ductus venosus collapses followed by fall in pressure in IVC and right
atrial pressure. The umbilical vein forms ligamentum teres and the ductus venousus
forms ligamentum venosum.
c. Closure of the ductus arteriosus: Within few hours of respiration, the muscle
wall of the ductus arteriosus probably in response to rising O2 tension of blood or due to
redaction of prostaglandins. The functional closure o£ the ductus may occur soon after
the establishment of pulmonary circulation. The anatomical obliteration takes 1-3
months and becomes ligamentum arteriosum.
d. Closure of foramen ovale: This is caused by an increased pressure of the left
atrium combined with a decreased pressure on the right atrium due to fall in PVR and
rise in S.VR. Functional closure occurs soon after birth but anatomical closure occurs in
about 1 year time.
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Within one or two hours following birth the C.O is estimated to be about 500 ml/min,
and the heart rate varies from 120-140/min.
PLACENTAL TRANSFER OF DRUGS:

Protective mechanisms to protect the fetus from drugs administered
to the mother:
a. Maternal liver metabolism: Drugs administered to the mother are metabolized
in the liver to non active metabolites thus, the actual concentration of drug delivered to
the fetus is less and is dependent on the maternal hepatic microsomal enzyme induction
or inhibition.
b. Placenta: The placenta serves as a semi permeable membrane and site of
metabolism. Drugs administered to the mother will have to cross this barrier to reach
the fetus.
c. Others: Drug uptake by fetal liver may protect the fetus against occurrence of
high drug levels in the fetal heart and CNS. Fetal microsomal enzyme activity, even
though it is less than in adult have significant levels of cytochrome P45Q and NADP
cytochrome C reductase as early as 14 weeks of gestation. This suggests that even the
premature human fetus has the capacity to metabolize various drugs.
Dilution of drug in umbilical venous blood in the right atrium and shunting of blood
across the foramen ovale and ductus arteriosus which also modify fetal drug
distribution.
PLACENTAL BARRIER/ MEMBRANE:

Inspite of close proximity of fetal and maternal blood, intermixing of blood never occurs
i.e. the two are separated by tissue, called placental membrane or barrier, consisting of
the following.
In early pregnancy, it consists of

Syncytiotrophoblast
Cytotrophoblast
Basement membrane
Connective tissue stoma of villus
Endothelium of fetal capillary wall.
Near term
Attenuation of syncytial layer
Sparse Cytotrophoblast
Fetal capillaries get distended and almost fill the villus.
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During early pregnancy thickness of membrane is about 0:025nun but near term it may
become thinner to the extent: of O'.002inm. These thinner zones of membranes take
part in materno-fetal exchange of nutrients, gases and drugs. The total surface area at
term – 10m2.
MECHANISM OF TRANSFER ACROSS PLACENTA

a. Simple diffusion: Most of the respiratory uses and anesthetic agents cross the
placenta by simple diffusion. The rate of diffusion across the placenta is according to
FICK'S LAW;
Q/t = KA (Cm – Cf) D
Where,
q/t = Rate of diffusion per unit time
K = Diffusion constant
A = Area available for diffusion
Cm = concentration in mother
Cf = Concentration in fetus
D = thickness of placental membrane.
b. Active transport; the molecule is transferred at the cost of energy in the form of
ATP e.g.: aminoacid, vitamins, some ions (calcium and iron).
c. Facilitated diffusion: E.g.: glucose
d. Pinocytosis (Cell eating) e.g.: Large molecules such as Immunoglobulins and
plasma proteins.
e. Breaks or leakage: Breaks in the placental membrane and mixing of maternal
and fetal blood are probably responsible for Rh sensitization.
FACTORS AFFECTING PLACENTAL TRANSFER OF DRUGS;

A maternally administered drug before it reaches the fetus must traverse the placenta.
This process is affected by drug factors, maternal factors, placental factors and fetal
factors.
1. Drug factors:
a. Lipid solubility: Compounds with high lipid solubility or large, lipid water
partition coefficients, readily cross the placenta. E.g. Thiopentone, benzodiazepines and
local anesthetics highly lipid soluble. Glycopyrrolate, scoline, NDMR are poorly HPW
soluble.
b. Molecular weight: Diffusion varies inversely with molecular weight.
Compounds with mole. weight < 600 readily cross the placenta, whereas those > 1000
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do not. Most anesthetic agents have mole. weight ranging between 250 - 400 and thus
cross the placenta.
c. Degree of ionization: Only unionized substances are transferred across the
placenta, substances that are ionized are not transferred except when the maternal -
fetal ratio is very high E.g. Scoline.
d. Protein binding: Highly protein bound drug do not cross the placenta for Eg:
Scoline, bupivacaine have limited transfer due to their high: protein binding.
e. PKA (pH at which drug 50% ionized): If PKA of drug is near physiological pH,
more drug is and greater transfer. E.g. Thiopentone with PKA 7.6 is more ionized and
hence greater transfer.
2. Maternal factors:
a. Total dose of the drug: Increasing the total dose of the drug regardless of the
route of administration increases he maternal arterial blood concentration. As a result
fetal drug concentration increases as well.
b. Injection site: IV route administration results in the highest peak concentration
of drug.
c. Adjuvants: for E.g.: Local anesthetics with epinephrine in epidural anesthesia,
the epinephrine reduces the peak maternal local anesthetic concentration by 30% to
50% by reducing LA absorption. Hence avoiding increased placental transfer and
adverse effect on fetus.
d. Maternal metabolism and excretion: This also reduces drug concentration in
blood perfusing the intervillous space. In conditions like preeclampsia, due to impaired
maternal hepatic metabolism and decreased hepatic blood flow, the concentration of
anesthetic agents in maternal blood are on the higher side. This may increase the
placental transfer.
e. Maternal protein binding: Protein binding of the drug reduces the placental
transfer. The reduction in the maternal level of plasma proteins, such as can occur in
severe, preeclampsia, can enhance fetal exposure to anesthetic agents.
3. Placental factors:
a. Placental blood flow: The transfer of highly lipid soluble drugs is directly
proportional to placental blood flow. If placental blood flow is decreased secondary to
maternal hypotension, cardiac failure, aortocaval compression and during uterine
contraction, the. drug transfer is also reduced. Certain drugs may directly affect
placental circulation and in turn produce changes both in drug transfer and transfer of
O2 and nutrients to the fetus Eg: Few opioids [morphine, pethidine and hallucinogen
substance such as LSD cause placental vasoconstriction.
b. Placental aging: As pregnancy advances, thickness of placental membrane
decreases and increased permeability to drugs.
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4. Fetal factors
a. Fetal circulation: Major portion of drug entering' fetal circulation is extracted
and metabolized by enzyme systems in fetal liver before it reaches fetal brain
and heart. This is one of the protective mechanism in fetus.
b. Fetal pH
↓ Fetal pH
(Fetal hypoxia & acidosis
More drug is ionized ↓ protein binding ↑ CO2
Incapable of transfer ↑ Free fraction of drug ↑ CBF & Increase
Across placenta Permeability of BBB
“Ion trapping”
↑ amount of drug available for uptake in the fetal brain and heart.
Categories of drugs used in pregnancy: Used by food & Drug administration (FDA)
1980
Class A : Controlled studies how no risk.
Class B : No rich in animal studies or no risk supported by controlled
human studies.
Class C : animal studies indicate a risk but no human studies available.
Class D : Evidence of fetal risk but benefits overweight risk.
Class E: Evidence of high risk of fetus, which overweight befits.
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Effect of anesthetic agents on pregnancy:
Indicatives agents:
o Thiopentone: approved as FDA pregnancy category C
It is characterized by high lipid solubility, ↑ protein binding low ionization and
low molecular weight. Therefore it rapidly crosses the placenta.
After single maternal i.v. dose the drug can be detected in umbilical venous blood
within 30 sec.
Despites rapid placental transfer, APGAR score and neurobehavioral scores are
satisfactory with does 4-5 mg/kg because fetal brain contractions get limited due
to
o Dilution at the liquor – most of drug first passes through the liver where it
other gets cleared by fiver of gets dilated by blood from the level
extremities and viscera.
Rapid Redistribution – which decreases the drug concentration in maternal
blood, so that thiopentone gets redistributed across the concentration gradient
back to the mother.
Ketamine: FDA pregnancy category D.
It is more lipid soluble and less protein bound than thiopentone.
It crosses the placenta rapidly, does not produce neonatal depression if dose is <
1.5 mg/kg
In doses 1.5 -2 mg/kg – low APGAR scoring and hypertonic.
In 1st trimester – cranial anomalies (rare)
Safe dose 1-1.5 mg/kg
3. Propofol; FDA Pregnancy category B
Transplacental transfer is rapid because it is lipid soluble, largely unionized drug

with a low molecular weight.
Safe dose – IV induction 1.5 – 2.5 mg/kg. continuous infusion < 100 µg/kg/min
associated with neonatal depression – low APGAR score, muscular hypotonus
and transient somnolence.
4. Benzodiazepines: FDA pregnancy category D
In obstetrics, they are used mainly as sedatives and anticonvulsants. Diazepam and
midazolam are two most frequently used drugs.
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a. Diazepam:
It is highly lipid soluble and has low molecular weight (285), hence crosses placenta
rapidly.
1st trimester – clefts, craniofacial asymmetry, cardiac defects and pyloric
stenosis.
During labor – it can decrease beat fetal heart rate variability, when used in large
doses i.e. . 0.5 mg/kg it produces fetal hypotonia, lethargy, feeding problems, low
APGAR, hypothermia. (Floppy baby syndrome).
Safe dose - < 5 mg i.v.
b. Midazolam:
Water soluble, shorter half life, less local irritation than diazepam.
At physiological pH, its structure changes and it becomes lipid soluble.
Placental transfer is less compared to diazepam hence preferred over diazepam.
At induction doses (0.2 mg – 0.3 mg/kg) it produces more adverse effects,
compared to thiopentone.
Safe dose i.e. 2 mg iv.
b. Inhalation Agents:
a. Nitrous oxide:
Most popular inhalation agent in obstetric anesthesia. The low blood solubility of
N2O renders maternal uptake and recovery very rapid.
In concentrations of 50%, it does not cause maternal and fetal cardiovascular or
respiratory depression and does not affect uterine contractility. In higher
concentrations and for prolonged periods can cause fetal respiratory depression and
acidosis.
Increased incidence of gestational defects and spontaneous abortion rate due to
prolonged exposure to N2O, as in female personnel working in operation theatre.
Increased incidence of neurological defects- (Anencephaly) in fetus due to
inactivation of Vit B12 which in turn effect on folate metabolism.
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b) volatile anesthetics
Are highly lipid soluble, unionized and low in molecular weight, thus cross
placenta freely.
The blood gas partition coefficient is lower in neonates than in adults, therefore
they are eliminated rapidly when respiration is established.
When used in love concentration (Halothane 0,5%, isoflurane. 0.75%, enflurane
1%) they does not cause neonatal depression. No change in uterine tone,
response to Oxytocin.
At higher concentrations (Halothane 2% enflurane 1.5%, isoflurane 1.25%) they
reduce maternal BP and cardiac-output, decreased uterine blood flow, neonatal
hypoxia and acidosis. Myometrial relaxation leading to increased incidence of
postpartum hemorrhage.
Muscle relaxant; FDA Pregnancy category C

Muscle relaxants have low lipid solubility and highly ionized at physiological pH
(quaternary ammonium compounds). They are highly protein bound, thus does not
cross placenta easily. Insignificant placental transfer occurs when used in clinical doses.
a. Succinylcholine:
In clinical doses, (1.5 – 2mg/kg) have no effect on the neonate; its rapid
hydrolysis by pseudocholinesterase limits its transfer.
In high doses i.e. >6mg/kg, enough placental transfer can occur to cause neonatal
paralysis.
In patients with very low pseudocholinesterase level and\or abnormal
pseudocholinesterase, prolonged maternal and neonatal paralysis can occur (due
to increased amount of unmetabolized drugs hence placental transfer).
b) Non depolarizing muscle relaxants
Fetal blood concentration of NDMR's following maternal administrations around

5-10%.
With clinical doses (vecuronium and pancuronium 0.0.5 mg/kg, atracurium 0.5
mg/kg, rocuronium 0.6 mg/kg, mivacurium 0.15 mg/kg). there are no adverse
neonatal effects.
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OPIOIDS: FDA Pregnancy category D
The opioids are potent analgesics mainly used during labour analgesia (Intraoperative
analgesia)
All opioids cause a variety of side effects in the mother like respiratory
depression, orthostatic hypo tension, nausea, vomiting, pruritis and delayed
gastric emptying.
They are highly lipid soluble and rapidly crosses placenta and are capable of
producing neonatal respiratory depression and changes in the neurobehavioral
of the child.
Spinal and epidural delivery of opioids diminishes the usual„ side effects
observed with systemically and parenterally administered opioids.
a) Morphine:
Causes greater maternal and neonatal depression and FHR - variability

compared to other opioids.
Due to its longer duration of action, its primary metabolite morphine -3-
glucronide, cleared slowly and may therefore accumulate in the fetus.
Maternal addiction causes withdrawal symptoms in neonate - trembling,
hypertonia, irritability, high pitched cry.
b) Pethidine:
More commonly used opioid in obstetrics, fetal exposure to pethidine is higher

2-3 hours after administration to mother.
Administered during 1st trimester – polydactyly and hypospadiasis.
Administered during labour – changes in FHR variability, low APGAR, changes in
O2 saturation and convulsions.
c) Fentanyl:
Rapid placental transfer,

A dose of 1µg/kg given iv to mother within 15 min. of caesarean delivery
considered safe i.e. no effect on APGAR scoring and neurobehavioral score.
d. Tramadol:
Is a weak opioid agonist
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In therapeutic doses (50-100mg iv), it has fewer side effects and especially less
respiratory depression.
Opioid antagonist: Naloxone:

Crosses placenta and detected in fetus in mins.
Indicated to reverse the respiratory depression in neonates exposed to narcotics
in utero.
Dose – 0.01 mg-0.1 mg/kg (im/iv/ETT/sc. Onset of action is rapid and lasts for 4
hrs.
Should not be given prophylactically to mother to antagonize the neonatal
effects, since it reverses maternal analgesia.
Local anesthetics; FDA Pregnancy category B

Local anesthetics are weak bases and non ionized hence readily cross placenta.
In clinical situations in which fetus is likely to be acidotic, the dose of local
anesthetics must be reduced or avoided because “ion trapping” may occur in
fetal circulation. (i.e. they cross the placenta in non-ionized form and become
ionized which cannot re-enter the maternal circulation).
a. Lignocaine:
It is less protein bound and rapidly cross placenta.

May cause fetal bradycardia and acidosis when used in large doses as in epidural
anesthesia.
When used in continuous epidural analgesia – tachyphylaxis, drug accumulation
and increased placental transfer.
B. Bupivacaine:
Limited placental transfer due to high protein binding (>30%)

When used for epidural labour analgesia and caesarean section, dose not
produce any adverse effects on the neurobehavioral score of the newborn. It
also does not have any detrimental effects on the utero-placental circulation,
provided that long hypotensive periods are avoided.
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c) Ropivacaine:
Has a lower lipid solubility and high protein bindings as compared to

bupivacaine.
Less cardiotoxic than bupivacaine, hence has a increased margin of safety.
Does not produce any adverse effects in the neonate, even in high doses (upto
25ml of ropivacaine 0.7%).
Anticholinergics and anticholinesterases:
a. Atropine: FDA pregnancy category C
Crosses placenta rapidly and reaches equilibrium with maternal blood within 10
mins.
Can cause transient fetal tachycardia in high doses.
b. Glycopyrrolate – FDA Pregnancy category B.
Since it is a quarternary ammonium compound (ionized) poorly crosses the

placenta and does not cause fetal tachycardia.
c. Neostigmine – FDA Pregnancy category C.
Quarternary ammonium compound

Although neostigmine is ionized at physiological pH, the low molecular weight
about 223 is low enough to cause placental transfer. In high does, >5mg, may
result in fetal bradycardia.
Effect of maternal alcoholism and smoking on pregnancy.
A. Alcohol-FDA pregnancy category D.
Ethyl alcohol is a potent teratogenic.

Fetal alcohol syndrome is usually seen among children of women who drink
more than 3 ounces of absolute alcohol daily throughout pregnancy. Lesser
amounts may be associated with a variety of less severe manifestations in
children.
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No safe level for maternal drinking during pregnancy has been established.
Fetal Alcohol syndrome:

Congenital anomalies; Brain defects, cardiac defects and spinal defects.
Craniofacial anomalies: Absent to hypopiantic philtrum, broad upper lip, flattened
nasal bridge, micrognathia microphthalmia, short nose.
Others: Prenatal and postnatal growth retardation, mental retardation, behavioral
disturbances.
b. Smoking: Maternal smoking in a does related fashion, is associated with
increased frequency of spontaneous abortion, low birth weight. Preterm labour,
perinatal mortality and placental abruption.
Immediate effects like increase in maternal heart rate, blood pressure, fetal heart rate,
increase in placental vascular resistance, increase in fetal aortic and umbilical vein
blood flow.
No major congenital anomalies were detected, but associated with placental changes
very early in pregnancy like increased placental calcification, thickening of villous
membranes and trophoblastic layers.
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Chapter 5 ANESTHESIA FOR PREGNANT PATIENTS WITH CO-EXISTING
DISEASES – VHD, DIABETES MELLITUS AND BRONCHIAL ASTHMA
INTRODUCTION:
Pregnant woman who has cardiac disease presents complex medical problems, because
Normal pregnancy produce cardiorespiratory symptoms which mimic cardiac
disease.
Circulatory changes during pregnancy may mask cardiac disease in a previously
asymptomatic woman.
Circulatory changes during pregnancy may aggravate pre-existing cardiac
disease.
Pre-existing cardiac disease can affect both mother and the fetus.
Circulatory changes of pregnancy which affect parturient with valvular heart disease.
Hemodynamic Change during Change during Change during
parameter normal pregnancy labour and postpartum
delivery
Blood volume ↑ 40-50% ↑ ↓
Heart rate ↑ 10-15 beats /min ↑ ↓
Cardiac output ↑ 30-50% above ↑ 50% addition ↑ initially with ↑ pre
baseline load then ↓ with
diuresis
Blood pressure ↓ 10 mm Hg ↑ Return to baseline
Stroke volume ↑ 1 and 2
st nd ↑ 300-500 cc per ↓
trimester slightly ↓ contraction
3 trimester
rd
Systemic vascular ↓ ↑ Returns to base line

resistance
Pulmonary ↓ ↑ Returns to baseline
vascular resistance
Colloid osmotic ↓ ↓ Returns to baseline
pressure
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Effect of cardiovascular drugs on pregnancy
Drug Fetal adverse effects

Warfarin Cross placental barrier; fetal hemorrhage
Heparin None reported
Digoxin Low birth weight
Quinidine Toxic dose may induce premature labour
Procainamide None reported
Disopyramide May initiate uterine contractions
Lidocaine High blood level may cause fetal acidosis
Mexilitine Fetal bradycardia, IUGR, low APGAR score, neonatal
hyperthyroidism
Flecainide Reported fetal death
Propafenone Non reported
Adenosine None reported, use during first trimester limited
Amiodarone IUGR, prematurity, hypothyroidism
Calcium channel blocking Fetal distress due to maternal hypotension
agents
Hydralazine Non reported
Organic nitrates Fetal heart rate deceleration and bradycardia
ACE inhibitors Skull ossification defect, IUGR. Premature delivery,
anemia, limb contractures
Diuretic agents Impairment of uterine blood flow and danger of
hyponatremia, bradycardia.
Classification of cardiac disease and pregnancy:

NYHA Classification of functional impairment;
Class I : Asymptomatic
Class II : Slight limitation of physical activities; comfortable at rest
Class III : Marked limitation with less than ordinary activity causing fatigue,
palpitation, dyspnea, or angina.
Class IV ; symptomatic at rest.
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Classification of valvular heart lesions according to maternal, fetal and neonatal
risk .
Low maternal and fetal High maternal and fetal risk High maternal High neonatal
risk risk
Asymptomatic aortic stenosis Severe aortic stenosis with or Reduced left Maternal age <
low mean outflow gradient without symptoms ventricular systolic 20 yr or > 35 yr.
(<50mm Hg) with normal left function (LVEF <
ventricular function 40%)
Aortic regurgitation of NYHA Aortic regurgitation with NYHS Previous heart Use
Cass I or II with normal left class III IV symptoms failure anticoagulant
ventricular systolic function therapy
throughout
pregnancy
Mitral regurgitation of NYHA Mitral regurgitation with Previous stroke or Smoking during
class I or II with normal left NYHA class III or IV symptoms transient ischemic pregnancy
ventricular systolic function attach
Mild moderate mitral stenosis Mitral stenosis with NYHA Multiple
(valve area > 1.5 cm2, gradient Class II, III, or IV symptoms gestations
< 5 mm HG) without severe
pulmonary hypertension
Mitral valve prolapse with no Aortic valve disease, mitral
mitral regurgitation or with valve disease, or both, resulting
mild to moderate mitral in severe pulmonary
regurgitation and with hypertension (pulmonary
normal left ventricular hypertension) (pulmonary
systolic function pressure > 75^ of systemic
pressures)
Mild to moderate pulmonary Aortic valve disease, mitral
valve stenosis valve disease, or both, with left
ventricular systolic dysfunction
(EF < 40%) maternal cyanosis
reduced functional class status
(NYHA class III or IV).
Table: Modified From Reimold and Rutherford
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Recognized risks:
An inability of the mother to meet the physiologic demands of pregnancy.
An inadequate supply of well oxygenated blood for fetal nourishment.
A worsening of maternal disease.
Infection, hemorrhage or thromboembolism.
Diagnosis and management during pregnancy:

Signs and symptoms
Serial measurement of a host of noninvasive, objective parameters can provide
important information.
a. Intermittent measurements of peripheral oxygen saturation with pulse-oxymeter
may provide early indication of heart failure.
b. Vital capacity measurement: Detect increase in blood volume that produce
pulmonary vascular engorgement.
c. Electrocardiogram and holter monitors: Can detect ischemia, arrhythmias
conduction defects and axis deviations.
d. chest radiograph: Exposes the mother to a maximum of 80 m rad of radiation, 50m
rad to chest, 5m rad to the gonads better to avoid.
A dose of 0.5 rad is recommended maximum radiation exposure to the pregnant
women. Some suggested even 10-rad exposure is safe.
Radionuclide techniques expose the mother to 500 to 800m rad better to avoid.
Cardiac cauterization exposes the patient to as much as 28,000 m rad of
radiation.
e. Flow directed right heart and pulmonary artery catheterization without
fluoroscopy: Can assess valvular function and chamber pressures.
f. Two dimentational contract echocardiography: Can evaluate valve and ventricular
function.
Management at term
Good communication between the obstetric anesthesiologist and obstetrician is
necessary.
Invasive monitoring
Antibiotic regimens
Anticoagulation
Termination of pregnancy
Route of delivery
Anesthetic management
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Maternal fetal priorities
Effect of cardiac and uterine therapeutic modalities should be discussed before
parturition.
Antibiotic prophylaxis for endocarditis:

Prophylaxis is optional for high risk patients undergoing vaginal delivery.
Prophylactic measures:
Ampicillin 2g IM or IV.
Plus Gentamycin 1.5mg/kg IM or IV (not to exceed 120mg) 30 min before start of
the procedure.
Plus Ampicillin 1g IM or IV or amoxicillin 1g, orally 6 hours after the procedure.
For patient allergic or resistant to ampicillin or amoxicillin.
Vancomycin 1g IV over 1 to 2 hours.
Plus gentamycin 1.5 mg/kg IV or IM 30 minutes before the start of procedure.
Anticoagulants; Certain patients must receive anticoagulants patient with cardiac
valve disease with chronic atrial fibrillation and a history of systemic emboli.
Warfarin: Crosses the placenta and increases danger of abnormal fetal
development. Congenital malformations, Abortion, stillbirth and hemorrhage.
Risks may be minimal with low doses (5mg or less daily)
Heparin: Is the preferred Anticoagulant.
Risks:
Maternal thrombocytopenia
Thromboembolism
Osteoporosis
Rare hypersensitive reactions
Retroplacental hemorrhage
Abruptio placenta
Heparin is safe for the fetus.
Low – molecular weight heparin (LMWH):
Advantage:
Less platelet aggregation
Does not cross the placenta
Reduced association with osteoporosis
Does not prolong activated thromboplastin time (APTT).
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At term discontinue heparin therapy 24 hours before induction and avoid
warfarin throughout.
If spontaneous labour occurs, carefully monitor aPTT.
If a PTT prolonged near delivery, consider protamine sulfate unless the patient
receiving LMWH.
Specific VHD:
Mitral stenosis: Is the most common acquired valvular disease in pregnancy
(Rheumatic origin)
Is associated maternal mortality of 10%
In patient NYHA functional class III and IV this increased > 50%.
Obstructive lesion usually develops 10-20 years after the initial infection. It may
develop after 6 years.
It may not tolerate the normal cardiovascular changes of pregnancy.
Sudden life-threatening pulmonary oedema may occur in previously
asymptomatic patients.
Symptoms occur in 25% of affected gravida.
Pathophysiology:
Normal mitral valve area; 4 to 6 cm2
Stenotic lesions are graded as follows
Mild : 1.5 to 2.5 cm2
Moderate : 1 to 1.5 cm2
Severe : Less than 1 cm2
Critical (tight) : Less than 0.6 cm2
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Pressure volume Loop:

Reduced preload
Diastolic compliance curve shifted (Ch. Under filled ventricle)
Little preload reserve, to difficult to adjust to a demand for greater output (In
pregnancy)
Symptoms:
Shortness of breath, dyspnea on exertion, orthopnea.
Recurrent bronchitis.
Hemoptysis
Systemic embolism
Acute pulmonary oedema may occur with the onset of atrial fibrillation or acute
pulmonary infection.
Physical findings:
First heart sound and mitral opening snap are loud with pliable value, faint with
calcified value.
Diastolic murmur: Low –frequency apical murmur is longer with more severe
stenosis.
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Investigations:
ECG:
Left atrial enlargement or atrial fibrillation
Right axis deviation
Rarely right ventricular hypertrophy
Broad notched ‘P’ wave in lead II (P Mitrale).
Chest radiograph: Not usually advocated because of radiation hazard. Increased
cardiac size, especially left atrium, calcification in mitral value, pulmonary congestion.
Straight left heart border. Kerly’s B lines.
Echocardiogram: left atrial dilation. Decreased left ventricular performance.
Characteristic value changes. Orifice – size, severity and pliability of valve, LV size, LA
size, clots in left auricle.
Hemodynamic changes: Diastolic gradient between pulmonary artery occlusion
pressure and left ventricular diastolic pressure.
Doppler flow study: Assessment of mitral value area.
Cardiac decompensation:
Most likely to occur at times of maximal increase in heart rate, systemic blood
volume, cardiac output and pulmonary blood volume.
Occurs with transvalvular pressure gradient greater than 25mm Hg.
Accompanying events – Atrial fibrillation, paroxysmal tachycardia, pulmonary
vascular congestion, infarction.
Late stage mitral stenosis:

Elevated pulmonary pressures leads to persistent pulmonary hypertension and
irreversible pulmonary arterial hyperplasia.
Right heart failure
Peripheral oedema
Hepatomegaly
Ascites
Distended neck veins
Ventilation perfusion mismatching, which worsens in the trendlenberg position.
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MEDICAL MANGEMENT OF MS IN PREGNANCY:

It should be directed to the
Reduction of blood volume
o ↓ Na intake
o Diuretic therapy
↑ left ventricular diastolic filling by
↓ heart rate towards lower margin of normal (60-70 beats/min)
o Bed rest
o Beta blockers
If atrial fibrillation: Anticoagulation is mandatory.
If mother life is at risk at any point of time in pregnancy.
Emergency intervention
o Balloon Valvuloplasty (PTMC)
o Closed mitral valvotomy
o Cardiac surgery – (valve replacement)
Closed mitral valvotomy does not carry an increased risk for mother and the
fetus.
Cardio pulmonary bypass, especially in first trimester may result in –
miscarriage, mental retardation.
To avoid these complication.
- Timing to cardiac intervention – second trimester
- (First trimester – organogenesis, third trimester – full blown
physiological changes).
- Short perfusion time
- High Flow rate for optimal perfusion should be attempted.
CPB has no higher risk for mother.
Patient with mitral stenosis without complication should generally be allowed to
enter into labor spontaneously at term.
ANESTHETIC TECHNIQUE FOR DELIVERY AND LSCS:

Preanesthetic evaluation:
Assess severity of disease as per NYHA classification of functional impairment as
described earlier.
Investigation: Hb TC, DC, ESR, ASO titer, aPTT (if on anticoagulants)
Specific investigations; should be evaluated as described earlier.
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Antibiotic prophylaxis: should be considered as explained before.
Anticoagulants: If on anticoagulants; it should be stopped 24 hrs before.
Premedication: 10mg diazepam night before surgery and 5mg IM 30 to 45min
before surgery.
Monitoring:
Use all available non invasive cardiovascular monitors like
Pulse
NIBP
Oxygen analyzer
Pulse oxymeter
Capnography
ECG
Special monitoring:
CVP monitoring for patient with significant symptoms.
Systemic and pulmonary artery catheters for most severe cases like pulmonary
hypertension.
Continues ECG
Greater risk of circulatory overload arises during the first 48 hours after delivery as the
contracted uterus displaces blood in to the systemic circulation.
ANESTHESIA AND ANALGESIA:
Goals:
↑ LV preload
↓ heart rate
contractile state to be maintained
Pulmonary vascular resistance to be decreased
Avoid maternal tachycardia

The pressure gradient across the valve is inversely proportional to the square of the
diastolic filling time.
Gorlin’s formula:
Stroke volume/Diastolic filling time
MV Gradient =
Mitral valve area
Small increase in heart rate results in marked increase in left atrial pressure.
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- Blockers can control heart rate.
Epidural block for labor analgesia unless it is specifically contraindicated.
If epidural analgesia is contraindicated;

NYHA functional class I an II manage well with intermittent parenteral analgesia,
provided maternal heart rate is kept under control. Fentanyl is drug of choice.
For NYHA grade III and IV intermittent analgesia is insufficient. Try continuous
or patient controlled intravenous opioid infusion.
Labor analgesia by continuous epidural provides pain relief and prevents stress
on cardia.
Cesarean section:
a. NYHA class I and II patients tolerate epidural block required for operative
delivery.
Monitor cardiac preload and adjust it as necessary.
b. NYHA class III and IV may fare better with epidural anesthesia.
i. although these patient do not tolerate any sudden reduction in cardiac after load,
they are often on the brink of pulmonary oedema with very high pulmonary arterial and
venous pressures.
Any sudden increase in after load or heart rate (intubation) may precipitate pulmonary
oedema.
ii. Slow venodilation produced by incremental epidural anesthesia should improve
maternal hemodynamic.
iii. In this setting pulmonary artery pressure must be monitored. Maintain adequate
left ventricular preload during the onset of sympathetic block. Avoid fluid over load.
c. General anesthesia:
i. Obtund the adrenergic response to intubation with -blockers.
ii. Xylocard 1.5mg/kg body weight 60 to 90 seconds before.
iii. Induction – Etomidate is the suitable intravenous induction agent (2-3µg/kg) or
Midazolam 0.1 mg/kg + Opioids (Fentanyl) 2-4 µg/kg.
Sleeping dose (2mg/kg) of thiopentone can be used.
iv. Intubation: Succinylcholine may be used rocuronium is better choice.
v. Maintain anesthesia with N2O/O2/ rocuronium (vecuronium) if succinylcholine
is used for intubation.
These patients are at greater risk of pulmonary oedema immediately postpartum.
Blood volume expands as the uterus contracts and vasodilator effect of regional
anesthesia wear off
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Because of high incidence of pulmonary oedema consider giving furosemide 20-
40 mg Iv with delivery of placenta. Closely monitor the patients volume states
for next 24-48 hours.
Maintain the patient on prophylactic ventilation at least for 24 hours.
Choice of anesthesia:
Spinal anesthesia: Contraindicated because of profound hypotension is
dangerous in mitral stenosis with under filled left ventricle.
General anesthesia: Tends to increase systemic blood pressure and heart rate
and can cause pulmonary oedema. So, reserve general anesthesia if epidural fails
or contraindicated.
Epidural; continues epidural is ideal if coagulation profile is normal (platelet . 1
lakh, BT, CT, PTT –normal) Graded epidural with increments will not affect blood
pressure and heart rate much.
Vasoactive drugs;
Use vasopressors and oxytocic agents cautiously
Avoid methergine totally as it increases SVR
Oxytocin infusion slowly can be given. Bolus dose should be avoided.
Prostadin: Not to be used because it decreases BP.
IV fluids to be given cautiously as overload can precipitate pulmonary oedema.
CVP monitoring is used as guideline.
Consider using a pure constrictor, like phenylephrine in patients with mitral
stenosis.
Diabetes mellitus in pregnancy:

Introduction: common complication encountered during pregnancy.
Incidence 5% of all pregnancies are affected with some degree of glucose
intolerance.
With the advent of exogenous insulin and the institution of intensive
management, maternal and fetal complications decreased.
Women achieving tight glycemic control can expect essentially normal out come.
High risk women are those with vascular complications of diabetes and with
poor glycemic control.
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MODIFIED WHITE’S CLASSIFICATION OF DIABETES IN
PREGNANCY:
Gestational diabetes mellitus non insulin requiring
Abnormal carbohydrate tolerance only during pregnancy not requiring insulin.
Gestational diabetes mellitus requiring insulin.
Abnormal carbohydrate tolerance only during pregnancy requiring insulin.
Class A: Abnormal carbohydrate tolerance in the non pregnant state identified
before the present pregnancy that does not require insulin either before or
during pregnancy.
Class B: Onset of insulin requiring diabetes after 20 years of age with duration of
less than 10 years.
Class C : Onset of diabetes mellitus between 10-20 years of age with duration of
less than 20 years or duration of 10-20 years regardless of age of onset.
Class D: Onset of insulin requiring diabetes before 10 years of age or duration
greater than 20 years regardless of the age of onset or insulin requiring diabetes
with chronic .Hypertension or IDDM with benign retinopathy.
Class F :Onset of insulin requiring diabetes with diabetic nephropathy
(Proteinuria of greater than 500mg in a 24 hour urine collection)
Class R: Insulin requiring diabetes with proliferative retinopathy.
Class T: Insulin requiring diabetes with renal transplant.
Class H: Insulin requiring diabetes with coronary artery disease.
Effect of diabetes on the mother:
1. Major changes in glucose metabolism occur with pregnancy.
In healthy pregnant women fasting for 12 hours can produce a plasma glucose
concentration of as low as 40-45 mg/dl
i. This reduces insulin secretion leading to ketosis.
ii. This exaggerated response is termed accelerated starvation of pregnancy.
Increase in maternal and fetal glucose utilization.
Volume of distribution for glucose are responsible for this effect.
Accelerated starvation and maternal hypoglycemia increase production of
ketoacids which crosses the placenta and results in fetal acidosis.
When healthy parturient eat, their plasma glucose concentration rises
This causes increase insulin production.
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Hypertrophy of the -cells of the islets of langerhans yields to hyperinsulinemic
response.
More evident during third trimester.
It signals hepatic resistance to insulin. The synergistic effects of placental
hormones such as – human placental lactogen, estrogen, progesterone and tumor
necrosis factor α are responsible for insulin resistance.
2. Diabetes during pregnancy exaggerates all of the these effects:

a. In early pregnancy, maternal hypoglycemia frequency occurs and necessitates
drastic reduction in insulin does.
b. latter half of pregnancy, insulin resistance develops, results in progressive
increase in insulin requirements.
c. Without tight metabolic control, these women are extremely prone to
ketoacidosis.
3. Incidence of obstetric complications such as pre-eclampsia, hydraminos, preterm
labour are higher in diabetic women.
4. Other complications of diabetes include retinopathy, nephropathy, hypertension
and coronary insufficiency.
5. These women are more prone for developing diabetes.
Effect of diabetes on the fetus;

Congenital anomalies:
The advent of insulin therapy in pregnancy reduced perinatal mortality to less
than 55.
Major congenital anomalies occur at a rate of 6 to 12%.
Mechanism remains a mystery.
a. Inadequate control of diabetes during early stages of pregnancy, particularly
organogenesis.
b. Strict control of diabetes beginning before conception significantly reduce the
incidence of congenital defects.
Macrosomia:
1. Maternal hyperglycemia provides excessive quantities of glucose to the fetus.
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Glucose crosses the placenta by facilitated diffusion, carrier mediated and non-
energy dependent.
Results in increased insulin secretion in the fetus.
Insulin is an anabolic hormone.
Increased fat deposition, hypertrophy of visceral organs and increased and
increased skeletal growth occur.
2. It manifests as fetal fat deposition in the shoulder and trunk.
Head is no longer the largest part.

During vaginal delivery, macrosomia (fetal weight > 4000g) contributes to a high
incidence of birth injuries – shoulder dystonia, facial N-Injury brachial plexus
injury and asphyxia.
Inspite of good metabolic control – incidence may as high as 20 to 30%
NEONATAL HYPOGLYCEMIA:
In infants of healthy non-diabetic mother, insulin concentration falls rapidly with
separation of placenta at delivery, compensating for sudden cessation of the fuel
supply.
Such hormonal adaptation fails to occur in infants of diabetic mother.
Chronic oversupply of glucose induces fetus pancreatic islet cell hypertrophy and
hyperinsulinemia, which persists after birth results neonatal hypoglycemia
(Blood sugar < 30 mg/dl)
Incidence 40% with macrocosmic and preterm infants at the highest risk.
Infants of diabetic mother secretes less glucagon and less catecholamines in
response to spontaneous hypoglycemia results decrease glucose production in
the liver.
Other neonatal metabolic derangements of both IDDM and GDM include –
hyperbilirubinemia, Acidosis, hypocalcemia, hypomagnesemia.
Respiratory distress syndrome:

Common cause of neonatal morbidity and mortality.
Fetal hyperinsulinemia interfere with surfactant production and delay lung
maturity.
5-6 fold greater risk of RDS in premature infant of inadequate controlled diabetic
mother.
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Changes in utero-placental circulation and fetal oxygenation:
Diabetes significantly impairs utero-placental perfusion.
Structure of the placenta itself is modified by diabetes. The villi are enlarged,
intervillous spaces are smaller and uterine blood flow is reduced.
The presence of increased maternal glycosylated hemoglobin (HBA1C) also
compromise fetal oxygenation.
Glucose covalently binds to the two -chains in the adult Hb (HBA) it creates
HBA1C which interferes with oxygen uptake.
Diabetic ketoacidosis:
Incidence : 0.7 % with GDM
1.7to 9.3% with IDDM
Etiology : Multifactorial. Common precipitating factors
Poor patient Compliance.
Undiagnosed diabetes
Administration of - mimetic agents
Emesis
Poor physician management
Sepsis.
Ketoacidosis may occur in gravid diabetics with lesser degree of hyperglycemia (150-
300 mg/dl) than in non gravid diabetics.
Symptoms:
Nausea and vomiting
Altered mental status (ranging from drowsiness to lethargy and coma)
Polydipsia
Polyuria
Abdominal pain
Signs:
Hyperventilation (Kussumal’s respiration)
Fruity or acetone breath odor
Dehydration
Hypotension
Investigations:
Plasma glucose greater than 300 mg/dl
Plasma HCO3 , 15 mEq/1
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PH < 7.30
Serum acetone at 1:2 dilution
Serum sodium potassium are decreased
BUN may be low, normal or high
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Treatment:
Lab Electrolyte, blood glucose, arterial blood gases, fluid intake/output
each hour.
Consider intra-arterial catheter and central venous catheter
Insulin Load 0.3 units / kg or 10-20 units regular insulin Iv infuse 5-10
units / hr until plasma glucose reaches 200mg/dl and then 1-2
U/hr.
If no appreciable decrease in 2 hrs increase rate.
Fluids Replace fluid deficit over 36-48 hours.
0.9% NaCl 4-6 L in first 12 hours.
1000-2000ml in 1st hour.
500-1000 ml/hr over next 3 hours
250ml/hr thereafter
give 0.45% NaCl if Na > 150 mEq/dl
Add 5% dextrose if plasma glucose < 200-250mg/dl (150mg/hr)
Potassium 40 mEq KCL/1 of fluid after 2-4 hr of insulin therapy and
establishment of urine output > 0.5 ml/kg/hr.
Bicarbonate Give 1 amp (44 mEq/) in 1 L of normal saline if Ph < 7.1
Monitoring ECG in electrolyte imbalance
Pulse oxymeter
Radial arterial catheter for BP and blood gas analysis
CVP to evaluate response to fluid therapy
fluid intake/output
Continuous fetal monitoring
Diagnosis of DM in pregnancy:
Screen all pregnant women at risk at first prenatal visit.
If initial test results normal, then repeat at 24 to 28 weeks of gestation.
Screening method:
Use oral glucose challenge (50-g) with plasma assessment in 1 hour.
130 to 150mg/dl are used as cutoffs for positive screen.
Positive patients subsequently undergo with 3 hour oral glucose tolerance test.
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Method: initial fasting glucose level followed by 100g oral glucose.

100g OGTT NDDG Criteria Carpenter – caustan criteria
Fasting 105 mg/dl 95 mg/dl
1 hr 190 mg/dl 180 mg/dl
2 hr 165 mg/dl 155mg/dl
3 hr 145 mg/dl 140 mg/dl
Patient with fasting blood sugars and adequate control with diet are classified as
A1.
Those with elevated fasting or 2 hour post-prandial requiring insulin are
classified as A2.
Obstetric management:
Intensive diabetic education
Nutritional counseling
Specific dietary guidelines
Exercise, weight control, glucose monitoring and warning signs of complications.
Insulin dosing strategies;

Typical regimen: Dosing 3 times /day
Total daily dose : Total body weight in kg X 0.7 in units
2/3rd in the morning
1/3rd at night.
Morning dose : 2/3rd NPH insulin

1/3rd regular insulin
Evening dose : 1/3rd regular insulin at dinner

2/3rd NPH at bed time
Frequent adjustments required depends upon glucose monitoring.
Oral hypoglycemic;
Traditionally avoided because of teratogenicity and fetal metabolic alterations.
Newer generation sulfonylurea’s such as glyburide appear safe, minimal passage
to fetus and favorable outcomes.
Timing of delivery:
1. Both maternal and fetal conditions must be considered.
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Normal glycemic with healthy fetus parturient may be allowed to progress to
term and experience spontaneous labour. Fetal maturation should be confirmed.
Premature labor should be treated with bed rest, IV fluids and magnesium
sulfate.
o - Sympathomimetic drugs are contraindicated.
Have direct anti insulin effects
Induce hyperglycemia and ketoacidosis.
Corticosteroids for fetal lung maturity may be justified, provided glucose
homeostasis is maintained.
If fetal surveillance suggests a compromised pregnancy, prompt delivery may be
necessary, even without evidence of fetal lung maturity.
2. Method of delivery;
Macrosomia, fetal intolerance to labor may make vaginal delivery unlikely.
Obese patient with GDM is at increased risk of fetal macrosomia.
Diabetic patient with all factors are more likely to require cesarean delivery than
normal patients.
Intrapartum management:
Preoperative evaluation should be directed at those organs most commonly
affected by chronic diabetes mellitus.
The presence of renal insufficiency, cardiac disease, peripheral or autonomic
neuropathy.
Physical examination:
Thoroughly evaluate the airway for signs of stiff joint syndrome and potential for
difficult intubation.
Look for signs of cardiac decompensation. The documented cardiac diseased
patient should have a recent ECG.
Laboratory investigation includes – electrolytes, BUN, Creatinine, Glucose.
Antepartum fetal assessment:

Antepartum testing with non-stress test are initiated at 39 weeks of gestation.
Patient requiring insulin and women with pre-existing type 2 diabetes, non-
stress test initiated at 32 weeks of gestation and obtained on a twice weekly
basic.
Ultrasound assessment of fetal weight is obtained late in third trimester.
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This assessment may provide insight into the decision to deliver and route of
delivery should take place.
Assessment of fetal lung maturity is not warranted before induction beyond 38
weeks of gestation.
Intrapartum glucose control:

Neonatal hyperglycemia and acidosis are most common complication.
Maintaining maternal plasma glucose a normal concentration (30-120mg/dl)
during labor reduces neonatal hypoglycemia and acidosis.
Commonly used insulin-glucose protocols can attain this goal.
Table 1:
Give the usual insulin dose the evening before surgery.
Measure fasting blood sugar on the morning of surgery or induction of labour.
Start 5% dextrose with insulin and infuse 1-2U/hr and glucose at 150mg/kg/hr.
adjust the dose of insulin and glucose, hourly blood sugar to maintain levels at
70-120 mg/dl.
Measure blood sugars each hour.
If glucose levels are > 120 mg/dl treat with a bolus of 1 unit of insulin and
increase infusion.
If glucose level < 70mg/dl administer 2-5 gms of glucose.
Table 2:
Blood glucose mg/dl Insulin dose U/hr IV fluids
< 80 0 Lactated ringer (D5) 125ml/hr
80-100 0 D5 LR 125 ml/hr
100-140 1.0 D5 LR at 125 ml/hr
140-180 1.5 0.9% NaCl at 125ml/hr
180-220 2.0 0.9% Nacl at 125 ml/hr
> 220 > 2.5+ 0.9% Nacl 125 ml/hr
Note:
Administer usual insulin dose the evening before induction/surgery.
NPO after midnight
With hold usual morning dose
Assess usual blood sugar hourly
Adjust fluid and insulin based on levels.
Glucose requirement during labor is constant 2.55mg/kg/min.
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Insulin requirement vary.
Insulin not needed during first stage of labor due to fasting and increased
glucose utilization.
Usual insulin requirement range from 0-5 U/hr. (regular insulin),
Glucose and insulin infusions should be maintained on separate mechanical
pumps.
Avoiding both hyper and hypoglycemia are important, because these imbalances
prolong labor and induce neonatal hypoglycemia.
Management of diet - controller: GDM: Intravenous fluids without dextrose.
Monitoring is continued as IDDM.
Immediately postpartum, insulin requirement drops to 60% of pre pregnancy
requirement. The dose will return to baseline in about 5-6 days.
THE AIRWAY AND DIABETES IN PREGNANCY

IDDM in parturient frequently begins in childhood as JODM (juvenile - onset diabetes
mellitus) and associated with stiff joint syndrome.
o Limited joint mobility is found in 28% JODM within 5 years of diagnosis.
o 1/3 of patients with LJM have involvement of the cervical spine.
o Impaired cervical spine movement (atlanto occipital joint) present
difficult intubation.
o 26% to 48% incidence of difficult intubation in diabetic patients.
o Difficult intubation correlates with inflexibility of the joints of the hand.
BED SIDE TEST: It is to have the patient oppose the palms of hands and see if proximal
interphalangeal joints of the fourth and fifth fingers wall touch.
The gravid of GDM is also at risk for difficult intubation because of obesity.
ANALGESIA FOR LABOR AND DELIVERY

In early stages of labor: Small dose of systemic opioids but have the risk of
neonatal respiratory depression.
o Epidural anesthesia and combined spinal anesthesia techniques are better
choice: Provides excellent pain relief and minimal effects on fetus.
Endogenous catecholamine and cortisol levels are decreased, and improve utero-
placental perfusion.
o Hyperglycemia is minimized so better glycemic control may be achieved.
o Both epidural and CSE may result in hypoglycemia (may be due to
decreased cortisol and catecholamines)
o So important to measure plasma glucose level frequently.
o Choice of local anesthetic - no special benefits for any given drug.
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o A second peripheral IV line should be established for hydration before RA.
Glucose free solutions should be infused to maintain BP.
o Left lateral position should be maintained to avoid supine hypotension
syndrome.
The dosing of epidural should be in small increments.
If BP falls ephedrine in doses of 5-10 mg IV is necessary.
Oxygen should be administered by mask.
ANESTHESIA FOR CESAREAN SECTION

Operated on first in the morning to ensure proper glycemic control during
perioperative period.
The usual dose of insulin administered the night before surgery.
In the morning of surgery both food and insulin should be withheld.
For maintaining euglycemia, one of the protocols explained earlier can be
followed.
CHOICE OF ANESTHESIA
Regional anesthesia is the choice. Epidural and CSE may be used.
Advantage of epidural analgesia

o Indirectly increase utero-placental blood flow by decreasing the
endogenous catecholamine concentrations.
o It will reduce the maternal lactic acid production, and, hence, reduce fetal
acidosis.
o It will provide excellent pain relief during the first, as well as the second,
stage of labor, especially during a difficult delivery.
o The existing epidural catheter can be used should lot emergency cesarean
section be necessary.
Dextrose free crystalloid 1500 to 2000m1 should be administered before R.A.

The block should be induced slowly to avoid sudden onset of sympathetic
blockade with precipitations hypotension.
Oxygen should be given continuously by facemask.
o Prompt treatment of hypotension with epidrine, left word displacement
of uterus to avoid aorto-caval compression, and oxygenation of the
mother excellent maternal and neonatal outcomes, can be expected.
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NEUROPATHY AND REGIONAL ANESTHESIA:
Autonomic neuropathy:
Occurs within 15 years of onset of insulin treatment in upto 30% of diabetics.
23% of gravida with IDDM have autonomic dysfunction.
Manifestations
a) Orthostatic hypotension or light headedness.
b) Diarrhea or constipation
c) Bladder complication
d) Resting tachycardia (diabetics experience less of an increase in resting heart rate
with pregnancy than do non diabetics).
e) Decreased heart rate variability with deep breathing or vagal stimulation.
General anesthesia in a parturient with autonomic neuropathy:

a) Hypotension
b) Less stress response follows tracheal intubation
c) 35% requires vasopressor treatment
d) The fetus of the IDDM mother tolerates hypotension poorly.
Regional anesthesia:
a) Greater degree of hypotension
Cardiac and vasoconstrictive responses to hypotension are blunted by autonomic

neuropathy.
Epidrine or phenylephrine are appropriate treatment of choice.
Peripheral neuropathy
o Upto 50% diabetics have some evidence of peripheral neuropathy.
o Distal sensory and motor lesions are most common.
o Symptom: - paresthesia, pain or hyperesthesia of distal extremities.
o Small fiber neuropathy is less common and presents as distal burning
pain or hyperalgesia. Autonomic neuropathy is more commonly
associated with small fiber neuropathy.
If contemplating regional analgesia - anesthesia, document the extent and type of
peripheral neuropathy.
o Chances of peripartum nerve injury is increased.
o Assure careful and proper positioning during anesthesia.
Ulnar nerve is most commonly affected during general anesthesia.
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Passage of fetus through pelvis, placement of forceps, and lithotomy position
may cause nerve injury.
Commonly affected are the lumbosacral trunk, sacral femoral, lateral femoral cutaneous
and lateral Popliteal nerves.
For general anesthesia usual protocol can be followed.
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Chapter 6 - ASTHMA IN PREGNANCY
Most common pulmonary disease in women of childbearing age.
Complicates 1% of pregnancies.
Pathophysiology:
Tracheobronchial tree is more sensitive to a variety of stimuli.
Bronchospasm occur in response to provocation.
Symptoms vary
Mild and undetectable
Severe and syndrome of status asthmaticus.
Physiologic effects:
Intermittent small airway obstruction.
Most marked on expiration (wheezing)
Leads to air trapping and hyperinflation.
Hypersecretion of mucus
Mucosal oedema
Smooth muscle hyper contractility.
Factors that can precipitate bronchospasm include –

IgE mediated hypersensitivity to inhaled irritants.
Acute inflammatory disease
Cold
Exercise
Aspirin
Non-immune mediated (direct) bronchoconstriction to inhaled substances
(animal dander, dust and smoke)
Emotional stress
Mechanical stimulation (Eg: Intubation)
THEORIES ATTEMPT TO EXPLAIN THE PATHOPHYSIOLOGY

a) Imbalance between the sympathetic and parasympathetic nervous system.
Vagal and a-adrenergic effects predominate over -adrenergic action.
Stimulation of parasympathetic airway fibers increases intracellular CGMP which
promotes bronchoconstriction and airflow obstruction.
b) Asthma patients may produce autoantibodies to A-adrenergic receptors.
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c) Asthma may arise from inflammatory pulmonary changes that various stimuli
produce in susceptible individuals.
Pre-exposure to a particular allergen
↓
Antigen antibody complex
↓
Binds specific mast cell receptors
↓
Mast cell degranulates
↓
Vasoactive and cell mediator biochemical
(Histamine, leukotrienes, prostaglandins,
platelet activating factor and cell chemotactic factors)
↓
Inflammatory cells Vascular and airway changes
(macrophages and esinophils)
↓
Capillary endothelial and Symptoms
Airway epithelial damage
Clinical symptoms and signs:

Wheezing
Hyper inflated lung volumes
o Ventilation perfusion abnormalities
Hypoxemia
Hypercapnea
EFFECT OF PREGNANCY ON ASTHAMA:

One third of women with asthma show improved asthma control during
pregnancy.
Another 1/3rd remain unchanged
The last one-third experience worsening of asthma.
o Patients with severe asthma before pregnancy will have most severe
exacerbations during pregnancy.
The course of asthma in previous; pregnancies is the best predictor of the course
in feature pregnancies.
o Most common causes for exacerbation
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o Respiratory tract infection
o Non compliance with therapeutic regimens.
o Pregnancy - related changes that may worsen asthma
o Prostaglandin F2a- (bronchoconstrictor) increases.
Changes in cell mediated immunity may increase susceptibility to infection.
Pregnancy - related changes that may improve asthma.
o Plasma concentration of cortisol and progesterone (which induce smooth
muscle relaxation) rise.
EFFECT OF ASTHMA ON PREGNANCY

1. Maternal asthma may increase the frequency of hemorrhage, hyper emesis,
toxemia, neonatal deaths, preterm deliveries and low birth weight infants.
2. Maternal hypoxemia and respiratory alkalosis may severely compromise the
fetus,
3. Maternal fetal oxygen exchange depends on maternal arterial oxygen level and
the oxygen affinity of maternal blood.
Maternal hypoxemia lessens the maternal fetal oxygen diffusion gradient results
in decrease oxygen delivery to the fetus.
Maternal alkalosis causes left word shift of the oxyhemoglobin dissociation
curve, resulting in greater affinity of maternal hemoglobin for oxygen and less
exchange to the fetus.
b) The fetus rapidly develops hypoxemia and risks vital organ damage.
3. Status asthmaticus during pregnancy can harm both mother and fetus.
4. Aggressive management of asthma to prevent episodes of status asthmaticus

may improve pregnancy outcome.
PHARMACOTHERAPY:
Management goals in treating asthma include
Identification and removal of precipitating factors
Proper rest, nutrition and hydration
Aggressive antibiotic treatment for infection
Pharmacotherapy where indicated
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Bronchodilator agents:
1. - agonists:
-adrenergic stimulation relaxes bronchial smooth muscles by increasing
intracellular concentration of CAMP.
-agonist - bronchodilators are safe for use throughout pregnancy.
-agonist may interfere with normal labor due to uterine relaxation, may contribute
postpartum uterine agony and haemorrhage.
Terbutaline, metaproterenol, salmetrol and albuterol are 2 selective agents.
Aerosol administration speeds onset and reduces side effects from systemic
absorption.
Epinephrine
Has α- adrenergic (utero-placental vasoconstriction) effects along with
nonspecific -adrenergic activity.
Not to hesitate to use epinephrine in case of life threatening bronchospasm.
2) Parasympatholytics:
Ipratropium bromide relaxes bronchial smooth muscles by competitive
inhibition of vagus mediated bronchoconstriction,
Aerosols administration minimizes systemic anticholinergic effects (tachycardia,
dry mouth).
3) Methylxanthines:
Theophylline and Aminophylline;
Mechanism of action
Inhibit - phosphodiesterase, the enzyme responsible for the breakdown of cAMP.
Modulate the interaction of actinomycin and calcium.
Antagonize prostaglandins.
Inhibit adenosine.
Release endogenous catecholamines.
Attenuates the release of mast cell mediators.
Methylxanthines arc safe during pregnancy.
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Anti-inflammatory agents:
Steroids;
Steroids function by altering protein production, inhibiting mediator release and
suppressing inflammatory mediator action. It increases the responsiveness of p-
receptors to catecholamines. Reduces airway oedema by inhibiting release of
chemical mediators.
Inhibit the formation of chemotactic mediators and inactivate inflammatory cells.
Steroid use in pregnancy
Similar to use in treating non-pregnant asthmatics
Use lowest effective dose
Long standing steroid use (more than 1 month) may result in adrenal
suppression.
Chromolyn sodium:
Is an aerosol agent
Prevents degranulation of mast cells by membrane stabilization
It is safe during pregnancy
It can't counter effect previously released substances.
Evaluation:
History of the disease
In acute crisis management of hypoxia and respiratory compromise are
important.
Physical examination
Marked tachycardia, cyanosis and fatigue.
Wheezing is evidence of diffuse broncho constriction, lack of wheezing denotes
inabilities to ventilate.
Increase use of accessory muscles and nostril flaring.
Note the patient ability to converse.
Tachycardia is compensatory response to stress and hypercapnea, bradycardia
may provide hypoxic cardiac arrest.
A elevated temperature may signal acute infection.
Laboratory investigation:
A complete blood count may suggest acute infection.
Grams stain sputum.
Chest radiograph: Hyperinflation, pneumothorax Pneumo-mediastinum.
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An arterial blood gas
Blood gas value normally changes in pregnancy
pH and PaCO2 are better parameter.
If patient has alkalosis and PaC02 lower than normal (<32 mmHg) the attack is
mild.
Acidosis and hypercapnia.
pH <7.35 PaCO2 > 35 to 38 mm hg Pa02 < 60 mm Hg. indicates impending
respiratory failure.
Serial spirometry: Determine efficacy of therapy.
TREATMENT:
Unstable asthma:
Correct hypoxemia and acidosis: Support ventilation, oxygen therapy.
Bronchodilators and steroids.
Treat underlying cause and proceed to stable asthma treatment.
Stable asthma
Remove precipitating factors
Hydration
Obtain clinical studies
Initiate pharmacotherapy - bronchodilators, steroids, consider aminophylline,
antibiotics.
Repeat clinical study to assess efficacy of treatment.
ANESTHETIC MANAGEMENT:
Preoperative evaluation
Assess the severity of asthma during pregnancy.
Examine the patient for bronchospasm.
Try Lo optimize maternal pulmonary status before induction of labor or cesarean
delivery.
Intrapartum bronchospasm
Occur only 10% asthmatic parturient.
Treatment
Supplemental oxygen
Adequate hydration
Treat precipitating actors like infection.
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Inhaled -adrenergic agonists. (Metaproterenol, albuterol)
Parenteral corticosteroid therapy.
Patient who have taken oral steroids during previous year (attack) should receive
steroid coverage during labor and delivery. IV hydrocortisone 100mg 6th hourly.
Patient receiving corticosteroids may have diabetes.
Analgesia for labor and delivery

o Systemic medication can provide analgesia in the early phases of labor.
o More active and painful labor, epidural analgesia has distinct advantages.
o Patient without analgesia pain of active labor increase minute ventilation
and oxygen consumption.
o In asthmatics this may precipitate bronchospasm,
Anesthesia for cesarean section:
Epidural anesthesia:
Regional anesthesia advantages:
Avoid endotracheal intubation decreases bronchospasm.
In the awake patient continuous verbal contact will elicit signs of respiratory
difficulty.
Respiratory effects of epidural anesthesia:

High motor block can impair pulmonary function arterial blood gas values are
unchanged in asthmatic parturient.
High block can reduce peak expiratory flow rate.
If cough is impaired avoid sedation.
Epinephrine (1:200,000) may aid in bronchodilation but not significant.
SPINAL ANESTHESIA:
Most data suggest that extensive sensory and sympathetic blockades lack effect
on respiratory function.
Reduction in peak expiratory flow rate occur during spinal anesthesia.
GENERAL ANESTHESIA: Rapid sequence induction and intubation can
precipitate bronchospasm. So deep plane of anesthesia helps prevent
bronchospasm.
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Induction:
a) Ketamine
Choice for induction of anesthesia in asthmatics
Bronchodilation begins within 1.5 minutes and lasts for 6-8 minutes.
Induction dose <1.5 mg/kg.
- Propofol or thiopentone can be used in hypertensive asthmatics.
- Other technique to prevent intubation related bronchospasm. IV lidocaine
- Small dose of opioid (fentanyl)
Intubation;
Avoid manipulation of airway until full muscle relaxation has been achieved with
succinylcholine.
Intraoperative bronchospasm
High concentration of oxygen
Inhaled bronchodilators can be given via ETT.
Volatile anesthetics are potent bronchodilators should be used to maintain
anesthesia.
Halothane and isoflurane provide bronchodilation.
Halothane is a better bronchodilator.
Maintain anesthesia with 50% oxygen + nitrous oxide + halothane + vecuronium.
Extubation:
Reverse with neostigmine + glycopyrrolate (atropine can be used).
Awake extubation: Minimize the chance of pulmonary aspiration.
ETT may prompt bronchospasm as level of anesthesia wanes.
Inhaled bronchodilators and small dose of IV fentanyl or lidocaine before
emergence can help to minimize airway reactivity to extubation.
UTERINE ATONY:
Inhaled -agonists and volatile anesthetics are uterine relaxants.
Some uterotonics are bronchoconstrictor.
Prostaglandins: PGF2α is potent bronchoconstrictor, avoid synthetic analogue of
this prostaglandin. (15 methyl PGF2 α, carboprost – tromethamine).
Ergot preparation: Bronchospasm observed.
Use uterine massage and IV oxytocin infusion as first treatment of uterine atony
in the asthmatic patient.
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Chapter 7 - EMERGENCY CAESAREAN SECTION: BEST
PRACTICE
What is an "emergency" caesarean section?
A four point classification of urgency of caesarean section.
Table: Categorization of urgency of Caesarean section

Grade Definition (at time of decision to operate)
Category 1 Immediate threat to life of woman or fetus
Category 2 Maternal or fetal compromise, not immediately life-threatening
Category 3 Needing early delivery but no maternal or fetal compromise
Category 4 At a time to suit the woman and maternity team
The National Sentinel Audit of Caesarean Sections defined 30 mins as a standard for
decision delivery interval in the category 1 situation.
Anesthetists involvement can begin only once they have been informed of a case, and
audits of response times should measure anesthetist informed - delivery' intervals. The
importance of good multidisciplinary communication (midwife-obstetrician-anesthetist
theatre practitioner) cannot be overstressed.
In utero fetal resuscitation

The anesthetist should also be an active participant in measures that might ameliorate
isolated fetal compromise and even avert the need for Caesarean section. Some clinical
scenarios (e.g. iatrogenic uterine hyperstimulation with synthetic Oxytocin) are
obviously more amenable to resolution than others (e.g. placental abruption). Whatever
the etiology of maternal or fetal compromise, measures to relieve aortocaval
compression are vital. Having moved the mother from labour bed to theatre table, left-
lateral tilt until delivery is all too easily forgotten.
Table: In utero fetal resuscitation

1. Oxytocin off
2. Position full left lateral
3. Oxygen
4. I.v. infusion of 1 litre crystalloid
5. Low blood pressure: i.v. vasopressor
6. Tocolysis: terbutaline 250µg (s.c), glyceryl trinitrate 40 NG (metered aerosol
doses)
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Anesthetic options
The Royal College of Anesthetists compendium of audit recipes, proposed that > 85% of
'emergency' Caesarean sections should be under regional anesthesia, and that fewer
than 3% of regional blocks should require conversion to general anesthesia.
The anesthetic technique of first choice for the woman laboring with epidural analgesia
will be top-up of that epidural. Unless contraindicated, single-shot spinal anesthesia is
appropriate for the majority of women without labour epidural analgesia who require
Category 2 Caesarean section.
Epidural top-up
Women receiving epidural analgesia in labour should be reviewed regularly to identify
suboptimal blocks (e.g. missed segments) that predict potentially inadequate surgical
anesthesia if topped up for Caesarean section. Women at risk of operative delivery, e.g.
'trial of scar' or non-reassuring cardiotocogram, should be given regular oral ranitidine
to reduce the acidity of gastric contents.
Only very rarely does the need for emergency Caesarean section arise 'out of the blue'.
Advance warning can provide the extra time that can prove crucial in allowing
successful conversion of labour analgesia to surgical anesthesia.
Extending a low-dose labour epidural block to provide a dense block for Caesarean
section anesthesia is not the same as establishing de novo single-shot epidural
anesthesia. The preferred choice of local anesthetic is levobupivacaine, the S-
enantiomer of bupivacaine, which is less cardiotoxic than racemic bupivacaine in the
event of accidental intravascular injection. Whether the top-up should be administered
in delivery room or theatre is controversial. Topping-up in the delivery room might gain
time, but maternal monitoring is suboptimal when the risk of high block or systemic
local anesthetic toxicity is greatest. Waiting until arrival in theatre before starting to
top-up can invoke obstetrician impatience and a call for general anesthesia. A
compromise is to administer a small initial dose in the delivery room (e.g. 5 ml
levobupivacaine 0.5%) and further 5-ng1 increments as required in theatre.
The efficacy of epidural anesthesia is consistently reported as inferior to that of spinal
anesthesia in both elective and emergency situations. Blockade of light touch sensation
from S5 to T5 should avoid the need for supplementation or conversion to general
anesthesia. Drops of ethyl chloride allow evaluation of both cold and light touch
sensation. The addition of epidural fentanyl 50 µg minimizes pain from visceral traction.
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Single-shot spinal
Contraindications:
1. Active bleeding
2. Cardiac disease
3. Uncorrected coagulopathy and
4. High suspicion of bacteraemia
An adequate block for starting surgery should be conferred by a majority of de novo

single shot spinals within 10-20 min. Hyperbaric bupivacaine 0.5%, 2.5 ml is a midrange
dose, appropriate for most women; the addition of diamorphine 0.25 mg probably
enhances blockade of visceral pain, and certainly provides postoperative analgesia.
When there is pressure of time, fentanyl 25 g is an alternative opioid that requires no
dilution. However, this short-acting opioid does not confer postoperative analgesia.
Preservative-free morphine is also available at an appropriate dilution (2 mg in 10 ml);
0.1 mg (0.5 ml of this solution) provides comparable. postoperative analgesia to diamor-
phine 0.25 mg. Obsessive maintenance of left-lateral tilt to offset aortocaval
compression and prompt use of phenylephrine (now widely regarded as the
vasopressor of choice) should mitigate the slight fetal acidosis that has been observed
after spinal compared with epidural or general anesthesia.
Preload (administration of fluid before spinal anesthesia) has been superseded by
colloid - a fluid bolus coinciding with the sympathetic blockade. Although phenylephrine
can be given by infusion, SO-100 µg boluses are as efficacious. Phenylephrine 100 µg is
equivalent to ephedrine 8 mg. Timing is everything; the first dose of phenylephrine
should be given presumptively rather than waiting for arterial pressure to decrease.
Subsequent doses are best given in response to symptoms (nausea or light-
headedness), which tend to precede hypotension. Reflex bradycardia (heart rate 4550
beat. min) is to be expected after an alpha adrenergic agonist, and an anticholinergic
agent should be immediately available, although administration is rarely necessary.
Women with preterm babies require more rather than less intrathecal local anesthetic,
presumably because of less engorgement of the inferior vena cava and therefore
epidural veins, and consequently less compression of the thecal sac.
The incidence of hypotension (a 30% decrease in mean arterial pressure) after single-
shot spinal anesthesia in women with treated preeclampsia has been shown to be less
than that in healthy parturient. Eclamptic women who have regained consciousness and
received intravenous magnesium can safely undergo regional anesthesia, provided
coagulation indices are acceptable (platelet count > 80x109.1-1).
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Combined spinal-epidural
In the event of failure of a topped-up labour epidural to produce bilateral loss of light
touch sensation from S4 to T5, single-shot spinal anesthesia using a dose appropriate
for a de novo spinal is not an inherently safe option because of the risk of excessively
high block. Combined spinal-epidural anesthesia is a useful recourse. A conservative
spinal dose (hyperbaric bupivacaine 0.5% 1 ml) might well, suffice and can be safely
augmented by subsequent increments of epidural local anesthetic.
General anesthesia
Arguably, historical and contemporary evidence does not suggest that 'traditional' rapid
sequence induction (thiopental, succinylcholine, cricoid pressure, intubation) is
necessarily the safest approach to general anesthesia for Caesarean section.
Depth of anesthesia
The effects on the fetus of anesthetics and opioid analgesics are 'innocuous and
reversible'. The choice of drug regimen or doses used for women with cardiac or
cerebrovascular disease should not be restricted on account of concerns for the fetus.
Dose-dependent respiratory depression is predictable and readily treatable by a
neonatal pediatrician, who should be present to receive all neonates born by Caesarean
section under general anesthesia.
There is no justification for administration of low inspired vapor concentrations that
risk awareness. To maintain bispectral index (BIS) values < 60 for 'adequate' depth of
anesthesia during. Caesarean section, end-tidal vapor concentration > 0.75 MAC (+ 50%
nitrous oxide) has been recommended. There is no evidence that neonatal outcome' is
adversely influenced by greater depth of maternal anesthesia; the relaxant effect of
modern, insoluble vapors on uterine tone is readily reversible. In the event of severe
hypovolemia, anesthesia can be induced and maintained with intravenous ketamine,
which has a useful sympathomimetic effect.
Pre-eclampsia
In pre-eclampsia, general anesthesia is indicated for uncorrected coagulopathy or
symptoms (piercing headache, in particular) or signs consistent with impending
eclampsia. An exaggerated pressor response to intubation, which would threaten the
integrity of the cerebral circulation, will be averted reliably by a neuro-anesthetic
induction regimen (thiopental supplemented by alfentanil 10 µg. kg1 or remifentanil 2
µg. kg1). The threat of dangerous hypertension remains at extubation; antihypertensive
pretreatment (e.g. labetalol in 10-20-mg increments) is effective. Non-depolarizing
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neuromuscular blockade is significantly enhanced by therapeutic serum magnesium
concentrations, and monitoring by peripheral nerve stimulation is essential.
Postoperative concerns
Intrathecal diamorphine is the mainstay of postoperative analgesia after single-shot
spinal anesthesia. For epidurals or combined spinal epidurals, 2.5 mg (10 times the
intrathecal dose) is appropriate. If there has been accidental or deliberate dural
puncture (i.e. combined spinal epidural) it should be borne in mind that there might be
a route for a dangerous excess of opioid to reach the intrathecal compartment. Unless
there is hepatic dysfunction, paracetamol is given regularly to all women. Diclofenac is
prescribed provided there are no contraindications (notably renal dysfunction, e.g. in
preeclampsia). Low molecular weight heparin is administered 2 hr after removal of the
epidural catheter. Synthetic oxytocin is given slowly as a 5-unit bolus immediately after
delivery, followed by an infusion (10 units.h-1 for at least 4 h) to prevent uterine atony.
The risk of postpartum haemorrhage is greater in women who have undergone
emergency as opposed to elective Caesarean section. Clinical observation (e.g. uterine
palpation) and physiological monitoring are configured to detect haemorrhage, which
can be covert (concealed within the uterus or Intraperitoneal) as well as overt.
Fluid balance
Around 1% of women will require high dependency care after Caesarean section.
Fluid input and output must be charted meticulously. In preeclampsia, oliguria (urine
output < 30 ml.h-1) after delivery is extremely common and does not necessarily imply
volume depletion. Acute tubular necrosis is exceptionally. rare in the absence of a
compounding factor such as major haemorrhage or injudicious administration of a non-
steroidal anti-inflammatory drug. No study has shown that crystalloid or colloid is
superior. Crystalloid infusion may reduce plasma colloid oncotic pressure, but the
longer half-life of colloid infusions may contribute to circulatory overload during the
period of postpartum mobilization of the increased extracellular fluid volume of
pregnancy. If synthetic oxytocin is to be continued beyond the immediate postpartum
period, administration should be in small diluent volumes by syringe pump (e.g. 60
units in 60 ml normal saline at 10 ml.h-1). Measurement of CVP can help substantiate a
diagnosis of hypovolaemia, and assist its correction. Cautious volume expansion can
reasonably be undertaken if CVP is ≤5 mmHg, but the circulating volume should be
considered as full if CVP is > 5 mmHg and minimal intravenous fluids (e.g. normal saline
20xnl.h-1) should suffice. Disparity between CVP and pulmonary artery wedge pressure
(PAWP) is a distinct possibility (PAWP may be considerably higher as a result of left
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ventricular dysfunction). Administration of blood and blood products seems to be a risk
factor for the development of pulmonary oedema.
Placenta praevia and accreta

The commonly held obstetric view that placenta praevia dictates general anesthesia is
not supported by available evidence. Guidelines from the Royal College of Obstetricians
and Gynecologists state that the choice of anesthetic lies with the anesthetist. The
difference between the mother who is actively bleeding (in whom sympathetic blockade
might be disastrous) and the stable, volume-replete mother is sometimes not
appreciated.
Reducing the depth of general anesthesia to treat intraoperative hypotension is not a
substitute for addressing the problem of hypovolaemia, which requires aggressive
management regardless of the type of anesthetic. Placenta praevia overlying a previous
Caesarean section scar raises the possibility of placenta accreta (abnormally firm
attachment of the placenta to the uterine wall) and a particularly high risk of massive
haemorrhage. General anesthesia with invasive monitoring, rapid fluid warming/
infusion device, cell salvage facility, and provision for postoperative ICU admission
might be considered prudent.
Conclusions
Good multidisciplinary communication is crucial; the categorization of urgency should
be discussed.
Anesthetists should participate actively in resuscitation of the fetus in utero;
relief of aortocaval compression is paramount.
Epidural top-up with levobupivacaine 0.5% and fentanyl is the anesthetic of choice for
the women receiving labour epidural analgesia who require Caesarean section.
Combined spinal-epidural is useful if epidural top-up has failed to provide
bilateral light touch anesthesia from S5 - T5.
Single-shot spinal anesthesia is appropriate for most Category 2 emergencies (in
women without labour epidural analgesia). Preeclampsia is not a contraindication.
Phenylephrine is the vasopressor of choice. Phenylephrine 100 µg = ephedrine 8 mg.
Induction and maintenance doses of general anesthesia drugs should not be reduced in
the belief that the baby will be harmed.
General anesthesia is not indicated by default for placenta praevia. Early postoperative
observations and monitoring are geared towards the detection of overt or covert
haemorrhage; sepsis is a later, insidious complication.
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Chapter 8 - ANESTHESIA FOR CAESAREAN SECTION AND NEONATAL
ACID
BASE STATUS; A META – ANALYSIS
Discussion:
The above study confirms that SA for CS is associated with greater degree of metabolic
acidosis compared to GA and EA.
Factors considered in this study:

1. UA and UV: It is noted that three will be acid excess (little) and base deficit
causing reduced PH the reduced PH could further impact upon out come of
already compromised fetus.
Even though GA reduces the Apgar score, it is short lived. It should be born in mind that
cord PH is also affected by maternal respiration and also with mechanical ventilation
given by different anesthetists during GA.
Result show that PH with SA were significantly low compared with GA at EA.
Normal UA PH or 7.2
Base excess 10 to 0 mEq L-1
With poor fetal perfusion of placenta – large difference between Ua and UV PH as
small volume of umbilical blood is readily serviced at the maternal –fetal inter
face.
But with maternal problems – low difference between UA and UV PH as both UA
and UV are affected.
2. Significance of Base Excess;

Base Excess quantifies metabolic (non respiratory) acid base status. And is
almost not affected by – alteration in PCO2.
HB Concentration
It is well established that UA PH is lower than UV, while UA PCO2 is higher
difference between UA and UV in base deficit may therefore vary either way.
When,
Reduced PH with normal base deficit → short term disturbance in placental blood
supply.
Increased base deficit → longer lasting problem.
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In the fetus, metabolic acidosis is mainly the result of anaerobic metabolism and
any increase in hypoxia cannot be desirable (and so SA)
Other factors influencing neonatal Acid – Base balance
1. Anesthetic technique: Not much difference between SA and GA but factors which
are of significance are
- Maternal posture
- Inhaled O2 concentration.
- Minute ventilation.
- IVF volume
- Vasopressor administration
- Extent of Sympathetic Blockade etc.
In pre-eclampsia, SA is advised as it causes less hypotension and thus less need for
Vasopressor than in normal parturient.
Maternal posture:
Aorto-caval compression in late pregnancy affects - maternal intervillous blood
flow - affect A-B status.
Also - Aortocaval compression increases spread of SA---worsening the condition.
Maternal inhaled O2 cone.
Studies have shown - improved neonatal PO2 and Apgar scores with increased
inhaled fractions of maternal O2
There will be - better tunic saturation and
Better UA base excess.
Maternal hypoxia is considered - as of high risk and also in apparently normal
oxygenated patients -transmission to fetus ceases after uterus incision after which
unexpected delays could cause damage.
Fluid load
It is more logical to administer fluid at the insect of vaso dilation rather than giving it
before and it has been shown that colloids are better than crystalloid preload and leg
wrapping.
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Vasopressor
Ephedrine has α and sympathomimetic effects thus thought to give ideal protection
for placental intervillous blood flow.
But now studies have shown that it is associated with more severe UA acidosis than
phenylephrine ((x-stimulant) and also phenylephrine causes less maternal hypotension.
Conclusion:
Although there is significant different in Punic pH between SA and EA and GA and a
consistent adverse effect on base deficit, the differences are not large.
Advantages of SA:
Evidence of reduce maternal mortality and perinatal mortality.
Simplicity of its administration.
Minimal amount of monitoring is needed.
Disadvantages of GA:
Sedate the baby even though the effect is short lived and easily overcome.
It is advise for reasons for hast e/ coagulopathy
EA is advised where
Fetus is at risk
Need to avoid both maternal risks and fetal sedative effects of GA.
No immediate hurry.
Now the dangers and inefficiencies of EA can be overcome by the use of epidural opioids
and less toxic LA drugs.
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Chapter 9 - INCIDENTAL SURGERIES DURING PREGNANCY
AND ITS ANESTHETIC IMPLICATIONS
Incidence:
Between 1.6% to 2.2% of pregnant women undergo surgery for reasons unrelated to
parturition. This-may be an underestimate due to surgery performed prior to clinical
recognition, of pregnancy.
The commonest indications for surgery in pregnancy are appendiectomy, breast biopsy,
cervical encircle, ovarian cystectomy and increasing trauma. Other less frequent, but
more challenging situations include laparoscopic surgery, cardiac surgery requiring
cardiopulmonary techniques, neurosurgery and more recently, fetal surgery.
Physiology of pregnancy and Anesthetic implications;

Physiologic changes resulting from pregnancy affect almost every organ system, and
these alterations influence anesthetic management of pregnant women. Some
anesthesiologists believe the physiologic alterations are significant enough that they
classify healthy pregnant patients as an American Society of Anesthesiologist physical
status 2 (a patient with a mild systemic disease). In order to provide safe anesthesia to
the pregnant patient, one must understand the physiological changes and how they
impact on administration of anesthesia.
Maternal consideration
a) Respiratory system;
1) Due to increased progesterone levels during the 1" trimester, minute ventilation
is increased by 50% because of increase in tidal volume by 40% and respiratory rate by
15%.
2) After the fifth month of gestation, the functional residual capacity, expiratory
reserve volume and residual volume are all deceased by about 20%, because of
the gravid uterus pushing on diaphragm.
These changes result in an increase in PO2 and a decrease in Pco2, resulting in
mild respiratory alkalosis. In the third trimester of pregnancy, normal Pco2, is 27
to 32 mm Hg and normal pH greater than 7.44.
3) Arterial Po2 rises by approximately 5 to 10 mm Hg in normal pregnancy.
However, in supine position, arterial Po2 decreases by at least 6-10 mm Hg.
4) Vital capacity is not changed from pre pregnancy levels.
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Anesthetic Implications
a) Increased alveolar ventilation and decreased functional residual capacity lead to
a more rapid uptake and excretion of inhaled anesthetics.
b) FRC decreases by about 20% a result of anatomic factors, puts the pregnant
patient at increased risk of small airway closure and atelectasis.
c) The decreases in FRC in conjunction with increases in cardiac output, metabolic
requirement and oxygen consumption makes the pregnant patient more
susceptible to arterial hypoxemia during periods of apnoea or airway
obstruction.
d) Edema, weight-gain and increase in breast size and capillary engorgement of the
mucosal lining of upper airway may make intubation of the trachea technically
difficult. Incidence of failed intubation in the term pregnant patient presenting
for the cesarean section is 8 times higher than in general population. The
incidence of fatal failed intubation is 13 times that in general population.
e) Use of nasal airway and nasotracheal intubation should be avoided.
b) Cardiovascular system:
1) An increase in the plasma volume by 40% and red cell volume by 25% leads to
physiological anemia of pregnancy.
2) Cardiac output is increased by 30 to 40% during the 1sttrimester and peaks in
the second trimester, is mostly directed to the uterus.
3) Vascular resistance is decreased as a result of direct vasodilatation from the
increased progesterone and possibly prostacyclin levels, which leads to an
increase in the resting pulse of about 10-5 beats per minute above the baseline.
4) Beyond 20 wks of gestation, the compressive effects of the uterus on the inferior
venacava lead to decrease in the venous return, with decrease in cardiac output.
The decrease in cardiac output can be as much as 25 to 30%. This decrease is
more often when the patient is in supine position and may manifest as dizziness
and syncope. This is known as supine hypotension syndrome.
a) The hemodilution causes a decreased plasma protein concentration. Thus a free
fraction of highly protein bound drugs (e.g. bupivacaine) may be increased
during pregnancy.
b) Increase in the cardiac output will hasten the speed of intravenous induction.
c) The effect of increased cardiac output and dilated peripheral vasculature is
increased blood flow, with preference to organs such as the placenta, uterus and
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skin. The uterine artery blood flow is at least 500-600 ml/minute; thus, an
obstetric haemorrhage during the last trimester can be catastrophic.
Gastrointestinal system:
1) Due to increased progesterone levels, gastrointestinal tract motility is decreased
by the end of first trimester.
2) The stomach is displaced upward by the enlarging uterus, assumes a horizontal
position further slowing gastric emptying with change in the position and
function of gastro intestinal sphincter.
Anesthetic implications
1) Above changes in the gastrointestinal tract by the end of 1sttrimester, place the
pregnant patient at increased risk for aspiration of gastric contents.
2) Triple aspiration precautions which includes a non-particulate antacid, H2
receptor blocker and Metoclopramide to decrease the acidity and volume of
gastric contents.
3) After the 1sttrimester, all general anesthesia should be conducted with a rapid
sequence induction, cricoid pressure and tracheal intubation.
Hepatic system
Plasma pseudocholinesterase activity is decreased by 20 - 25%, this moderate decrease
is usually clinically insignificant. Prolonged apnoea is rarely a problem following a
standard close of succinylcholine.
Hematologic system:
1) Pregnancy is a hypercoagulable state, with a rate of thromboemobolic
complications as high as five to six times that of non pregnant women.
2) Physiologic anemia decrease oxygen carrying capacity. A haemoglobin level of <
11 g/dl is considered abnormal.
Renal system:
1) Renal blood flow and GFR increase.
2) Increased frequency of urinary tract infections due to pressure of the gravid
uterus on the ureter with obstruction of flow.
3) Drugs with significant renal clearance may need to be administered at higher or
more frequent doses to account for the increased clearance.
4) Sodium excretion remains normal.
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Central nervous system
The minimum alveolar concentration (MAC) or median effective dose (ED50) for
volatile agents is reduced by 25 to 40%. This is related to progesterone and
endorphin effect.
Epidural venous engorgement due to compression of inferior venacava by gravid
uterus decreases the size of the epidural and intrathecal spaces.
The decrease in MAC along with an increase in alveolar ventilation places the
pregnant patient at risk for the anesthetic overdose.
The dose of local anesthetic required for a major conduction block is decreased
due to decrease in the size of epidural and intrathecal spaces.
FETAL CONSIDERATIONS
There are 3 main areas of concern.
i) Maintenance of fetal oxygenation
ii) Avoidance of teratogenic agents
iii) Prevention of preterm labour
Maintenance of fetal oxygenation:

The maintenance of normal maternal PaO2 and PaCO2, maternal blood pressure and
uterine vascular resistance determine the status of fetal oxygenation.
i) Maternal administration of increased inspired oxygen will increase fetal
oxygenation. Fetus is never at risk for hyperoxia, because fetal oxygen tension
will not exceed approximately 65 mm Hg, even with maternal administration of
100% O2.
ii) Pregnant women lives with a compensated respiratory alkalosis, so
hyperventilation should be avoided. Respiratory alkalosis shifts the
oxyhaemoglobin dissociation curve to the left and could impair the transfer of
oxygen across the placenta. Umbilical flow is also decreased with alkalosis by
direct vasoconstriction.
iii) Maternal hypercapnia will lead to respiratory acidosis in fetus.
iv) Excessive IPPV leads to increased intrathoracic pressure, decreased venous
return, decreased cardiac output which leads to decrease in the uterine blood
flow.
v) Uterine arterial blood flow is directly dependent on maternal blood pressure. A
decrease in the maternal blood pressure leads to decrease in the uterine blood flow
followed by decrease in the intervillous blood flow and fetal asphyxia.
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vi) Deep levels of inhalation anesthetic agents lead to hypotension and fetal
asphyxia.
Avoidance of teratogenic agent:

Teratogenicity of a drug depends on the following factors:
a) Dose and duration of exposure
b) Embryonic or fetal stage at which drug is administered.
c) Species specific-genetic susceptibility to the agent.
In human, the critical time is during organogenesis, which extends 15 days through 55
days of gestational age. The critical time for central nervous system extend beyond
gestation.
Critical factors in teratology Mechanisms of teratogenicity
1) Specificity 1) Mutation
2) Dosage 2) Chromosomal dysfunction
3) Time of exposure during embryogenesis 3) Interference with substrate precursors
4) Depletion of energy sources
5) Enzyme inhibition
6) Altered membrane permeability
7) Osmolar imbalance
The U.S. Food and Drug Administration has developed a system to categorize each
specific drug. Categories range from category A, well studied drugs that carry no risk;
through B, C and D which are progressively less well studied or possibly risky, to
category X, in which fetal risk has been clearly demonstrated. Most anesthetic agents,
including the intravenous induction agents, local anesthetics, opioids and
neuromuscular blocking drugs are under category B or C classification.
The danger of teratogenic effects from currently available anesthetic or sedative drugs
remains only a potential risk.
Anesthetic agents with suspected teratogenic effects was mainly nitrous oxide. Nitrous
oxide inactivates methionine synthetase which is responsible for conversion of
Homocysteins and methyl tetrahydrofolate to methionine tetrahydrofolate which is
needed for synthesis of DNA. Thus avoiding Nitrous oxide in first and second trimester
of pregnancy was thought to have a preventive role in avoiding these effects. At that
time (1985), there was no human data to support the view regarding teratogenicity and
N20, but subsequently a number of publications have proved this hypothesis to be
unequivocally negative. There is now strong evidence against human developmental
toxicity of N20. Thus, acute exposure to anesthesia for surgery during pregnancy is not
associated with an increase in congenital malformation rates.
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No anesthetic, opioid analgesic, sedative-hypnotic, or anxiolytic agent appears to be
teratogenic or safer than another agent.
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Prevention of 'preterm labour:
Anesthesia and surgery during pregnancy have been found to increase the incidence of
preterm labour and spontaneous abortions. The rate of preterm labour after non
obstetric surgery during pregnancy tends to increase with gestational age and depends
on the type and duration of the procedure. The overall risk of the preterm labour given
pelvic or lower abdominal surgery during pregnancy is 4 to 6%.
Some obstetricians prefer to use prophylactic tocolytics like beta adrenergic agonists
(Ritodrine and terbutaline) and magnesium -sulfate, though their efficacy is doubtful.
Each of these agents has potential maternal and fetal side effects and concomitant
anesthetic implications.
Side effects of -adrenergic agonists include hypokalemia, hyperglycemia, pulmonary
edema, tachycardia, premature ventricular contractions (PVCs), chest tightness,
myocardial ischemia, ST-segment and T- wave changes on the ECG, atrial fibrillation and
rarely, maternal death associated with unrecognized heart disease. Because of these
potential side effects prophylactic use of -agonists are not recommended. Precautions
to be taken while using Beta adrenergic agonists are
1. Avoid sympathomimetic agents like Ephedrine, Halothane, ketamine and
pancuronium due to increased risk of dysrrhythmias.
2. Avoid hyperventilation, as intracellular movement of K' may precipitate
hypokalemia.
3. Careful monitoring of fluid status to avoid pulmonary oedema.
While using MgS04 following precautions should be taken:

1. Renal functions should be adequate.
2. Patients become more sensitive to depolarizing and non-depolarizing muscle
relaxants, hence neuromuscular monitoring is essential.
3. Adequate monitoring of cardiac and respiratory functions.
4. Baseline MgSO4levels should be available prior to anesthesia.
All patients treated with tocolytics agents should have the agent continued 24-48
hours postoperatively. All patients should be monitored postoperatively for the
presence of uterine contractions.
Tocolysis is not recommended in presence of maternal infection.
General recommendations:
1. Avoid all elective surgical procedures during pregnancy. If this is not possible,
then the 1sttrimester should be avoided.
2. Confirm that elective surgery patients are not pregnant.
3. Document FHR tones prior to surgery.
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4. Monitor uterine tone and FHR tones during and after surgery.
5. Avoid premedication. If necessary, barbiturates can be given for sedation.
6. Transport with left uterine displacement to avoid aortocaval compression and
minimize uterine hypoperfusion and fetal asphyxia.
7. Regional anesthesia is favored over general anesthesia as maternal mortality is
16 times higher with general anesthesia.
8. Triple aspiration precautions

Non particulate antacid
H2 blocker
Metoclopramide
9. If regional anesthesia
It is preferable to use spinal anesthesia rather than epidural to limit the amount
of drug exposure.
Fluid preloading
Treat hypotension with fluid administration and / or ephedrine.
10. If general anesthesia:
Fluid preloading
denitrogenate with 100% O2
Rapid sequence with cricoid pressure induction.
Use drugs with history of relative safety.
Adequate oxygenation
Maintain normocarbia.
Treat hypotension with fluid administration and / or ephedrine.
Recommendation for anesthetizing the pregnant patient for non-obstetric surgery:

Avoid surgery during the first trimester
o Document FHR tones prior to surgery
o Monitor uterine tone and FHR tones during and after surgery
o Avoid premedication
o Transport with left uterine displacement
o Regional anesthesia is recommended whenever possible
o Aspiration prophylaxis after the first trimester
o Non-particulate antacid
o H2 blocker
o Metoclopramide
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If regional anesthesia
o Fluid preloading
o Treat hypotension with fluid administration and / or ephedrine
If general anesthesia
Fluid preloading
Denitrogenate with 100% oxygen
Rapid sequence with cricoid pressure induction
Use drugs with history of relative safety
Adequate oxygenation
Maintain normocarbia
Treat hypotension with fluid administration and/or ephedrine
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Pregnant surgical patient
Elective surgery Essential surgery Emergency surgery
Delay until 1st 2nd/3rd trimester

Postpartum trimester
If no or minimal increased risk

to mother, consider delaying
until mid-gestation
If greater than minimal Proceed with optimal anesthetic for

increased risk of mother, mother, modified by considerations
Proceed with surgery. for maternal physiologic changes and
fetal well being. Consider consulting
a perinatologist or an obstetrician.
Intraoperative and postoperative
fetal and uterine monitoring may be
useful
Summary recommendations for management of the pregnant surgical patient
Intra-operative monitoring:
1. Blood pressure, heart rate, respiratory rate, temperature.

2. Electrocardiogram
3. Oxygen saturation
4. end-tidal carbon dioxide
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5. fetal heart (FHR)
6. Uterine activity (when feasible)
Fetal heart Rate monitoring:

After 16thweek, it is technically feasible to monitor FHR. A normal FHR is
between 120 and 160 beats / min with 3 to 7 beats variability. Variability is decreased
by hypoxia and sedative drugs as well as periods of fetal sleep. Slowing of fetal heart
rate in the operative setting suggests hypoxia.
In the fetus, cardiac output is rate-dependent. If the heart rate falls to 80 beats / min,
cardiac output is significantly reduced and at a rate of 60 beats / min, the fetus is in
jeopardy.
Logically, fetal heart rate monitoring is an indirect reflection of utero-placental
blood flow, so careful attention to avoid hypotension during the surgery, with the goal
of maintaining systolic blood pressure within 20% of baseline and a left or right uterine
displacement of the uterus off the vena cava are recommended.
IMPLICATIONS OF ANESTHESIA FOR SPECIFIC SURGERY
a) Common General Surgical Diseases:
1. Appendiectomy
It is more frequent in the II and III trimester.
In a pregnant patient, appendix lies above the iliac crest and nearer to the right
sub-costal area, so caution is to be exercised while giving regional anesthesia.
In early pregnancy, where possible, regional anesthesia is preferred to avoid any
side effects of anesthetic agents. In later pregnancy. GA is preferred to allow
maximum oxygenation, uterine relaxation and avoidance of hypertension.
2. Gall Bladder and Biliary tract diseases

Diagnosing this group of diseases during pregnancy is difficult because of certain
physiological hepatic changes which are peculiar to pregnancy. Certain
conditions unique to pregnancy affect liver functions, e.g.,
o Acute fatty liver, severe PET and intrahepatic cholestasis.
Severe Eclampsia - HELP syndrome.
Deranged liver functions include: Increase in Serum Alkaline Phosphatase.
Serum Globulin and Carrier proteins; Decrease in Total Proteins and Serum
Albumin. If coagulopathy is confirmed by decreased platelet counts. Regional
anesthesia should be avoided.
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Indications for emergency cholecystectomy include;
If ascending cholangitis develops

Common Bile Duct obstruction
Severe Pancreatitis
GA with controlled ventilation is the technique or choice in these patients.
3. Ovarian Disease
Ultrasonography has helped in detecting mere adnexal masses with pregnancy.
Conservative management of ovarian cysts may lead to torsion, rupture or
spread of an undiagnosed malignancy.
Adnexal surgery should be ideally done between 14-18 weeks of gestation.
GA or Regional anesthesia can be given along with tocolytics therapy.
LAPAROSCOPIC SURGERY DURING PREGNANCY
The major advantages of laparoscopic surgery during pregnancy are;

1) Small abdominal incisions result in rapid postoperative recovery and early
mobilization.
2) Early return of gastrointestinal activity.
3) Smaller scars.
4) Fever incisional hernias.
5) Decreased rate of fetal depression due to decreased pain and less narcotic use.
6) Short hospitalization time and prompt return to regular life.
Laparoscopy holds an increased risk to the fetus

1) It decreases uterine blood flow by increasing intra-abdominal pressure.
2) It causes fetal hypotension and hypoxia because of decreased maternal venous
return and cardiac output.
3) Although not proven in humans, it may cause fetal acidosis by CO2 absorption.
Suggested precautions:
Suggested precautions that should be exercised when laparoscopic surgery is
performed in pregnant patients include
1) Intraoperative fetal monitoring.
2) The patient should be positioned in left lateral decubitus position.
3) A Hasson trocar open technique is safer to prevent inadvertent puncture of the
uterus, especially with increasing gestational age. Ultrasound guidance during
the insertion of a Veress needle can decrease the danger of injury to the uterus.
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4) Intra-abdominal pressure should be kept low and should be no higher than 15
mm Hg.
5) Maternal end-tidal volume CO2 should be monitored and kept within normal
range.
6) Tocolytic agents need not be used prophylactically.
7) A gestational age of 26 to 28 wks seems to be the limit for successful completion
of laparoscopic surgery. Late in the second trimester, the size of the uterus
interferes with adequate visualization of intra-abdominal organs.
Anesthetic management of pregnant women for laparoscopy

Position Left or right uterine displacement
Premedication Oral sodium citrate, 30 mL; metoclopramide, 10mg i.v.
Induction Rapid-sequence induction (thiopental sodium and succinylcholine)
Ventilatory To keep end tidal PCO2 between 32 and 34 mmHg.
adjustments
Positioning Gradual changes to reverse trendelenburg
Fetal heart rate Around 16 weeks, pre-and immediate postoperative period
monitoring
Insufflations Open trochar method
technique
Tocolysis Terbutaline 0.25 mg subcutaneous, if needed
Hypotension Increments of ephedrine, 5-10 mg
Postoperative Left/ right uterine displacement oxygen supplements, fetal heart
period rate monitoring.
CONSIDERATIONS FOR SPECIALIZED PROCEDURES:
a) Cardiac surgery during pregnancy

The cardiovascular changes of pregnancy include a 30 to 50% increase in blood volume
and a similar increase in cardiac output. These effects peak at 24 to 28 wks of gestation
and are maintained until parturition. Thus, the patient with preexisting cardiac disease
is exposed to major stress during 2nd and 3rd trimesters of gestation. Although pregnant
patients with heart disease are usually managed with medical therapy, those with
severe decompensation (i.e. cardiac disease leading to pulmonary edema which is
resistant to medical therapy) require surgery. The most common indication is
rheumatic valvular heart disease particularly mitral stenosis.
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Indications for surgery:
1) Medical treatment fads to control heart failure.
2) When less invasive procedures (balloon valvotomy) are failed or are
inappropriate. No specific anesthetic drug regimen is preferred.
Use of cardiopulmonary bypass during pregnancy

CPB increases the risk, particularly for the fetus.
Factors related to cardio-pulmonary bypass, which can adversely effect fetal
oxygenation.
- Nonpulsatile perfusion.
- Inadequate perfusion pressure.
- Inadequate pump flow.
- Embolic phenomena to the utero-placental bed.
- Release of renin and catecholamines in response to CPB.
Recommendation regarding management of CPB in pregnant patients undergoing

open heart surgery:
1) Avoid aortocaval compression.
2) Maintain pump flow at up at 40% to 50% above usual to stimulate the cardiac
output of pregnancy.
3) Maintain mean arterial pressure at 60 mmHg to ensure adequate utero-placental
perfusion.
4) Maintain normothermia or only mild hypothermia (32°C).
5) Optimize acid - base status, oxygenation and ventilation.
b) Neurosurgery
a) Controlled hypotension: may be required for craniotomy in a pregnant patient or

for repair of a vascular lesion. Commonly used agents are volatile anesthetics,
sodium nitroprusside, nitroglycerin, or trimethaphan.
- A reductions in systolic blood pressure of 25 to 30% or a mean blood pressure of

less than 70 mm Hg will lead to reductions in utero-placental blood flow. All of
these drugs cross the placenta and induce hypotension in the fetus.
- Volatile anesthetic agents- they should be avoided as they cause maternal
hypotension and decrease uterine blood flow with resultant fetal hypoxia.
- Sodium nitroprusside is degraded to cyanide which is fetotoxic. If this agent is
used, it should be used for only a short time and should be discontinued if the
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infusion rate exceeds 0.5 mg/kg/hr, if maternal metabolic acidosis ensues, or if
resistance to the agent is apparent.
- Nitroglycerine is associated with adverse fetal effects, it is metabolized to nitrites
and produced methemoglobinemia.
- Trimethaphan leads to tachyphylaxis and interacts with neuromuscular blocking
agents, thus making it a poorer choice.
b) Hypothermia: It is used to decrease metabolic requirements in the brain and other
organs and reduces cerebral blood flow. The usual goal is to achieve a temperature
of 30°C. This should not be harmful and does not appear to increase the risk of fetal
mortality.
c) Hyperventilation: Is commonly used during neuro anesthesia because the decrease in
C02 reduces cerebral blood flow. The normal flow of 50 m1/100g per minute is reduced
by 1 ml/100g/min for each 1 mm reduction in C02. This is effective until the C02 reaches
approximately 20 mm Hg. The potential adverse effects of hyperventilation on the fetus
of decreased placental oxygen transfer and umbilical vessel vasoconstriction should not
be a problem to a healthy fetus whose mother receives moderate hyperventilation i.e.
C02 of approximately 25 mmHg. Fetal heart rate monitoring must be mandatory if
hyperventilation is instituted.
d) Diuretics: These drugs should be used with caution because these can cause
significant negative fluid shifts for the fetus.
e) It is highly recommended that atropine be used instead of glycopyrrolate for the
reversal of muscle relaxant. Because glycopyrrolate does not cross the placenta where
as neostigmine does to some degree, resulting in fetal bradycardia and lead to caesarean
section in some cases.
IMPLICATIONS OF ANESTHESIA FOR SPECIFIC SURGERY
A. Fetal surgery
The most common interventions used are intrauterine exchange transfusions,
placement of diversion catheters and aspiration of cystic masses. Maternal sedation
with 1-2 mg Midazolam with Fentanyl 50-100 microgram intravenously to provide mild
sedation or analgesia and 0.4 mg/kg of Atracurium into the umbilical vein of the fetus
result in immediate cessation of fetal movement lasting for 30-60 min. This technique
provide; optimum operating conditions for the surgeon while avoiding excessive
maternal sedation. In fetal cardio-pulmonary surgery, diaphragmatic hernia repair etc.
fetus is usually anesthetized from placental transfer of maternal anesthesia conducted
with high doses of inhalational halogenated agents to facilitate uterine relaxation. Fetal
immobility is achieved with IM nondepolarizing muscle relaxants.
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B. In vitro fertilization
Technique of in-vitro fertilization with embryo transfer is now widely used in infertile
couples. Two methods namely Laparoscopy and ultrasonically guided oocytes
collection arc commonly used. The later method requires local anesthesia and mild
sedation. GA or Regional anesthesia is required where Laparoscopy techniques are
used. There is a theoretical concern of possible effects on the oocyte of higher systemic
levels of multiple anesthetic agents may change the concentration of certain regulatory
peptides found in follicular fluid leading to increased incidence.
CONCLUSION
The major considerations for providing anesthesia care for the pregnant patient
undergoing non-obstetric surgery should include
1. Understanding the physiological changes of pregnancy and their influence on the
patient.
2. Maintaining an adequate utero-placental perfusion by avoiding and treating
hypotension and avoiding aortocaval compression.
3. Selecting anesthetic drugs and techniques that have a good track record for
safety.
4. Using regional anesthesia whenever possible.
5. Remembering that no anesthetic agent or adjuvant drug has as yet been proven
to be teratogenic in humans. (This information should be transmitted to the
patient before administering anesthesia).
6). Providing fetal surveillance with external fetal heart rate monitoring and uterine
activity monitoring whenever feasible.
7). Making appropriate adjustments in technique as guided by the results.
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Chapter 10 - OBSTETRIC HAEMORRHAGE
Haemorrhage from the genital tract is defined by the amount and the time when
it occurs.
Antepartum haemorrhage: Occur after 20 weeks of pregnancy and before delivery of
the baby.
Postpartum haemorrhage: Occurs in the first 24 hrs after delivery of the baby.
Obstetric haemorrhage: It is defined as an acute blood loss of greater than 500ml or a
major obstetric haemorrhage – where blood loss is > 1000 ml.
It is not easy to assess blood loss from the genital tract unless it is overt,
Often, it is concealed. The muscular blood loss plus an estimate of the concealed loss
should be added together. A prediction of the continuing risk and extent of blood loss
should be made in order not to delay treatment.
Management strategies for the treatment of major haemorrhage:

Assessment of severity
Determination of etiology
Treatment of haemorrhage, including resuscitation of the patient and control of
bleeding site.
Reassessment of the patient including the effectiveness of resuscitation and
continuing blood loss.
Assessment of blood loss:
The severity of haemorrhage is dependent on both the actual blood loss and rate
of haemorrhage. The greater the blood loss, the greater the discrepancy between the
actual and estimated volumes.
Assessment of blood loss may be difficult in pregnancy:
Physiological anemia:
Plasma volume >> increased blood cell mass. Therefore larger blood volume loss
before compensatory mechanism occur.
CVS physiology altered in normal pregnancy increased heart rate and decreased
systemic vascular resistance. Therefore classical signs of acute blood loss may be
affected.
Patients generally young and healthy. Therefore may compensate without
cardiovascular parameter changes.
Blood loss may be concealed (contained in uterus)
Effects of auto transfusion from contraction of uterus. Therefore decompensation may
be slowed.
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Amniotic fluid contamination with blood. Therefore visual assessment blood loss may
be inaccurate.
Estimate of blood loss may be obtained from visual assessment and the clinical features
of shock.
Acute % blood loss Clinical findings
1) 15-20% None
2) 20-25% Respiratory rate 14-20/min. Increased heart rate 100/min.
Mild hypotension. Peripheral vasoconstriction.
3) 25-35% Respiratory rate 20-30 / min. Increased heart rate 100-120 / min.
Hypotension 80-100 mm of Hg. Restlessness. Oliguria.
4) > 35% Respiratory rate > 35 / min
Heart ate > 120 / min
Hypotension < 60 mm of Hg. Altered consciousness. Anuria.
Management of major obstetric haemorrhage:

Ensure adequate oxygenation / ventilation
Maintain patient airway
Supplement oxygen. FiO2 100% by non-rebreathing face mask, intubate
trachea if loss of consciousness, respiratory failure or cardiovascular collapse.
Restore circulating volume and cardiac output
Lateral wedge if Antepartum
Two large intravenous cannula (16 to 18 G)
Expand circulating volume (crystalloid + colloid / blood)
Consider warmer fluid and use of pressurized injection devices.
Treat severe hypotension with ephedrine 5-50mg or phenylephrine 50-200 IV.
Order, required units of blood:
Cross matching, type specific, ‘O’ Rh –ve defending on urgency.
Baseline investigations:
Blood count, platelet count, electrolytes, coagulation screen, ionized calcium.
Monitoring:
Patient colour, respiratory rate, consciousness, ECG, BP, oximetry, urine output, fetal
heart rate (if appropriate)
Rapid assessment:
Severity of blood loss, etiology.
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Brief history (including anesthetic history) and examination.
Treat causes.
Medical (oxytocin with atony)
Surgical (exploration operation, remember aspiration prophylaxis prior to rapid
sequence induction).
Reassess: Continuing blood loss / effectiveness of resuscitation consider
insertion of CVP line / temperature probe consider further blood and blood
products (fresh frozen plasma, platelets)
Continuing care
Intensive care admission
Monitoring
Treatment of complications e.g., Coagulopathies, adult respiratory distress
syndrome, acute tubular necrosis.
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Chapter 11 - ANTE PARTUM HAEMORRHAGE (APH)
A.P. haemorrhage – complicates about 4% of pregnancies.
Causes:
Placenta praevia, Abruptio placenta, Uterine rupture.
Haemorrhage results in a reduction in the oxygen supply to both fetus and maternal
organs following the loss of circulating volume and red cell mass. Consequent cellular
hypoxia and acidosis may lead to organs dysfunction.
The utero-placental unit is at particular risk during haemorrhage due to:
Compensatory selective vasoconstriction results in division of blood from less vital
organs (skin, gut, muscle, kidneys, utero-placental unit) to maintain perfusion of the
more critical organs (heart, brain).
Absent auto regulatory capacity, reduction in maternal blood pressure results in a
decrease in the uterine blood flow with detrimental effects on the fetus.
Therefore during haemorrhage, rapid restoration of maternal blood volume with
adequate oxygen carrying capacity and treatment of the underlying causes improves
fetal well-being.
ABRUPTIO PLACENTAE
Definition:
Abruptio placenta is defined as the premature separation of the normally implanted
placenta.
It involves haemorrhage into the decidua basalis which splits and the decidual
hematoma leads to separation, compression and ultimate destruction of placenta
adjacent to it. This process occurs after 20 weeks of gestation but before delivery of the
baby.
Risk factors: Chronic hypertension, advanced maternal age, abdominal trauma,
multiparity and history of prior abruption.
In 85% of cases, at least part of the bleeding is external, but in 15% of cases, bleeding is
occult or concealed. Where fetal death occurs, blood loss is more than 2.5 liter. Uterine
tenderness, back pain, fetal distress or death, uterine irritability could be the other
forms of presentation.
Grade 0 – Clinical features of suggestive of abruption may be absent, the diagnosis is
made after infection of placenta following delivery.
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Grade I – 1) External bleeding is present
2) Tenderness on the uterus may or may not be present

3) Shock is absent
4) FHS is good.
Grade II – External bleeding may or may not be present
Uterine tenderness +
Shock is absent
Fetal delivery or even death.
Grade III – External bleeding may or may not be present
Uterine tenderness +
Shock pronounced
Fetal death
Associated coagulation defect may complicate
Mechanism of coagulation failure:

Consumptive coagulopathy
Enhanced fibrinolytic activity
The sequence of reverse abruption include
Haemorrhage, sometimes out of proportion to preventing symptoms and signs.
DIC (20-40% of cases)
Acute renal failure
Major organ necrosis
Anesthetic management:
General principles:
Maternal monitoring should include BP, ECG, urine output, CVP, pulse oximetry,
blood gas analysis, coagulation profile, serum electrolytes.
Establishment of two IV line (16 or 18 G cannula)
Immediate correction of fetal distress.
Placing the mother in the left lateral position.
Maternal oxygenation
Correcting maternal hypotension
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Discontinuing oxytocin.
{Hematological picture in Abruptio
1) Thrombocytopenia - < 1 lakh / cu mm
2) Depletion of fibrinogen - < 19 m / lit or < 150 mg / 100 ml
3) Prolonged PTT - > 1.5 times of normal, low level of V & VIII factors – reflects DIC.
1 unit of blood –
1) Raises platelet count by 10,000-15,000 cells / mm3
2) Hb by 1gm%
3) Hematocrit by 3%
4) Fibrinogen by 0.1g / litre.}
Correction of maternal hypovolemia, hypotension a major organ damage.
Safe delivery of fetus ( caesarean section)
Extraction of thromboplastic material by delivery of placenta and treatment of
coagulopathy.
In cases of consumption coagulopathy, fresh whole blood is the treatment of
choice, as it replaces volume and coagulation factors.
If fibrinogen level has fallen below 1gm/lit, fresh frozen plasma should be
preferred to fibrinogen concentrate. Platelet concentrate may be needed if
platelet count is less than 1 lakh cells / mm3
All this is usually necessary only when stored and not fresh blood is used in
therapy.
In an oliguric state, after correction of hypovolemia – mannitol in a dose of
0.5g/kg or dopamine about 1-2 µg/kg/min may be useful in restoring renal function.
PLACENTA PRAEVIA
Definition:
When placenta is implanted partially or completely over the lower uterine segment.
Classification:
Type I – lateral: The major part of the placenta is attached to the upper segment and
only the lower margin encroaches on to the lower segment but not upto the os
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Type II – Marginal – placenta reaches the internal os but does not cover it.(Placental
Position – anterior or posterior)
Type III – Incomplete central: Placenta entirely cover the os when closed but does not
entirely do so when fully dilated.
Type IV – central – placenta completely cover internal os even after it is fully dilated.
{History of previous placenta previa or cesarean section ensures the risks of placenta
accreta, placental increta and percreta}.
In these conditions, the placenta becomes adherent to the surface, invades the
muscle or completely penetrates the myometrium. It is difficult to or impossible to
separate from it. Moreover these conditions regularly produce life threatening maternal
haemorrhage.
Hysterectomy following delivery of the fetus is usually required to control
profuse bleeding following separation of the placenta. Coagulopathy is common.}
Clinical purpose:
Mild degree – type I and type II anterior
Major degree – Type II posterior and III and IV – frequently complicated with
bleeding.
Diagnosis is suspected from the C/S of painless bleeding and confirmed by
ultrasonography.
Pre-disposing factors:
Advanced maternal age and multiparous.
If the placenta praevia associated with bleeding due to uterine contractions – tocolytic
therapy is instituted.
Depends on the degree of urgency and the maternal and fetal status.
General principles:
Being the same as in case of abruptio placentae
Establishment of two IV lines (if maternal haemorrhage present)
Correction of fetal distress
Correction of maternal hypovolemia, hypotension
Tocolytic therapy – Bleeding associated with uterine contraction
Safe delivery of fetus (caesarean section).
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Chapter 12 - UTERINE RUPTURE
Uterine rupture is less common (0.4%) but potentially devastating cause of
obstetric haemorrhage.
It may occur in
Previously scarred uterus (previous C. section)
Uterine manipulation (forceps delivery)
CPD
Excessive uterine stimulation.
Multiparous
Rapid spontaneous delivery
Other risk factors include uterine anomaly, tumour, placenta percreta rupture of an
unscarred uterus can result in massive maternal haemorrhage.
Symptoms being – Severe abdominal pain, Maternal hypotension, Fetal distress.
Treatment
– Emergency laparotomy and may require obstetric hysterectomy.
General principles being the same –
Establishment of an IV line.
Correction of maternal hypovolemia.
Correction of fetal distress (by placing mother in left lateral position, maternal
oxygenation and correction of maternal hypotension) and
Safe delivery of fetus.
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Chapter 13 -ANESTHESIA FOR CAESAREAN SECTION IN
APH (EMERGENCY)
General anesthesia is the right choice, if maternal hypovolemia, hypotension
persists due to haemorrhage.
The usual precautions against a full stomach should not be forgotten.
Once the initial resuscitation has been effected and essential monitoring setup
1) Pre-oxygenation is done
2) Rapid sequence induction should be done with induction agent with:
a) Ketamine 0.5 – 1 mg /kg IV in decompensated bleeding. Or
b) Thiopentone 2-4mg/kg or sleeping dose in compensated bleeding.
No induction agent in a unconscious moribund patient.
3) Cricoid pressure is applied and 1.5mg/kg of succinylcholine administered
4) Endotracheal intubation performed. Cricoid pressure released after inflation of cuff.
5) Maintain N2O and O2 at 50%
6) After delivery of fetus, IV opioids and benzodiazepines can be supplemented.
7) Maintenance of relaxants is done by non-depolarizing relaxants – preferably
atracurium.
8) Oxytocin, ergometrine and prostaglandins are used to aid in uterine contraction.
Abruptio is often associated with uterine atony and post partum haemorrhage.
Because elevated fibrin degradation products cause uterine relaxation and inhibit the
action of oxytocin. In this situation, the alternatives are:
Intra-myometrial oxytocin
Prostaglandin F2
IV ergometrine.
Regional anesthesia in antipartum haemorrhage:
Regional anesthesia has no role in massive active haemorrhage. But in a stable
patient with no active haemorrhage, and an ultrasound diagnosis of placenta praevia
and mild abruptio placenta – regional anesthesia could be considered along with several
advantages.
The time taken to initiate the block can be deleterious particularly to the fetus.
Sympathetic blockade resulting in severe hypotension in a hypovolemic patient
by abolishing compensatory sympathetic stimulation.
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Abnormal coagulation parameters, if present could complicate a regional technique.
In a stable patient with mild abruptio or placenta previa with no active bleeding,
regional anesthetic cannot be dismissed because:
Retrospective studies have shown that when bleeding did occur, it will less in
patient who received regional blocks.
Other hazards under GA in emergency obstetric, such as the full stomach
problem is reduced.
Hence if a large bore IV access is established and if adequate colloids and
vasopressors are available, then regional blockade can be a good alternative to general
anesthesia in a stable patient with mild abruptio or placenta praevia with no active
bleeding.
POST PARTUM HAEMORRHAGE

Post partum haemorrhage complicates about 10% of deliveries
It is defined as blood loss greater than
500ml in vaginal delivery.
1000 ml in caesarean delivery
Causes:
Uterine atony
Retained placenta
Placenta accreta
Birth trauma
Uterine inversion
UTERINE ATONY
It is the most common cause of post-partum haemorrhage. It is due to failure of
uterine contraction which leads to uterine bleeding after delivery of placenta.
Risk factors for uterine atony:

Prolonged labour
Grand multiparous
Over distended uterus
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Twin gestation or more
Polyhydramnios
Big baby (Diabetic in pregnancy )
Tocolytic therapy
Chorioamnionitis.
Use of drug known to decrease uterine contractibility e.g. Inhalation agents.
Treatment:
Includes volume resuscitation and
Administration of utero tonic medications.
Oxytocic drugs for use in PPH:
Drug Dose Side effects
Oxytocin 5-10 units IV and 10-50 units Hypotension (due to peripheral
/ 1000 ml/NS IV at sufficient dilatation)
rate to produce uterine Tachycardia
contractions Pulmonary oedema (due mild
ADH effect) Water intoxication or
hyponatraemia.
Methyl ergometrine 0.2 mg IM or 0.2mg diluted in Nausea / vomiting, sever
10 ml NS slow IV or intra- hypertension, coronary artery,
myometrial injection spasm bronchospasm.
Prostaglandin 15- 0.25 mg 1M or 0.25 mg Nausea / vomiting, severe
methyl F2 diluted in 10 ml NS for intra hypertension, bronchospasm ,
myometrial injection Increased inter pulmonary shunt.
In rare circumstances where haemorrhage is not controlled with administration

of oxytocic drugs, necessitate for surgical intervention.
Bilateral ligation of ascending uterine artery
Bilateral ligation of ovarian artery
Ligation of internal iliac or hypogastric artery
Hysterectomy
Radiological intervention: Percutaneous arterial embolism.
Anesthetic management: It includes correction of maternal hypovolemia and surgical
intervention done under general anesthesia.
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Chapter 14 - RETAINED PLACENTA
Retained placenta exists when all part of the placenta fails to deliver
spontaneously within 1st hr of birth of baby. Haemorrhage results from failure of the
uterus to contract where the placenta is adherent.
Treatment:
Manual removal of placenta or via curettage
Volume resuscitation
Provision of adequate analgesia.
Regional technique:
Epidural or spinal anesthesia is performed if maternal volume states allows.
Uterus relaxation is obtained with intravenous administration of nitroglycerin
50-100 µg bolus dose with careful monitoring of maternal blood pressure.
General anesthesia
– including administration of volatile anesthetic to provide uterine relaxation, will be
necessary if the uterus remains firmly contracted around the placenta or os starts
closing.
Intubation of the trachea is necessary when general anesthesia is used to relax
the uterus.
Ketamine in a dose exceeding 1mg/kg i.e, not recommended in view of dose-
related increase in uterine tone produced by this drug.
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Chapter 15 - PLACENTA ACCRETA, INCRETA &
PERCRETA
In these conditions placenta becomes adherent to the surface, invade the muscle
or completely invades the myometrium. It is difficult or impossible to separate from it.
However these conditions regularly produce life threatening maternal haemorrhage.
Hysterectomy following delivery of the fetus is usually required to control
profuse bleeding following separation of placenta – It is ideally done under general
anesthesia. Coagulopathy is common.
Uterine inversion:
It is a rare cause of PPH in which fundus actually inverts through the cervix into
vagina and preventing uterine contraction.
Risk factor: Adherent placenta, prolonged labour.
Clinical features:
Patient will suffer severe shock either neurogenic (vasovagal effects) or
hemorrhagic
Anesthetic management – Rapid induction of general anesthesia with uterine
relaxation is necessary.
Uterine relaxation either by inhalation agents or nitroglycerin 50-100µg IV bolus.
Versions:
1) External cephalic versions – for transverse lie
2) Internal podalic version – for II twin
Anesthetic technique would be epidural analgesia.
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Chapter 16 - ANESTHETIC MANAGEMENT OF
OBSTETRIC PATIENTS FOR NON-OBSTETRIC SURGERY
Introduction:
Non-obstetric surgery in pregnant patients is becoming more common with the
advent of laparoscopic surgery.
Approximately 2% of pregnant women need to undergo incidental surgery
during pregnancy.
The common indication for surgery in pregnancy are appendiectomy, cervical
encirclage, ovarian cystectomy and increasingly trauma.
In the I and II trimester laparoscopy is the most common procedure followed by
abdominal genitourinary gynecological and endoscopic procedures.
The anesthetic management of obstetric patients for incidental surgery needs
special care to avoid maternal morbidity and fetal loss.
The basic objective in such a situation are:
Maternal safety
Avoidance of teratogenic drugs
Avoidance of intrauterine fetal asphyxia
Prevention of abortion or preterm labour.
FACTORS INFLUENCING ANESTHETIC CONSIDERATIONS:

During pregnancy the maternal anatomical and physiological changes as well as
the hormonal effects on various organs result in certain implication for administering
anesthesia which may have potential adverse effects on fetus.
I) Maternal considerations. II) Fetal considerations
I) Maternal considerations:
Cardiovascular system:
Increase blood volume (more increase in plasma volume than in red blood cell –
haemodilution and decrease in Hb concentration)
Increased cardiac output.
Decreased peripheral resistance and mean arterial pressure
Assumption of supine position by the pregnant patient beyond 16-20 weeks of
gestational age results in partial or complete obstruction of inferior venacava and aorta.
Significant hypotension may develop, so a left lateral tilt is advocated in all
pregnant patients.
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Distention of epidural veins cause a reduction in volume of extradural and
intrathecal space.
Thus a given volume of local anesthetic solution spread over more segment than
would normally. So 30-50% reduction in dose requirements of local anesthetic solution
for epidural and sub-arachnoid anesthesia in pregnant women is considered.
Respiratory system:
Decreased FRC, Increased oxygen consumption and diminished buffering
capacity result in rapid development of hypoxia and acidosis during periods of
hypoventilation or apnoea.
This indicates the importance of pre-oxygenation before any anticipated period
of apnoea in pregnant women.
FRC, minute volume, hastens inhalational induction and depth of anesthesia
when breathing spontaneously. Another factor that accelerated induction of anesthesia
is a decrease in MAC by 20-40% in pregnant women.
Women are more prone for anesthetic over dosage.
Gastro-intestinal system:
gastrointestinal motility gastric emptying time
in gastric volume with in gastric pH
LES tone (owing to progesterone levels)
Cephaloid displacement of stomach and intestine, positions the stomach
vertically with increase in intra-gastric pressure along with change in angel of gastro-
oesophageal junction leads to a greater oesophageal reflux.
It therefore seems prudent to consider any pregnant patient at risk for aspiration
after 18-20 weeks of gestation.
Central-nervous system:
in MAC % of inhalation agent
sensitivity of nerve to local anesthetic drugs.
Hematological system:
protein binding associated with low albumin concentrations during pregnancy
may result in a greater percentage of unbound drug needs in reduction of induction
agent dosage.
Plasma cholinesterase activity is decreased as gestational age increases.
Fortunately prolonged N-M blockade is uncommon because the large volume available
for drug distribution affects the impact of decreased drug by hydrolysis.
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Miscellaneous:
Enlarged breasts in an obese parturient with a short neck may lead to difficulty
in laryngoscopy. This may overcome by the use of a short handled laryngoscope.
II) Fetal considerations:
a) Avoidance of teratogenic agents:

Although maternal catastrophe that causes severe maternal hypoxia or
hypotension pose the greatest risk to the fetus, considerable attention has been focused
on the teratogenicity of anesthetics. Most commonly used anesthetics and pre-
mendicant drugs are teratogenic in some animal species, However whether such data
from animals studies could be extrapolated to humans is not clear. For a drug to be
teratogenic, it must given to a susceptible species in an appropriate dose for an
adequate duration of time and during a specific period of organ development. The stage
of gestation at which exposure occurs determines the target organ/tissue, the type of
defect and the severity of damage. Each organ and each system undergo a critical stage
of differentiation during which vulnerability to teratogens is greatest.
For instance the period of sensitivity of the heart is – 18-40 days, limbs – 24-34 days.
In general, the critical period of organogenesis in human is between 15 and 56
days of gestation. Surveys of women have received anesthesia for operations during
pregnancy have failed to demonstrate that any anesthetic by itself produces abortions
or congenital malformations.
Nitrous oxide:
It is known to inhibit Methionine synthase by oxidizing Vit. B12 resulting in impaired
DNA synthesis. Thus prolonged exposure to N2O may lead to abnormal cell
multiplication in rapidly growing tissues such as the developing embryo. In view of
sufficient circumstantial evidence of the harmful nature of N2O, it is rational to avoid its
use in I and II trimester of pregnancy.
Diazepam:
Association between the intake of diazepam and the occurrence of oral clefts has been
observed, although it is doubtful whether a single dose of diazepam used in pregnancy
would be harmful.
Using the above two examples, no anesthetic drugs or local anesthetic drug has
been proved to be teratogenic in humans. However in the wake of proven teratogenicity
of anesthetic agents in animal studies, it would be wise to minimize or eliminate fetal
exposure to drugs during the first trimester.
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Drug factors such as hypoxia, hypercapnia, hyperpyrexia and severe
hypoglycemia which can occur during the perioperative period can themselves be
teratogenic or they may enhance the teratogenicity of other agents.
Ionizing radiations is also a known human teratogens, dose related effects on
reproduction range from an increased risk of childhood cancer in offspring of exposed
mothers to congenital anomalies or fetal death. There is evidence to suggest that no
increase in major anomalies or growth restriction results from exposures below 5-10
rads.
Fetal exposure from a chest radiograph is estimated at 8 milli rads barium enema
– 800 milli rads.
b) Avoidance of intra uterine fetal asphyxia:

Fetal hypoxia is the commonest and most important form of fetal stress which
occurs in a pregnant woman during surgery, early intra-uterine hypoxia may cause
abortion / congenital malformations. Hypoxia occurring later in gestation causes fetal
death or brain damage.
Fetal oxygenation depends upon maintenance of maternal oxygen flux and utero
placental blood flow.
Maternal factors which can result in fetal hypoxia include Hypotension and
Arterial hypoxemia.
c) Prevention of abortion or preterm labour:

Most studies of non-obstetrical surgeries during pregnancy have reported an
increased incidence of abortion and preterm delivery. It appears from these studies that
the underlying pathology necessitating the operative intervention, rather than any
particular anesthetic technique and determines the occurrence of abortion.
The surgery involving pelvic viscera are more likely to be associated with
abortion as compared to extra pelvic procedures.
Second trimester procedures that do not involve uterine manipulation has the
lowest risk for preterm labour.
Although volatile anesthetic depresses uterine contractility and theoretically are
advantageous for abdominal procedures, there is no evidence that any anesthetic agent
or technique influence the risk of preterm labour.
The prophylactic use of tocolytic agents such as ritodrine, Isoxsuprine,
terbutaline and magnesium sulphate is controversial, they are not without risk and it is
unclear whether their use alters outcome.
Selective administration to those patients at highest risk such as those undergoing
cervical encirclage has been suggested.
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Intravenous ketamine in dose of > 1mg/kg should not be used – as it causes,
increases in uterine tone and probably should be avoided. Rapid IV injection of
neostigmine might stimulate acetylcholine release and increase uterine tone and
stimulate pre-term labour. Neostigmine when used to reverse the effects of muscle
relaxants, should be administered slowly and even then should be preceded by
adequate dose of glycopyrrolate or (atropine).
It was believed that maternal hypoxia would cause utero placental
vasoconstriction with possible impairment of fetal oxygen delivery. This fear has proved
baseless in studies in pregnant women have demonstrated improved fetal oxygenation
with increasing maternal PaO2. Fetal PaO2 were exceeds 60 mm Hg even when maternal
PaO2 increases to 600 mmHg because of large maternal fetal oxygen tension gradient.
The reasons for the large maternal – fetal oxygen tension gradient are high oxygen
consumption of the placenta and venous distribution of the maternal and fetal blood
flow in the placenta. Thus maternal hypoxia cannot produce retrolental fibroplasia or
premature closure of the ductus arteriosus in utero.
Maternal hypercapnia can cause fetal acidosis because fetal PaCo2 correlates
directly with maternal PaCO2. Although mild fetal respiratory acidosis is of little
consequence, severe acidosis can cause fetal myocardial depression and hypotension.
Maternal hyperventilation should be avoided inter operatively or excessive
positive airway pressures may decrease uterine blood flow. In addition, the respiratory
alkalosis which results increases the affinity of maternal haemoglobin for oxygen. Thus,
oxygen delivery to the fetus is hampered.
Maternal hypotension from any cause can jeopardize utero placental blood flow
and cause fetal asphyxia. Hence maternal hypotension should be meticulously avoided
and aggressively treated, utero placental blood flow can be adversely affected by high
levels of circulating catecholamines, either endogenous (or in apprehension, light plain
of anesthesia or pain) or exogenous (following administration of -adrenergic agents).
FHR monitoring:
1) Heart rate with beat to beat variability running from 120-160 beats / min is
normal to the fetus.
Continuous fetal heart rate monitoring using a trans-abdominal Doppler is
feasible beginning at approximately 16 wks of gestation. However fetal heart rate can be
monitored in even earlier to it by using trans-vaginal ultrasound prob. However
technical difficulties may be encountered during abdominal operations or when the
mother is very obese. Fetal heart rate variability, which is usually an indicator of fetal-
well being is present by 25-27 wks of gestation. Changes in baseline FHR and FHR
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variability caused by anesthetic drugs should be distinguished from changes that result
from fetal hypoxia.
Persistent severe fetal bradycardia usually represents true fetal distress. The
greatest value of intra operative FHR monitoring is that it allows optimization of
maternal conditions if the fetus shows sign of compromise.
An explained change in FHR mandates evaluation of maternal position, blood
pressure, oxygenation and acid base status and inspection of the surgical site to ensure
that neither surgeons nor retractors are impairing uterine perfusion.
External tocodynamometer:
2) Uterine activity should be monitored continuously with an external
tocodynamometer both during surgery and also for several days post
operatively. This helps in the early detection of preterm labour and the timely
institution of appropriate tocolytic therapy.
Timing of surgery:
Elective surgery should be deferred until 6 weeks after delivery when the
physiological changes of pregnancy would have returned to normal. When possible
surgery should be avoided during the I trimester, especially during the period of
organogenesis. Non urgent surgery should be postponed to the second trimester or the
risk of preterm labour is lowest. Only emergency surgery should be undertaken during
the I trimester. In any serious maternal illness, the remote possibility of fetal risks
imposed by anesthesia and surgery assume secondary importance. The primary goal is
to preserve the life of the mother. Whether to perform simultaneous caesarean delivery
depends on a number of factors including the stage of pregnancy, the risk to the mother
of a trial of labour at a later date and the presence of intra abdominal sepsis. If decided
appropriate, the caesarean delivery must be performed immediately before the surgical
procedure to avoid risks to the fetus.
Monitoring:
Maternal monitoring should include:
Non-invasive blood pressure measurement
E.C.G.
Pulse oximetry
Capnography
Temperature monitoring
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Special monitoring during surgery:
FHR monitoring
External tocodynamometer
During the pre-operative visit, women of child bearing age scheduled for elective
surgery should be carefully questioned regarding the possibility of being pregnant and
also should be evaluated for possible co-existing diseases.
No effort should be spared during the pre-operative visit to alloy maternal
anxiety and apprehension. If pre-medication is necessary to alloy anxiety and
apprehension, barbiturates are preferred to minor techniques such as diazepam.
Glycopyrrolate, unlike atropine does not cross the placental barrier can be used.
Pregnant women should never be allowed to assume the supine position after 20
weeks of gestation. They should be nursed or transferred to the operation theatre in the
lateral position.
Local or regional anesthesia:

Should be used whenever possible as local anesthetics are not teratogenic. Crystalloid
preloading and use of left uterine displacement can prevent hypotension occurs despite
the above precautions, one may treat with additional IV fluids and -adrenergic agonists
(ephedrine) and to avoid -adrenergic drugs as these adversely affect the utero-
placental circulation.
General anesthesia:
If GA is chosen, it must be remembered that pregnant women may be at increased risk
for pulmonary aspiration of gastric contents. Hence, measures such as pre-operative
administration of oral-antacids and the use of cricoid pressure and rapid sequence
induction are essential. Pre-oxygenation is mandatory to avoid maternal and fetal
hypoxia.
The anesthetic technique should ensure adequate support of ventilation and
avoid maternal hyperventilation at all costs.
Scientific evidence does not support the avoidance of nitrous oxide during
pregnancy, particularly after the 6th week of gestation. Omission of N2O may increase
fetal risk, if inadequate anesthesia results or if a high dose of volatile agent causes
maternal hypotension. A caution approach would be to restrict N2O administration to a
concentration of 50% in operations of short durations and to avoid its use altogether in
extremely long operations.
Post-operative case:
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It should ideally be in an obstetric unit so that fetal heart and uterine activity can
be closely monitored. Attention should be paid to the provision of adequate post-
operative analgesia, either with acetaminophen or narcotic analgesics. Patient receiving
potent narcotic post analgesics may be unaware of mild uterine contractions. Personnel,
taking care of such patients in the post-operative period should be aware of the
possibility and exercise additional surveillance to detect pre-term labour. Avoid
acetosalicylic acid and NSAID’s as they may stimulate in utero closure of the ductus
arteriosus via inhibition of prostaglandin synthesis.
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Chapter 17 - LAPAROSCOPY DURING PREGNANCY
It is routinely being performed for cholecystectomy, appendiectomy, ovarian
torsion and surgery for adnexal masses.
The II trimester laparoscopic surgery is safer is the risk of spontaneous abortion
and risk of congenital malformations is low as compared to II trimester.
The risk of preterm labour and restriction of surgical access and vulnerability to
uterine trauma during trocar placement in the III trimester is also avoided.
Two major problems encountered are 1) Maternal hypotension
2) Gas embolism.
Pregnant patient are more susceptible due to the venous distention associated
with pregnancy and the high inflation pressure of 20-40 mm Hg in gynecological
surgery.
Recommendations for safe laparoscopy:

Surgery should occur in II trimester before 23rd week of pregnancy
Avoid using the trocar, use the open technique of trocar and needle placement.
Continued monitoring of ECG, BP, O2 saturation and end tidal carbon dioxide.
FHR monitoring with trans vaginal ultrasound probe
CO2 pneumoperitoneum cause significant fetal acidosis. Maternal ventilation
should be adjusted to maintain physiological alkalosis.
If maternal PaCO2 level are kept at basal values, fetal placental perfusion blood flow, pH
and blood gas tensions are unaffected.
Tocolytic agents may be helpful in alerting preterm labour.
The intra-abdominal pressure caused by pneumoperitoneum is much less than
the physiological pressure tolerated by the fetus during mid pregnancy uterine
contractions.
General anesthesia with endothelial intubation and controlled ventilation is
safest.
PCO2 should be maintained at approximately 35mm Hg.
Trauma and pregnancy:
Trauma occurs in 5-10% of pregnancies and it is responsible for 36 maternal
deaths / 100,000 pregnancies.
Fatigue, anemia, unsteadiness of gait and ligamentous laxity associated with
pregnancy predispose the parturient to fall and blunt abdominal trauma. Penetrating
abdominal injury from violence and accidents are also common.
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Precautions:
Fetal status may be jeopardized like pre-term labour, placental abruption, direct
fetal injury and hemorrhage.
Intrauterine fetal death can lead to disruption of utero placental unit which
carries the potential of returning tissue thromboplastins into the maternal circulation.
DIC and potential ARDS may further complicate the perioperative management.
Aim of anesthesia for:

Delivery Non-obstetric surgery
1) Pain free labor and delivery without To provide surgical anesthesia without
interfering with the progress of labour stimulating uterine activity and
precipitating premature labour or abortion
2) Obstetric anesthesia should provide To maintain utero-placental perfusion but
maternal analgesia without fetal neurologic without consideration for fetal neurologic
depression and delayed neonatal breathing or respiratory depression.
LAPAROSCOPIC TUBAL LIGATION:

Physiological changes of pregnancy persist till 6 wks of post partum.
Preoperative concerns include.
Decreased blood Hb concentration (physiological and blood loss).
The persistent increased risk of pulmonary aspiration.
Laparoscopic sterilization is commonly associated with minimal blood loss. Hb
levels as low as 7g/dl are considered safe.
The risk of pulmonary aspiration is diminished by

Minimum of 8hours of fasting
Premedication with an H2 histamine blocker.
A clear antacid (sod. Citrate)
Metoclopramide
Decrease plasma concentration of plasma cholinesterase
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Problems with laparoscopy
Technique of anesthesia:
For laparoscopic sterilization general endotracheal anesthesia is preferred.
Preoxygenation with 100% 2 for 3-5 minutes.
Rapid sequence induction and intubation: Inj thiopentone 3-5 mg/kg i.v once the
patient loses consciousness apply cricoid pressure. Under succinylcholine 1-2 mg/kg IV,
endotracheal intubation should be done. After inflation of cuff to adequate level cricoid
pressure can be released B/C air entry confirmed.
Maintenance of anesthesia: N2O – O2 – atracurium (0.5mg/kg i.v solutions 0.1 mg/kg
iv. supplement) – opioids (Fentanyl 2µg/kg IV) – IPPV.
Monitoring: Apart from routine monitoring
Monitoring for IAP < 15cm H2O
Monitoring for Air embolism
Reversal: Neostigmine 0.05mg/kg iv. + anticholinergics, atropine 0.02 mg/kg i.v.
Extubation: After thorough suctioning when the patient is fully awake extubation can
be done.
Post-operatively: Patient should be given analgesia. Monitoring should be
continued.
Post operative advice to the patient  to avoid breast feeding 12-24 hours
following general anesthesia.
Problems associated with laparoscopic procedures are due to

Insufflations of gases – CO2 has least potential for air embolism but can cause
hypercarbia arrhythmias and past-operative shoulder pain due to formation H2CO3 due
to diaphragm irritation.
Position of the patient

The trendelenburg position (10-20 degrees)
1. It increases the central blood volume and CO but reduces VC, FRC and lung
compliance thus predisposing to atelectasis.
Therefore work of breathing is increased and so spontaneous respiration should not
be considered.
2. It increases intracranial and intra ocular tension.
3. An inadvertent right main stem bronchial intubation due to cephalad displacement
of the carina and diaphragm might result in hypoxia.
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Pneumoperitoneum: Pneumoperitoneal and the accompanying raised intra abdominal
pressure (IAP) results in cardio respiratory instability and other side effects.
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Chapter 18 - AMNIOTIC FLUID EMBOLISM
Rare (1:20,000) catastrophic and life threatening complication of pregnancy that
occurs in the setting of a disrupted barrier between the amniotic fluid and maternal
circulation.
80% mortality. And 50% mortality in the first hour.
3 common sites of entry of amniotic fluid into maternal circulation are
Endocervical veins, Placenta and Uterine trauma site.
Can occur during labour or delivery, cesarean section or post partum.
- Amniotic fluid contains, Desquamated fetal debris, Prostaglandins and
leukotrienes.
- Alternative term “anaphylactoid syndrome of pregnancy” suggested to
emphasize role of chemical mediators in this syndrome.
Signs and symptoms:

Onset – dramatic and abrupt.
Dyspnoea, Arterial hypoxemia,
Cyanosis, Seizures,
Loss of consciousness, Hypotension (Disproportionate to blood loss)
Acute pulmonary embolism, Uterine atony,
Fetal distress is present at the same time,
Cardiopulmonary arrest in 80%,
Coagulopathy resembling DIC with associated bleeding, May be the only presenting
symptom.
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Pathophysiology:
Amniotic fluid embolism
eeeeembolism
Mechanical obstruction Humoral obstruction
Critical pulmonary vessel obstruction Pulmonary Vessel vasospasm
Acute Pulmonary HTN & Hypoxemia
Severe neurologic Spontaneous resolution LVF

impairment/death
Diagnosis: Signs of symptoms.

Increase pulmonary artery pressure.
Decrease cardiac output.
Amniotic fluid material in the parturient blood aspirated from a central venous
or pulmonary artery catheter - Confirmatory.
Autopsy lung biopsy.
Differential diagnosis:
- Aspiration of gastric contents (bronchoconstriction)
- Pulmonary embolism (chest pain)
- Venous air embolism
- Local anesthetic toxicity (high spinal level)
- High epidural anesthesia
- Total spinal anesthesia
Treatment: Arrest – CPR

 Tracheal intubation and mechanical ventilation of lungs with 100% O2. PEEP is
often helpful.
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 Inotropic support – guided by CVP and PAC dopamine, dobutamine and
norepinephrine – to treat acute LVF and hypotension.
 Fluid therapy – guided by CVP. - Prone for pulmonary edema.
 DIC treated with FFP, cryoprecipitate and platelets.
 Uterine atony – oxytocin and methylergometrine.
 Expeditious delivery appears to improve maternal and fetal outcome 
immediate cesarean delivery.
CPR:
Before delivery of fetus – difficult.
Chest compressions marginally effective.
Aortocaval compression impairs resuscitation in supine position.
Chest compressions are less effective in a lateral tilt position.
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Chapter 19 - LABOUR ANALGESIA
INTRODUCTION:
Labour and delivery are very different from any other physiological condition.
Not only these are associated with changed physiological parameters, but also it is
indeed the only physiological state that is painful. It is perhaps the only painful
condition that is always temporary, even without treatment, and usually associated with
a wonderful outcome.
Despite the finite nature of pain, labor has been described as more painful than
most clinical pain syndromes and pain resulting from chronic as well as accidental
injury. Indeed only causalgia in chronic pain patients and the traumatic amputation of
digit have been associated with more pain than labor.
For this reason, it is no surprise that long before the era of modern anesthesia,
attempts were made to relieve labor pain.
Pain as defined by international Association for study of pain as "an Unpleasant
sensory and emotional experience associated with actual or potential tissue
damage, or described in forms of such damage".
Pain pathways:
There are 2 pain pathways associated with labor, which are carried by different
peripheral nerves.
The first stage of labor starts with the onset of regular strong uterine
contractions causing changes in cervical dilation and lasts until there is full cervical
dilation. The pain of this stage is visceral in nature, and is associated with the stretching
or dilation of the cervix and lower uterine segment. As such it is modified through the
different nerve supply of the uterus via the sympathetic nerves and it is referred to the
dermatomes supplied by the T10-L1 spinal nerves.
The second stage of labor starts from the time from the full cervical dilatation
until the delivery of the neonate. This pain is somatic in nature due to pressure of
presenting part of the fetus leading to distension of the outlet and perineum which
causes intense stretching of the fascia and subcutaneous tissues. The peripheral somatic
nerve pathways are carried via pudendal nerve that is derived from the posterior roots
of S2 S3 and S4 spinal segment.
NERVE SUPPLY OF THE UTERUS AND THE BIRTH CANAL

Somato-sensory fibers from the body of the uterus bilaterally reach the
paracervical tissues, traverse the cervical plexus and confine in the base of broad
ligament passing through the inferior, middle and superior hypogastric plexus entering
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the sympathetic chain in the lumbar and lower thoracic region and centrally
connected by the white rami communicants of T10-L1.
Impulses from the vagina, vulva and perineum reach S2 to S4 through the
pudendal nerve, some areas of perineum and vulval skin are innervated by
ilioinguinal, genitofemoral, posterior femoral cutaneous nerves and by cutaneous
branches of S2-S4.
Labor and vaginal delivery produce tissue damage, and like tissue injury from
any other causes, result in pain and local, segmental, supra segmental and
cortical responses. There are different reflex autonomic responses at various
levels.
1. Local effects.
Pain, hyperalgesia and tenderness,
2. Segmental changes
Raised skeletal muscle tension
Decreased chest wall compliance and decrease in gastrointestinal and genito
urinary motility.
3. Supra segmental changes

Neuroendocrine responses-increasing in catabolic hormones.
Increased sympathetic tone, Rise in Cardiac output, fall in gastrointestinal,
genital and urinary motility.
Medullary center response-hyperventilation
Cortical responses-pain, perception, anxiety, fear and apprehension.
Physiological changes secondary to pain in labor.

Effects of Analgesia:
Maternal hyperventilation is reduced as a result of adequate pain relief. Thus
periods of hyperventilation during contraction followed by hypoventilation in between
contraction is also avoided.
Epidural analgesia, by blocking pain impulses as well as sympathetic efferent
reduces the release of catecholamines, cortical and ACTH, reducing the stress response.
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Analgesia also reduces the marked rise in CO and blood pressure due to pain.
This may be especially beneficial to the patients with cardiac disease, PIH and
Pulmonary HTN. Maternal and fetal metabolic acidosis is also reduced.
OBSTRETIC EPIDURAL:
Epidural Space in Pregnancy.
Alterations in the anatomy of the epidural and subarachnoid spaces are influenced
by pregnancy and labor are responsible for the reduced local anesthetic dose
requirement for pregnant women.
OBSTETRICAL REFLEXES:
First described by Ferguson in 1941
It is a neurohumoral reflex. The stimulus for evoking this response is distension
of the birth canal. Uterine contractions and impulses from the lower uterine segment
produce a certain degree of stimulation, referred to as the first Ferguson reflex.
With cervical dilatation and the onset of the second stage, from full dilatation 10
crowning, there is a marked increase in impulses referred to as the second
Ferguson reflex, which markedly augments the secretion of oxytocin.
Indications:
Patient request, pain relief in labor
Pre-eclampsia, in-coordinate uterine action, premature labor, maternal CVS or
respiratory disease, DM, Breech presentation, multiple pregnancy.
Contra-Indications:
Patient refusal -Local infection
Coagulopathy or anti coagulant therapy
Hypovolemia, hemorrhage or shock
Inadequate facilities or supervision.
Epidural Analgesia and Anesthesia:
First achieved by CORNING unintentionally in 1884, epidural analgesia and
anesthesia are the gold standards against which other techniques are compared.
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Optimal time for starting Analgesia:
Depends on several factors, including: (1) Whether epidural analgesia is
being used for spontaneous or induced labor (2) Severity of the pain (3) the
obstetric conditions (4) Preference of the obstetrician regarding use of oxytocics, out
let forceps (5) the presence of special indications for the procedure.
Conditions Essential to Initiation of Epidural Analgesia or Anesthesia

1. The parturient should be in active phase of labor and experiencing moderate or
severe pain during uterine contraction.
2. The contractions should be regular, of good intensity and occurring at intervals
of 3 min or less and lasting 35-40 sees or longer.
3. The presenting part should be engaged in the pelvis
4. The cervix should be dilated 3 to 4cm in multipara and 4 to 5cm in primipara.
Some technical considerations:
Preliminaries:
Explanation to familiarize the mother with the concept of epidural analgesia.
Written Consent should be taken
A brief history should search for any major contra indications
Check fetal FHS and maternal blood pressure and commence the IV fluid
preloading before positioning the patient for epidural injection.
Pre-hydration:
An IV fluid load of 500-1000ml of Hartmann's solution should be given to every
mother which will reduce the incidence of FHR disturbance and maternal
hypotension.
Position of Patient:
Left lateral position is the best
Sitting position is the best for the patient with a difficult back, in the obese
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Approach to the Epidural Space:
The midline approach between lumbar spines is most commonly used.
Identification of the Epidural Space:

Loss of resistance should be sought using a freely sliding syringe filled with air or
saline.
Insertion of Epidural catheter and Timing of injections:

If labor is progressing rapidly or the pain is severe, the first dose should be
injected through the Touhy needle before the catheter in inserted.
Catheter should not be inserted during a contraction
Injections should be made between contractions so as to avoid the risk of
increased spread.
Injections in the Lateral Position:
Strict avoidance of the supine position is vital.
Test dose in obstetric epidural:
The purpose of the epidural test dose in the obstetric patient is to assure that the
bulk of the injected is in the epidural space.
Potential spaces for the injected are a blood vessel or the intrathecal or subdural
space.
Another very important role, and perhaps the most significant of the test dose is
to detect intravascular position of epidural catheter. In pregnancy there is
engorgement of the vertebral venous plexus and this is directly connected to the
heart by the azygous venous system. The vertebral venous plexus is also directly
connected to the cerebral circulation. There is a 4-fold increased incidence of
epidural catheter migration into a vessel in parturient and also increased
chances of CNS as well as CVS toxicity,
Local anesthetic with or without epinephrine is used as the test dose.
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Segmental block technique:
a. Intermittent technique:
- Initial procedure
1. Procedure done during latent phase
2. Needle puncture L3 - L4 space
3. Advance catheter 3cm-L2
4. Withhold injections until onset of moderate labor pain
5. Inject test dose
Drugs and dosage used in this technique:

Bupivacaine. 0.25% 6-10ml.
0.125% 10-15m1. 0.1 - 0.125% + opioid. 10 - 15ml
Ropivacaine. 2mg/ml 8 - 12ml
1mg/ml + opioid. 10 -15ml
Fentanyl - 2 -5 g/ml
Sufentanil - 0.5 - 1 g/ml
b. Double catheter technique:

Initial Procedure
1. Needle puncture at L2 - L3 - catheter advanced 5cm to T12
2. Needle puncture through SCH (Sacrococcygeal hiatus) -advance catheter 2cm in
sacral canal to S3 vertebra.
3. Both catheter inserted at same time during latent phase
c. Continous epidural infusions (CEI):

After a satisfactory block in the standard technique is obtained, the CEI is
started.
Advantages: Constant analgesia, less motor block, lower medication dosages, more
constant level of block, less variation in the vital signs.
Drugs and dosage in CEI:

Bupivacaine - 0.125% or 0.0625% + opioid, 8 - 10ml/hr.
Ropivacaine - 0.08 - 1mg/ml + opioid
Fentanyl - 1 - 2 g/ml
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Adrenaline 1:800000
Sufentanyl - 0.5 g/ml
The term “walking epidural” was coined by Breen. He introduced an ultra-low dose
Bupivacaine (0.04%), epinephrine (1.7 g/ml), and Fentanyl (1.7 g/ml) solution for
labor (15 ml bolus followed up by an infusion at 15ml/hr) which allowed the
parturient ambulate.
Combined spinal epidural technique (CSE):

The CSE technique has gained increasing popularity since the introduction of
neuraxial opioids.
It can be done by needle-through-needle technique, single segment or double
segment technique.
Advantages:
Faster onset of analgesia, decreased incidence of motor blockade, greater degree of
patient satisfaction, decreased incidence of accidental dural punctures and a lower
amount of local anesthetics in the systemic circulation.
A common side effect of intrathecal lipid soluble opioids is pruritis. The Medullary
dorsal horn is the area most likely responsible for this effect. (Treatment Nalbuphine
5-10mg), or naloxone (40 to 80 g), Propofol (10mg) and diphenhydramine
(25mg) Ondansetron 8mg)
Other side effect is nausea and vomiting secondary to the cephalad spread of the
opioid reaching the vomiting center and (CTZ).
Another side effect of concern of the CSE technique is fetal bradycardia.
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Suggested drug doses and mixtures for labor CSE:
Administration Local anesthesia Opioid
Intrathecal injection Bupivacaine l - 2.5mg Fentanyl 20-25 g or
Sufentanyl 3-5 g
Epidural top-ups Bupivacaine (0.1%-0.125%) Fentanyl 20 - 25 g
10-15mg for first stage of labor. Sufentanyl 5 - 10 g
During 2nd stage this dose usually
will be sufficient
PAIN RELIEF IN LABOR - NON REGIONAL

The three forms of non-regional analgesia available to women in labor most
familiar to anesthetists are TENS, nitrous oxide (Entonox) and systemic opiodis.
However, in this era of "changing child birth" it is important that anesthetists working
on the labor wards are familiar with alternative approaches.
Psychological methods:
A number of psychological techniques have been used to assist women with the
pain of labor, including hypnosis and psycho prophylaxis.
Physical methods:
a. Transcutaneous electrical nerve stimulation (TENS)
TENS is a method of pain management that is non-invasive, portable, easy to use
and quickly discontinued if necessary.
Used originally for the relief of chronic pain, trauma and post-surgical pain,
recently it is a popular analgesic technique for the relief of pain in labor.
Efficacy: In general TENS is most effective of reducing the back pain associated with the
first stage of labor.
Side effects and complications:
TENS appears to be free from significant side effects and complications for
both mother and baby. Some women find the tingling sensation unpleasant or the
electrodes irritating.
MASSAGE: In 1990, Massage was the most popular form of simple analgesia despite the
fact that efficacy was low and supplementary techniques were usually required.
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Other physical methods:
Water Baths: Water baths are used as an analgesic relaxation technique by many
women before admission to the delivery unit and during labor.
Temperature should be restricted 37°C
Water Blocks: The water block technique involves a series of injections of sterile water
(0.1-0.5ml) at 4-6 points over the sacral border in the lower back.
Abdominal decompression: Abdominal decompression was a technique developed in
1955 by South African professor O.S. Heyns. The Technique involved encasing the
abdomen in an airtight shell and exposing it to a negative pressure of 20- 15mm Hg.
The technique has been largely abandoned since 1960’s c
Inhalation agents:
Ether and chloroform:

Ether was the first inhalation agent used for analgesia in labor.
In January 1847, James Young Simpson first documented the use of ether in
obstetrics when, it was given to deliver a dead fetus following an obstructed
labor.
When John Snow administered chloroform to Queen Victoria for the birth of
Prince Leopards on 7th April 1853, it marked a turning point in the history of
obstetric analgesia.
Despite this, chloroform remains the most commonly used inhalational analgesic
in labor until the wide spread introduction of nitrous oxide in the 1930's.
Nitrous Oxide:
History:
Nitrous oxide, identified by Joseph Priestly in 1772, was first investigated
clinically by Sir Humphrey Davy in 1798.
Nitrous oxide was first used in obstetric practice in 1880 by stanislav
kilkowitsch. Because of expense in production and difficulty in developing
delivery systems, nitrous oxide did not become widely available until the
1930's.
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In 1933 Minnitt designed a system for premixing Nitrous Oxide and air in a 50:
50 mixture. However, it rapidly became apparent that such mixtures caused
hypoxia, delivering as little as 8% of O2 and harmful to both mother and fetus.
In 1963, Tunstall demonstrated that, when mixed with 50% oxygen, N2O did not
separate into the liquid phase at a pressure of 2000 lb/ln2 and an adequate
degree of analgesia that could be safely administered.
Physical properties:
Entonox is a mixture of 50% N2O in 50% O2 that is supplied in cylinders at a
pressure of 137 bar (2000 .b/in2). At this pressure the two gases, "dissolve"
into each other, preventing the liquefaction of N2O.
Analgesia is rapid in onset due to the low blood gas solubility coefficient.
It is rapidly eliminated from the lungs between contractions such that there is
minimal accumulation in mother or fetus even during prolonged use in labor.
Other agents:
Trichloroethylene (Trilean)
Methoxyflurane:
Systemic opioids:
Meperidine (Pethidine):
IM dose is 50 to 100 mg and IV dose is 25 to 50mg.
Peak analgesic effect occurs 40 to 50 minutes after IM administration and 5 to 10
minutes after IV administration. The duration of action is 3-4 hours.
Meperidine used for labor analgesia can produce dose dependent neonatal
depression, decreased APGAR scores and abnormal results from neuro
behavioral examination.
Fentanyl:
The usual doses of Fentanyl used during labor are 50 to 100µg IM and 25 to 50 g
IV. After IV administrations the peak effect occurs within 3 to 5 minutes and the
duration is 30 to 60 minutes.
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Placental transfer is rapid. Temporary analgesia and mild sedation were
apparent after administration of 50 to 100 g. A transient decrease in FHR
variability was noted.
Morphine:
The peak analgesic effect of morphine occurs 1 to 2 hrs after IM administrations
and 20 minutes after IV administration. The duration of action is 4 to 6 hours.
In equianalgesic doses, morphine produces more respiratory depression of new
born than doses of pethidine.
Morphine is no longer used in labor analgesia.
Ketamine: Has been used to produce analgesia during labor (0.25mg/kg).
REGIONAL BLOCKS:
- Local Infiltration n
- Pudendal Block
- Transvaginal Pudendal Block
- Transperenial Pudendal Block
- Paracervical Block
CONCLUSION:
Is there a need to relieve labor pain? Women have delivered for eons without
pain relief.
American Society of Obstetricians and Gynecologists (ASOG) Statement.
"Labor results in severe pain for many women. There is no other circumstance,
where is considered acceptable for a person to experience sever pain amenable to safe
intervention, while under physician's care. Maternal request is a sufficient justification
for pain relief during labor”.
As stated by Hippocrates, “DIVINE IS THE TASK TO RELIEVE PAIN”.
This is especially so when we are considering two lives.
Having established the need to relieve labor pain the question to be answered is,
Is epidural analgesia the best method of pain relief in the world today?
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Anesthesiologist’s View:
Epidural analgesia is regarded by anesthesiologists as the gold standard by
which other analgesic techniques are compared. Epidural analgesia provides good to
excellent pain relief, is rapid in onset, and flexible, with minimal morbidity, when
administered by trained personnel.
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Chapter 20 - WALKING EPIDURALS IN LABOUR
Epidural blockade used for pain relief in labour should produce a barely sensory
block from T10 – S5 with retention of sensation without pain and maintenance of motor
power.
Mobile epidural
Advantages:
1. Increase maternal satisfaction.
2. Reduce long term maternal blockade.
3. Reduce the requirement of forceps delivery.
4. Less (or)can avoid supine hypotensive syndrome
5. Decrease incidence of deep vein thrombosis and pulmonary embolism
6. Less use of local anesthetics and can avoid the side effects of L.A.
7. Less (or) reduced need to catheterize the bladder.
8. Reduction in nursing problems.
When motor power is maintained, it is possible for the women to get up and walk
about (or) sit in the chair rather than bed.
Advantages:
Less pain
Shorter labour
Better fetal heart rate
Less difficulty in bearing down
Greater maternal acceptance
Walking epidurals are one, result of balanced analgesia, which first like balanced
general anesthesia, uses smaller doses of more than one drug to reduce unpleasant side
effects.
Side effects:
Medico-legal consequences of falls.
Fall due to hypotension
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Dizziness
Difficulty in fetal monitoring
Requisite:
Always advisable to have the patient accompanied by another adult when walking.
Dose:
Bupivacaine: 0.125% + 1 – 2 µg/ml fentanyl.
Bupivacaine: 0.125% + Tramadol 50mg
Fentanyl – 50 µg (or) 10 µg sufentanyl. Bupivacaine 0.04 – 0.25% in 10 ml.
Indications Contraindications
1)PIH 1) Patient refusal
2)MS 2)Blood coagulopathy
3)Pulmonary HTN 3)Infection of intended site of puncture
4)In-coordinate uterine contractions 4)Generalized septicemia
5)Pain free labour 5)Allergy to local anesthetic affect
6)Failure to progress 6)Lack of adequate facility or staff
7)Premature labour 7)CPD
8)For up delivery 8)Previous LSCS
9)Maternal distress 9)Malpresentation
10)Patient request 10)Large babies
11)DM
203

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2011

Dr Azam's Notes in Anesthesiology

Obstetrics and Gynecology

Dr. Mohammed Azam Danish

Dr Azam’s Notes in Anesthesiology

Obstetrics and Gynecology

www.DrAzam.com Obstetrics &Gynecology

Graphic representation of data is an excellent form of data compression; figures or

I constructed parts of Dr Azam’s Notes in Anesthesiology for Postgraduate students

Dr Azam’s Notes is aimed primarily at trainees in Anesthesia though more experienced

The format is designed to provide easy access to information presented in a concise

www.DrAzam.com Obstetrics &Gynecology

Anesthesiology is an ever-changing field. Standard safety precautions must be followed,

However, in view of the possibility of human error or changes in medical sciences,

www.DrAzam.com Obstetrics &Gynecology

To Mohammed Shafiulla, my father, my oxygen,

I also would like to thank my mom (Naaz Shafi), my wife

I also thank my Colleagues Dr Rajshekar Reddy & Dr Sachin for

Finally, I would like to thank my teachers. The dream begins

www.DrAzam.com Obstetrics &Gynecology

www.DrAzam.com Obstetrics &Gynecology

CHAPTER 1 - PHYSIOLOGICAL CHANGES OF PREGNANCY ............................................................................... 11

WEIGHT GAIN AND WATER METABOLISM: .................................................................................................................. 11

CHAPTER 2 - PLACENTAL CIRCULATION .......................................................................................................... 39

CHAPTER 3 - ANESTHESIA FOR PET................................................................................................................. 46

CLASSIFICATION OF HYPERTENSIVE DISEASES IN REGNANCY: ......................................................................... 46

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CHAPTER 4 - PLACENTA AND ITS CIRCULATION .............................................................................................. 78

PLACENTA AND ITS CIRCULATION: ................................................................................................................... 78

CHAPTER 6 - ASTHMA IN PREGNANCY ......................................................................................................... 120

PATHOPHYSIOLOGY: ............................................................................................................................................ 120

CHAPTER 7 - EMERGENCY CAESAREAN SECTION: BEST PRACTICE ................................................................ 130

TABLE: CATEGORIZATION OF URGENCY OF CAESAREAN SECTION ................................................................................... 130

DISCUSSION: ...................................................................................................................................................... 137

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CHAPTER 10 - OBSTETRIC HAEMORRHAGE .................................................................................................. 158

Physiological anemia:................................................................................................................................ 158

CHAPTER 11 - ANTE PARTUM HAEMORRHAGE (APH) .................................................................................. 161

CHAPTER 12 - UTERINE RUPTURE ................................................................................................................. 167

TREATMENT ....................................................................................................................................................... 167

CHAPTER 13 -ANESTHESIA FOR CAESAREAN SECTION IN APH (EMERGENCY) ............................................... 168

REGIONAL ANESTHESIA IN ANTIPARTUM HAEMORRHAGE ............................................................................................. 168

CHAPTER 14 - RETAINED PLACENTA ............................................................................................................. 171

Treatment: ................................................................................................................................................ 171

CHAPTER 15 - PLACENTA ACCRETA, INCRETA & PERCRETA .......................................................................... 173

CLINICAL FEATURES: ............................................................................................................................................ 173

FACTORS INFLUENCING ANESTHETIC CONSIDERATIONS: .............................................................................. 174

CHAPTER 17 - LAPAROSCOPY DURING PREGNANCY..................................................................................... 182

RECOMMENDATIONS FOR SAFE LAPAROSCOPY: ......................................................................................................... 182

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CHAPTER 18 - AMNIOTIC FLUID EMBOLISM ................................................................................................. 187

SIGNS AND SYMPTOMS:........................................................................................................................................ 187

CHAPTER 19 - LABOUR ANALGESIA .............................................................................................................. 190

CHAPTER 20 - WALKING EPIDURALS IN LABOUR .......................................................................................... 202

ADVANTAGES: .................................................................................................................................................... 202

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Weight gain and water metabolism:

The total weight gain at term is distributed as

1) Reproduction weight gain =6 kg

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Plasma protein changes during pregnancy:

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What are the anatomical changes seen?

What are the physiological changes seen?