Download Neuropathic pain

Our view of pain has changed over the
centuries as our understanding of this
universal condition has improved.
 Early humans viewed pain as a
punishment from the deities for a variety
of sins as exemplified by the legend of
Prometheus.
 Prometheus was sentenced by Zeus to
eternal torture for giving the fire reserved
for the gods to mortals

Artist's depiction of Prometheus
The seventeenth-century scientist and
philosopher, Descartes(Fig. 17.2),
changed this view in a single instant by
his drawing of a fire burning the foot of a
man.
 Descartes postulated a rational basis for
pain premised on the then radical notion
that pain was sensed in the periphery
and then carried via the nerves and
spinal cord to the brain (Fig. 17.3).

In 1965, Melzack and Wall2 proposed the gate control
theory of pain. The final model, depicted in Figure 1.1D in
the context of earlier theories of pain, is the first theory of
pain that incorporated the central control processes of
the brain.
 The gate control theory of pain2 proposed that the
transmission of nerve impulses from afferent fibers to spinal
cord transmission (T) cells is modulated by a gating
mechanism in the spinal dorsal horn. This gating
mechanism is influenced by the relative amount of activity
in large- and small-diameter fibers, so that large fibers
tend to inhibit transmission (close the gate), whereas small
fibers tend to facilitate transmission (open the gate).
 In addition, the spinal gating mechanism is influenced by
nerve impulses that descend from the brain.

Pain may be roughly divided into two broad
categories: physiologic and pathologic
pain.
1. Physiologic (acute, nociceptive) pain is an
essential early warning sign that usually
elicits reflex withdrawal and thereby
promotes survival by protecting the
organism from further injury.
2. In contrast, pathologic (e.g., neuropathic)
pain is an expression of the maladaptive
operation of the nervous system; it is pain
as a disease.

Physiologic pain is mediated by a sensory
system consisting of primary afferent
neurons, spinal interneurons and ascending
tracts, and several supraspinal areas.
 Trigeminal and dorsal root ganglia give rise
to high-threshold Aδ and C fibers
innervating peripheral tissues (skin,
muscles, joints, viscera).
 These specialized primary afferent neurons,
also called nociceptors, transduce noxious
stimuli into action potentials and conduct
them to the dorsal horn of the spinal cord

When peripheral tissue is damaged, primary
afferent neurons are sensitized or directly
activated (or both) by a variety of thermal,
mechanical, and chemical stimuli.
 Examples are protons, sympathetic amines,
adenosine triphosphate (ATP), glutamate,
neuropeptides (calcitonin gene–related
peptide, substance P), nerve growth factor,
prostaglandins, bradykinin,
proinflammatory cytokines, and
chemokines.



These agents lead to opening (gating) of cation
channels in the neuronal membrane. Such channels
include the capsaicin-, proton-, and heat-sensitive
transient receptor potential vanilloid 1 (TRPV1) or the
ATP-gated P2X3 receptor. Gating produces an inward
currentof Na+ and Ca2+ ions into the nociceptor
terminal.
If this depolarizing current is sufficient to activate
voltage-gated Na+ channels (e.g., NaV1.8), they too
will open, thus further depolarizing the membrane
and initiating a burst of action potentials that are then
conducted along the sensory axon to the dorsal horn
of the spinal cord.



Thereafter, these impulses are transmitted to
spinal neurons, the brainstem, the thalamus,
and the cortex.
Transmission of input from nociceptors to spinal
neurons that project to the brain is mediated by
direct monosynaptic contact or by multiple
excitatory or inhibitory interneurons.
The central terminals of nociceptors contain
excitatory transmitters such as glutamate,
substance P, and neurotrophic factors that
activate postsynaptic N-methyl-D-aspartate
(NMDA), neurokinin, and tyrosine kinase
receptors, respectively.


Repeated nociceptor stimulation can sensitize
both peripheral and central neurons (activitydependent plasticity).
In spinal neurons such a progressive increase
in output in response to persistent nociceptor
excitation has been termed “wind-up.” Later,
sensitization can be sustained by
transcriptional changes in the expression of
genes coding for various neuropeptides,
transmitters, ion channels, receptors, and
signaling molecules (transcription-dependent
plasticity) in both nociceptors and spinal
neurons.
INFLAMMATION/NOCICEPTIVE
Peripheral Sensitization
Central Sensitization
Damaged Zone
ALLODYNIA
HYPERALGESIA
Sensitization and activation
COX1 - COX2
BK2 - BK1
PGs, H+
CNS
ATP
NGF
blood
vessel
C-fibre
SP, CGRP
BK
5HT
Vasodilation+plasma extravasation
Transmitter
release - neuronal
excitability
Spike firing frequency
After
Before
Increased suprathreshold firing
Spontaneous firing
Stimulus intensity
Reduced
threshold
Tissue damage
Hyperalgesia
PERIPHERAL
ACTIVITY
Nerve damage
Spontaneous
pain
Allodynia
CENTRAL
SENSITIZATION
Decreased
threshold to
peripheral
stimuli
Increased
Expansion of spontaneous
activity
receptive
field
Important examples include the NMDA
receptor, cyclooxygenase-2 (COX-2),
Ca2+ and Na+ channels, and cytokines
and chemokines expressed by neurons
and glial cells.
 In addition, physical rearrangement of
neuronal circuits by apoptosis, nerve
growth, and sprouting occurs in the
peripheral and central nervous systems.




Concurrent with the events just described,
powerful endogenous mechanisms
counteracting pain unfold both in the periphery
and in the central nervous system.
In injured tissue this occurs by interactions
between leukocyte-derived opioid peptides
and peripheral nociceptor terminals carrying
opioid receptors [10] [11] and by the action of
anti-inflammatory cytokines.
Inflammation of peripheral tissue leads to
increased expression, axonal transport, and
enhanced G protein coupling of opioid
receptors in neurons of the dorsal root ganglia.
These phenomena are dependent on
sensory neuron electrical activity,
production of proinflammatory cytokines,
and the presence of nerve growth factor
within the inflamed tissue.
 In parallel, opioid peptide–containing
immune cells extravasate and accumulate
in the inflamed tissue.
 These cells upregulate the gene expression
of opioid peptide precursors[15] and the
enzymatic machinery for their processing
into functionally active peptides.


In response to stress, corticotropin-releasing factor,
cytokines, chemokines, or catecholamines, leukocytes
secrete opioids, which then activate peripheral opioid
receptors and produce analgesia by inhibiting the
excitability of nociceptors or the release of excitatory
neuropeptides, or both

The clinical relevance of these mechanisms has been
shown in studies demonstrating that patients with knee
joint inflammation express opioid peptides in immune cells
and opioid receptors on sensory nerve terminals within
synovia .After knee surgery, such patients exhibited
significantly enhanced postoperative pain and analgesic
consumption when the interaction between opioid
peptides and receptors was blocked by intra-articular
application of the antagonist naloxone.



In the spinal cord, inhibition is mediated by the
release of opioids, γ-aminobutyric acid (GABA), or
glycine from interneurons, which then activate
presynaptic opioid or GABA receptors (or both) on
central nociceptor terminals to reduce the release of
excitatory transmitters.
In addition, opening of postsynaptic K+ or Clchannels by opioids or GABA, respectively, evokes
hyperpolarizing inhibitory potentials in the dorsal horn
neurons.
During ongoing nociceptive stimulation, spinal
interneurons upregulate gene expression and the
production of opioid peptides.



Powerful descending inhibitory pathways from the
brainstem also become active by operating mostly
through the noradrenergic, serotonergic, and opioid
systems.
A key region is the periaqueductal gray matter. It
projects to the rostral ventromedial medulla, which
then projects along the dorsolateral funiculus to the
dorsal horn.
Integration of signals from excitatory and inhibitory
neurotransmitters with cognitive, emotional, and
environmental factors (see later) eventually results in
the central perception of pain. When the intricate
balance among biologic, psychological, and social
factors becomes disturbed, chronic pain can
develop.
Clinical definition of pain1
“An unpleasant sensory and emotional experience
associated with actual or potential tissue damage,
or described in terms of such damage...
1. IASP Pain Terminology. In Merskey H & Bogduk N eds. Classification of Chronic Pain, Second Edition,
IASP Task Force on Taxonomy. IASP Press, Seattle 1994:209-14.
‫درد یک ترکیب فیزیولوزی و رویداد احساسی است و‬
‫یک حس ساده و آسان نیست‪.‬‬
‫درد شامل‪:‬‬
‫‪ ‬تجربه حسی ناخوشایند‬
‫‪ ‬رویداد عاطفی ناخوشایند‬
‫‪ ‬ترکیبی از عناصر اجتماعی‪-‬روحی و معنوی‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫‪‬‬
‫ایجاد دپرشن‬
‫برانگیختن اضطراب‬
‫تداخل با عملکرد اجتماعی‬
‫تاثیر منفی بر توانایی جسمی‬
‫ممانعت از حرفه و شغل‬
‫کاهش درآمد‬
‫ترغیب به انزوا و گوشه گیری‬
‫آسیب به کیفیت روابط اجتماعی‬
‫ایجاد ناهماهنگی و استرس در خانواده‬
‫ایجاد تزلزل در ایمان و اعتقاد‬
Good pain management
will aid the treatment of
future pain
Physical
Pain
Previous/multiple or
Progressive pains
Other Physical
Symptoms
Psychological
Problems
Failure to
recognise &
treat
psychological
distress is a
common
cause of
unrelieved
pain
Palliation of other
symptoms will
improve pain
control
Social
Difficulties
Spiritual
Concerns
Cultural
Issues
Clinical
Pain
What the patient says it is
What must be treated
Culturally appropriate
management &
circumvention of
language barriers may
lessen pain
‫دردی است ناشی از تحریک اعصاب محیطی که با یک‬
‫سیستم عصبی‬
‫غیرمعیوب منتقل شده‪.‬ایمپالس های درد وارد طناب نخاعی‬
‫می شوند در‬
‫مسیر شاخه دورسال جایی که به مراکز باالتر در مغز صعود‬
‫می‬
‫کنند‪.‬ایمپالس های مهارکننده ‪,‬انتقال در شاخه دورسال در‬
‫طناب نخاعی را‬
‫بلوک می کنند و از انتقال بعدی ایمپالس های درد جلوگیری‬
‫می کنند‪.‬این‬
‫دردها معموال به اپیوئیدها حساس می باشند و پاسخ‬
‫نشان می دهند‬
‫‪ ‬شامل‪:‬‬
‫‪ :Peripheral pain ‬درد نوروپاتیک محیطی توسط‬
‫آسیب سیستم عصبی محیطی ایجاد شده و اغلب‬
‫اطراف عصبی که آسیب دیده ‪,‬منطقه ای با‬
‫حساسیت تغییر یافته وجود دارد‪.‬‬
‫‪:Central pain ‬درد نوروپاتیکی است که ناشی از‬
‫آسیب سیستم عصبی مرکزی می باشد و معموال‬
‫یک ناحیه با حساسیت تغییر یافته آمیخته با ناحیه‬
‫درد وجود دارد‪.‬یک حادثه سربرو واسکوالر یا آسیب‬
‫طناب نخاعی ممکن است مرتبط با درد سنترال باشد‬
Nociceptive pain

Transient pain in response to noxious stimuli ›
Inflammatory pain

Spontaneous pain and hypersensitivity to pain in ›
response to tissue damage and inflammation
Neuropathic pain

Spontaneous pain and hypersensitivity to pain in ›
association with damage to or a lesion of the
nervous system
Woolf. Ann Intern Med. 2004;140:441-451.
Is responsive to NSAID’s, coxibs,
and opiates
Noxious paracetamol
Peripheral Stimuli
Pain-Autonomic Response
Heat
- Withdrawal Reflex
Cold
Intense
Mechanical
Force
Nociceptor Sensory
Neuron
Brain
Chemical
Irritants
Spinal Cord
Woolf. Ann Intern Med. 2004;140:441-451.
Is responsive to NSAID’s,coxibs,
paracetamol, and opiates
Inflammation
Macrophage
Mast Cell
Neutrophil
Granulocyte
Spontaneous Pain
Pain Hypersensitivity
-Allodynia
-Hyperalgesia
Nociceptor Sensory
Neuron
Brain
Tissue
Damage
Spinal Cord
Woolf. Ann Intern Med. 2004;140:441-451.
Spontaneous Pain
Pain Hypersensitivity
Peripheral Nerve
Damage
May respond to•
local anaesthetic•
anticonvulsants•
antidepressants
•
Brain
Stroke
Less responsive to opioids•
Spinal Cord Injury
No response to NSAID’s, coxibs, or •
paracetamol
.
Woolf. Ann Intern Med. 2004;140:441-451
Perception
Is responsive to
NSAID’s,coxibs,
paracetamol and
opiates
Modulation
Transmission
Transduction
Reuben et al. J Bone Joint Surg. 2000;82:1754-1766.
Acute Pain
Increased
sympathetic
activity
GI effects
Splinting,
shallow
breathing
Increased
catabolic
demands
Anxiety
and fear
Peripheral/
central
sensitization
Myocardial
O2
consumption
GI motility
Atelectasis,
hypoxemia,
hypercarbia
Poor wound
healing/muscle
breakdown
Sleeplessness,
helplessness
Available
drugs
Myocardial
ischemia
Delayed
recovery
Pneumonia
Weakness
and impaired
rehabilitation
Psychological
Chronic
pain
Courtesy of Sunil J Panchal, MD
Pain pathway and modulation1
Ascending nociceptive pathways
Interpretation in
cerebral cortex:
pain
Activation of serotoninergic
and noradrenergic pathways
Stimulation of nociceptors
(A and C fibers) /
Release of neurotransmitters
and neuromodulators (i.e. PG)
Histamin,bradikinin,
serotonin
Descending inhibitory controls /
Diffuse noxious inhibitory controls
Injury
Release of serotonin,
noradrenalin and enkephalins
at spinal level
The Anatomy
and
Physiology of Labor Pain
‘LABOUR can be defined as spontaneous
painful uterine contractions associated
with the effacement and dilatation of
the cervix and the descent of the
presenting part’
Pain is a noxious and unpleasant stimulus—
produces fear and anxiety.
Unrelieved stress in labour produces increased
plasma cortisol and catecholamine
concentrations.
Leads to reduction in utero-placental blood flow.
Effective pain relief reduces plasma noradrenaline, prevents the rise during first & second
stage of labour.
Prevents metabolic acidosis by reducing the rate
of rise of lactate and pyruvate.
Decreases maternal O2 consumption by 14%.






First stage pain is due to uterine 
contractions causing stretching, tearing
and possibly ischaemia of the uterus and
dilatation of the cervix.
Second stage pain is caused by 
distension of pelvic structures and
perineum following descent of the
presenting part.
First stage: early, active, transition 
Dilatation ›
Second stage 
Pushing and birth ›
Third stage 
Delivery of placenta ›
Fourth stage 
Postpartum ›
Uterine contractions: o
Myometrial ischemia o
Causes release of potassium, bradykinin, histamin,
serotonin
Distention of lower uterine segments and o
cervix
Stimulates mechanorecoptors o
Impulses follow sensory-nerve fibers from paracervical
and hypogastric plexus to lumbar sympathetic chain
Enter dorsal horn of spinal cord at T10-12, L1
Transition associated with greater o
nocioceptive input related to increased
somatic pain from vaginal distention
Distention of vagina, perineum, pelvic floor, o
stretching of pelvic ligaments
Pain signal transmitted to spinal cord via S2-S4 o
(includes pudendal nerve)
Pathways of
Placement of Anesthetics for Labor
Pain
Eltzschig H et al. N Engl J Med 2003;348:319-332
From onset of regular
uterine contractions to full
dilation of cervix.
.I
From full cervical dilation to
delivery of the fetus.
.II
From delivery of the fetus to
delivery of the placenta.
.III
METHODS OF PAIN RELIEF
IN LABOR
NON-PHARMACOLOGICAL METHODS

PHARMACOLOGICAL METHODS

ADVANTAGES—Drugs administered may cross
the placenta and depress the fetus.
Any method that avoids or restricts their use
deserves attention.
LAMAZE Preparation 
It is not just a birthing method but a birthing philosophy.
A psycho prophylaxis in labor.
HYPNOSIS 
based on the power of suggestion.
self-hypnosis or receive assistance from a hypnotherapist.
training sessions are required.
Many methods are based on the work of Grantly DickRead, MD,
ACUPUNTURE 
Generally two local points and two distal points on the arms
or on the legs are selected.
Begin Acupuncture 4 weeks before the expected time of
delivery.
Needles are placed once a week using the specific points.
Points 
LI.4 Hegu, SP.6 Saninjiao, Extra Neima
PC 6 (Neiguan), Du.20,Du.2,Du6, GB.21,
He.7(shenmen)
Beneficial in patients with moderate to severe contraction 
pains in an otherwise reasonably
normal labor.
Very popular in Europe. 
Easy to apply, non-toxic and frequently effective. 
4 electrodes are placed one on either side of the 
spine in the lower thoracic region (T 10) and one
on either side of the spine in the sacral area.
The patient may control up to 3 levels of intensity 
of stimuli, and she can switch it off if she wishes.
Mechanism of action:
Inhibits transmitter 
release along pain
pathway by
stimulating the
myelinated Aβ fibres
of the spinal nerve
roots T10-L1 & S2-4.
Neuronal release of 
Endorphins in to the
CSF may result in a
feeling of well being as
well as analgesia.
Regional Analgesia
SPINAL ANALGESIA
EPIDURAL ANALGESIA
COMBIND SPINAL EPIDURAL
CAUDAL
PUDENDAL
PARACERVICAL
Systemic Analgesia
Intra Venous Analgesia
Inhalational Analgesia
Entonox
(50:50 N2O/O2)
Isoflurane ( 0/2%)
Enflurane (0/2%)
Desflurane (0/2%)




LIMITED USE
Drowsiness ,Unpleasant smell, High cost,
Accidental overdose
N2O does not interfere with uterine
contractions.
No effect on fetus too.
Premixed nitrous oxide &oxygen.
N2O 50% and O2 50%.
ENTONOX-cylinders with a capacity of 500 L
are available.
Inhalation should begin 45 seconds before
the onset of pain.
If the patient holds her mask -it will fall from
her hand, should unconsciousness
supervene . (safety factor)







OPIOIDS
PETHIDINE (MEPERIDIN)
FENTANYL
SUFENTANIL
REMIFENTANIL
MORPHINE
PENTAZOCINE
NALBUPHINE
TRAMADOL








SEDATIVE-TRANQUILIZER
BENZODIAZPINES 
BARBITURATE 
KETAMINE 
PROMETHAZINE 
Ketamine 0.5 to 1 mg/kg every 5 min 
Remifentanil 0.4 μg /kg lockout 1 min 
Promethazine 25-50 mg 
Tramadol 1 mg/kg/Im 
Active phase, dilatation 3-4cm,
fully effaced
A. Sympathetic
From T 6- L 2. 
Motor to upper uterine segment via splanchnic nerves & 
coeliac, aortic, renal &hypogastric plexuses and then to
great cervical ganglion of Frankenhauser.
B. Visceral afferent
T 11-L 1 
Sensory from uterus 
Block of these eases pain of first stage of labour.
C. Visceral afferent & efferent Parasympathetic
Sensory and Motor to cervix 
Inhibitory to uterus 
S2,3,4. 
The 33 articles selected included 14 studies, 1 metaanalysis, and 2 systematic reviews
obstetrics in rural and small urban centers might find
single-dose ITN a useful alternative to parenteral or
epidural analgesia for appropriately selected patients.
A combination of 2.5 mg of bupivacaine, 25 μg of fentanyl,
and 250 μg of morphine intrathecally usually provides a
4 hour painless window.
The Cochrane Library
Date review completed: pre 2004 
Number of trials included: 16 
Control group: various non-epidural analgesic interventions

Main outcomes: 
pain relief better than cobntrol group
Placement of epidural catheter

Test dose 3ml of lidocaine 1.5% with adrenaline (?)

Initial loading dose 10ml of bupivacaine 0.25% or lidocaine 1% and
fentanyl 50 μg .

Does Epidural Analgesia Increase the 
Incidence of Cesarean Section?
NO
Does Epidural analgesia prolong 
labor ?
NO
American Journal of Obstetrics and Gynecology 171(5), 1994, 1398
Anesthesiology 80(6), 1201-1208, 1994
American Journal of Obstetrics and Gynecology
185(1), 2001, 182-134
Test dose : 3 ml of 0.125% Bupivacaine

Blouse : 8ml of 0.125% Bupivacaine +
50 μg of Fentanyl.

Maintenance: 0.125% Bupivacaine +2 μg /ml Fentanyl
at the rate of 10ml/h

3ml/5min P.R.N 3 times
for breaking through pain upon patient request
PATIENT CONTROLLED ANALGESIA 
EPIDURAL (PCEA)
INTRAVENOUS (PCA)
COMBINED SPINAL EPIDURAL (CSE) 
Advantages:
Ability to minimize drug dosage
.1
Flexibility and benefits of self-administration
.2
Reduced demand on professional time
.3
0.0625% Bupivacaine +Fentanyl 2 μg /ml 
Demand dose: 3ml , Lockout interval 6 min 
Background infusion 6 ml/h 
3ml/5min P.R.N 3 times
for breaking through pain upon patient request
0.125% Bupivacaine with 1:400,000
Epinephrine Plus Fentanyl 2 μg /ml
2ml bolus /10min lockout interval 
3ml bolus/15min lockout interval 
4ml bolus/20min lockout interval 
6ml bolus/30min lockout interval 
Needle” through “Needle”
“ Back “ eye”
Needle” through “Needle” technique is the best 
Can be placed in lateral or sitting position 
Walking Epidural possible 
Rapid onset of analgesia 
Reliable, fewer failed or patchy blocks 
Effective sacral analgesia in advanced labor 
Less motor block 
Better patient satisfaction 
Aids epidural localization in difficult backs 
Faster cervical dilation in early nulliparas 
Placement of epidural catheter

Test dose 3ml of lidocaine 1.5% with adrenaline (?)

Initial loading dose 10ml of bupivacaine 0.25% or lidocaine
1% and fentanyl 50 μg .

Start the infusion 
as soon as adequate 
anesthesia is achieved. 
Initial infusion rates are - bupivacaine 0.25% 8-12 
ml/hr or lidocaine 0.5% 10-15 ml/hr.
PCEA: 20ml BUP 0.125% + fentanyl 2mcg/ml, 
then 6 ml/hr infusion, 6ml bolus, 15min lockout
CSE: 2.5mg BUP + fentanyl 25mcg 
No test dose, start PCEA 
PCEA: 0.0625% + 2 mcg/ml fentanyl. 15ml/hr basal 
infusion, 5ml bolus, 10min lockout, 30ml/hr max. If
patient requires manual rebolusing they change to
0.11% BUP
CSE: early labor 25mcg fentanyl + test dose 
Regular labor or multip: 15mcg fentanyl + ›
2.5mg BUP + test dose. Start PCEA
CSE: 2.5mg BUP + 25mcg fentanyl 
No test dose 
Infusion started 
Ropivacaine 0.1% + SUF 0.5mcg/ml 
Test dose + 5ml loading dose ›
PCEA: 4ml doses, 20min lockout ›
CEI: 6ml/hr ›
Rescue: 5ml if VAS > 5 ›
No epidural before cervical dilatation of 4 cm 
No epidural in the second stage 
IV hydration before/during epidural 
Bupivacaine 0.0625% ± fentanyl 2μg/ml 
Infusion rate 8~15 ml/hr ± initial loading 5~10 ml 
Essentially nurse-control analgesia 
Van Gessel et al. demonstrated that 59% of 
dural punctures were performed 1 or 2 spaces
higher than assumed
Broadbent et al. demonstrated in a group of 
experienced anesthesiologists that when they
believed they were at L3-L4, in 85% of the
cases the space was 1 to as many as 4
segments higher
A.ABSOLUTE
Maternal refusal 
Coagulation disorders 
Local sepsis 
Patient on anti-coagulant therapy 
B.RELATIVE
Shock 
Hypovolaemia 
Neurological disease 
Previous spine surgery 
Difficult anatomy 
C.MISCELLANEOUS
Inexperienced anesthetist 
Inadequate supervision, facilities, apparatus and personnel 
Very obese patients 
Allergies to local anesthetic drugs 
Immediate
Hypotension
Urinary retention
Local anestheticinduced convulsions
Local anestheticinduced cardiac arrest
Delayed
Postdural puncture headache
Transient backache
Epidural abscess or meningitis









A.MATERNAL
Needle or catheter-insertion
Wrong place
Penetrates blood vessels,dura,neural tissue. 
Broken catheter. 
Injection
Sub-arachnoid 
Intravascular 
Adverse reaction to local anesthetics 
Neural blockade
Hypotension 
Motor blockade 
Bladder dysfunction 
Shivering. 
Inadequate Anaesthesia
Total failure 
Partial failure 
Progress of labour
Prolongs labour 
Increased instrumental deliveries. 
A. BLOODY TAP:

Epidural venous plexuses are distended during pregnancy.

Accidental intravenous injection causes—

Hypotension
.1
Convulsions
.2
Unconsciousness.
.3
B. DURAL PUNCTURE:
Incidence-13% (in the hands of inexperienced anesthetist)

Sequelae of dural puncture

PDPH
.1
Sub-dural or extradural haematoma
.2
Total spinal block.
.3
NEUROLOGICAL
Injury to peripheral nerves 
Femoral & common peroneal nerve 
HEADACHE- Post-dural puncture
headache (PDPH).
Concentration
(%)
Dose
(mg*segment-1)
Onset
(min)
Duration
(min)
Chloroprocaine
2-3
45
5-15
30-90
Lidocaine
1-2
25
5-15
60-120
10-20
120-140
Bupivacaine
0.25-0.75
7
Ropivacaine
0.25-.75
9
10-15
120-160
Visceral pain comes from outer covering of abdominal 
viscera which are innervated by autonomic nervous
fibres , pain is due to distension or muscular contraction
of a viscera
It is typically vague , dull and nauseating , percieved in
areas corresponding to embryonic dermatome origin
Somatic pain comes from parietal peritoneum which 
are innervated by somatic nervous fibres pain is due to
irritation from inflammation ,infection , chemical
It is typically sharp and well localised
Referred pain is pain percived distant from its source 
and result from convergence of nerve fibres at spinal
cord
Usually performed by obstetrician 
Blocks the visceral afferent nerve fibres that pass 
through the paracervical ganglion of
Frankenhauser
Gives good analgesia without motor blockade 
Does not block the progress of labour 
Disadvantages:
Does not provide perineal analgesia 
High incidence of fetal bradycardia-due to high 
levels of local anesthetic entering the uterine artery
and reaching the fetus
Trauma to fetal scalp or maternal vagina. 
Indirectly by changes in uterine blood flow

Effect exerted directly by local anesthetic drugs

Changes in uterine contractility

Epidural blockade-produces fall in fetal
oxygenation-if hypotension is allowed to develop

If MAP remains<70mmHg for more than 3 hrsneonatal neuro – behaviour will be impaired.

Usually performed by obstetrician 
Provides good analgesia for somatic 
perineal pain in the second stage of labour.
Disadvantages:
Trauma to mother & fetus 
Accidental intravascular injection into the 
adjacent pudental vessels
Vaginal & ischiorectal haematoma 
Retropsoal & subgluteal abscess. 
Newer drugs for epidural:
Sufentanil---- potent opioid 
Levobupivacaine—less motor blockade 
Ropivacaine----- less motor blockade 
Walking epidurals 
Increased maternal comfort
Improved neonatal outcome
Ability to walk & change positions in bed are
supporting reasons for walking epidurals.
CONTINUOUS SPINAL ANALGESIA 
Using micro catheters--- 28 G.
Loading dose: 
11ml Ropivacaine 0.2%
Maintenance: 
6ml/h Ropivacaine 0.1% plus Fentanyl 2 μg /ml
Demand dose of 5ml,lockout interval 10min
Maximum 31ml
Epidural initiated: 8 ml
0.25% BUP
0.125% BUP
PECA: 4 ml basal, 4 ml
bolus,
Lockout 20 min, 16 ml/hr max
CIEA: 12 ml/hr infusion