prof.dr. manar mahmoud elkholy assist.prof.dr. enas...

Spinal Anesthesia in Caesarian Section: Sitting versus Lateral position Approach

A Thesis study

Submitted for the fulfillment of the master degree in Anesthesiology, surgical ICU and Pain Management

Presented by

Mohammad Ahmad Mohammad Yusuf Ollaek

M.B.B.Ch

Faculty of Medicine, Cairo University

Supervised by

Prof.Dr. Manar Mahmoud Elkholy Professor of Anesthesiology


Assist.Prof.Dr. Enas Mohamed Samir Assistant professor of anesthesiology

Faculty of medicine, Cairo University

Dr. Ahmad RagabAbd Elhakim Lecturer of anesthesiology


2011

ACKNOWLEDGEMENT

Thanks to Allah for giving me the power and strength to carry out

this work.

Words stand short where they come to express my gratitude to my

supervisors.

I would like to express my thanks and deepest gratitude to Prof. Dr.

Manar Mahmoud Elkholy, Professor of Anesthesiology, Faculty of

Medicine, Cairo University, for her great support and her continuous

generous advice.

My deep gratitude goes for Prof. Dr. Enas Mohamed Samir,

Professor of Anesthesiology, Faculty of Medicine, Cairo University, for her

kind help and great support throughout this work.

I would like to sincerely thank Dr. Ahmed Ragab Abd Elhakim,

Lecturer of Anesthesiology, Faculty of Medicine, Cairo University for his

valuable advice, honest assistance and fruitful suggestions throughout my

daily work.

I would like to express my thanks to all members of my family especially

my father and my wife for giving me love and care till I have finished this

work and forever.

II

DEDICATION

This work is dedicated to the soul of my mother,

who stood beside me through my entire life, gave me all

the support and taught me honesty and sincerity.

III

Abstract

Regional anesthesia became of choice in obstetric patients for

its characteristics in providing almost rapid onset of anesthesia,

allowing the mother to immediately interact with her baby; it is

safer for mother than general anesthesia.

After compatison of sitting versus lateral position approach

regarding spinal anesthesia in caesarian section, It proves that

sitting approach produces less hypotension, less cephaled spread

and less post dural puncture headache than lateral approach.

Key Words : Spinal anesthesia ‐ Caesarian Section ‐ Sitting ‐ Lateral.

Table of Contents

Contents Page

List of abbreviations ……………………………………….………………………….….. II

List of tables …………………………………………………...……………………….….. IV

List of figures …………………………………………...…………………………….…… V

Introduction ……………………………………………………………………….............. 1

Aim of Work......................................................................................................................... 5

Review of Literature:

Chapter (1): Anatomy of Spinal Cord and Vertebral Column…………………………. 6

Chapter (2): Physiologic Changes during Pregnancy…………………………………… 18

Chapter (3): Post Dural Puncture Headache………………...………….………………. 29

Patients and Methods…………………………………….………………………………... 50

Results ………………………...............…………………………………………………… 55

Discussion…………………………………………………………………………………... 64

Conclusion ………………………………………………………………...………….……. 70

Summary ………………………………………………………………...……………….... 71

References ………………………………….………………………………...……….…… 75

Arabic Summary ………………………….………………………………...…………..…

IV

List of Abbreviations

ACTH Adreno-cortico-trophic hormone

AED Antiepileptic drug

ASA American Society of Anesthesiologists

CC Closing Capacity

C.S. Caesarian Section

CT Computed Tomography

CSF Cerebrospinal Fluid

ECG Electrocardiogram

FRC Functional residual capacity

G Gauge

GA General Anesthesia

GABA Gamma-amino butyric acid

GFR Glomerular Filtration Rate

H Hour

Kg Kilogram

L.P Lumber Puncture

PDPH Post dural puncture headache

VC Vertebral Cloumn

ug Microgram

5-HT1D 5 hydroxytryptamine receptor 1D

V

List of Tables

Table Page

Table (1): Cardiovascular Changes in Pregnancy ……………………………………….. 21

Table (2): Coagulation Factors in Pregnancy ……...……………………………………... 24

Table (3): Values for Renal Function …………………...……...………….………………. 28

Table (4): Estimated rate of spontaneous recovery from post-dural puncture Headache 37

Table (5): Bromage scale……………………………………………………………………. 52

Table (6): Demographic data and Operative time of patients during study…………….. 57

Table (7): Systolic Blood Pressure of patients during study……………………………… 58

Table (8): Systolic Blood Pressure less than 100 mmHg of patients during study………. 59

Table (9): Heart Rate (HR) of patients during study……………………………………... 60

Table (10): O2 Saturation of patients during study……………………………………….. 60

Table (11): Incidence of Nausea and Vomiting of patients during study………………... 61

Table (12): Level of Sensory Block of patients during study……………………………... 62

Table (13): Incidence of PDPH within 48 hours of patients during study……………….. 63

VI

List of Figures

Figure Page

Figure (1): Vertebral Column …………………………………………...……………...…. 8

Figure (2): Vertebra ………………………….………………………...………………...…. 9

Figure (3): Ligaments of V.C. …………………................................……...………….…… 11

Figure (4): Sagittal Section of V.C…………………...……...…………………...…….…… 11

Figure (5): Cross Section of spinal cord …………………………....……...………….…… 15

Figure (6): Midline Sagittal view of the lumbar spine……………..……...………….…… 17

Figure (7): Types of Needles …………………...……...……………………………….…… 32

Figure (8): MRI showing diffuse dural enhancement……………………………………... 36

Figure (9): Systolic Blood Pressure of patients during study……………………………... 58

Figure (10): Systolic Blood Pressure less than 100 mmHg of patients during study in T3………………………………………………………………………………. 59

Figure (11): Incidence of Nausea and Vomiting of patients during study……………….. 61

Figure (12): Level of Sensory Block of patients during study…………………………….. 62

Figure (13): Incidence of PDPH within 48 hours of patients during study……………… 63

Introduction

Introduction

2

Since, regional anesthesia became of choice in obstetric patients for

its characteristics in providing almost rapid onset of anesthesia, allowing

the mother to immediately interact with her baby; it is safer for mother

than general anesthesia. So, the complications following regional

anesthesia became of great interest either to the anesthesiologist or to the

parturient(1) (2).

Complications of spinal or epidural block are either acute in the form

of pain on injection, high(total) spinal anesthesia and hypotension or

postoperative complications as backache, Post Dural Puncture Headache

(PDPH), urine retention, meningitis and nerve injury(3). Several studies

were done to detect and to role out incidence, pathophysiology and

effective measures to minimize or prevent these complications.

Post Dural Puncture Headache was described since more than 100

years and it presents one of the major complications of spinal and

epidural block annoying to the patients especially parturient with

incidence varies between 0.1 – 36 % in parturient because of sex, young

age and the wide spread application of regional anesthesia(4)(5)(6).

The actual mechanism producing PDPH remains unclear. However,

the widely accepted theory explaining the pathophysiology of PDPH is

based on the assumption of persistent leakage of the CSF through the hole

made by the spinal or epidural needle and decrease in CSF volume or

pressure or both, which leads to shift of intracranial contents and traction

on pain sensitive structures(4). The classic symptoms of PDPH consist of

photophobia, nausea, vomiting, neck stiffness, tinnitus, diplopia and

dizziness in addition to often severe cephalgia(4).

Introduction

3

Many studies implementing incidence of PDPH following different

techniques like median and para-median approach or usage of different

sizes and types of spinal needles. The outcome of these studies revealed

increased incidence with para-median technique in young patients and

decrease incidence while using smaller sizes spinal needles(7)(8).

Following subarachnoid injection, local anesthetics have been found

to be most highly concentrated in the lateral and posterior columns.

Intermediate concentrations are found in ventral roots, with the lowest in

dorsal root ganglia and gray matter of the anterior horn. The dorsal roots

are the primary targeted area when spinal anesthesia is performed. The

dorsal roots contain small-diameter nerve fibers carrying preganglionic

autonomic fibers, temperature, dull pain, and touch fibers. Large-diameter

fibers, centrally embedded in the nerve bundle, carry motor ability and

proprioceptive senses. The majority of the physiologic effects of spinal

anesthesia and essentially all the cardiovascular effects, are mediated by

preganglionic sympathetic blockade. Sympathetic nervous system fibers

are more peripherally located in the nerve roots than are the sensory

fibers (9).

The level of sympathetic fiber blockade is produced at two or more

dermatomes higher than the sensory blockade. These conclusions are

clinically confirmed by the loss of cold sensation and an increase in skin

temperature (thermography)(9).

Maternal hypotension is the most frequent complication of spinal

anesthesia for caesarean section. Most workers define hypotension as a

maternal systolic blood pressure below 70-80% of baseline recordings

and/or an absolute value of < 90 - 100mmHg. Hypotension is often

Introduction

4

associated with nausea and vomiting and, if severe, poses serious risks to

mother (unconsciousness, pulmonary aspiration) and baby (hypoxia,

acidosis and neurological injury) (10) (11).

Aim of Work

5

Aim of Work

The purpose of this study was to determine the effect of sitting versus

lateral techniques spinal anesthesia on incidence of PDPH, severity of

hypotension, block characteristics and the interrelation between severity

of hypotension and PDPH.

Chapter 1:

Anatomy of Spinal Cord and

Vertebral Column

Review of Literature

7

Anatomy of Vertebral Column (V.C.):

The vertebral column composed of 7 cervical, 12 thoracic, 5 lumbar, 5

fused sacral vertebrae and the coccyx. The vertebral column has four

characteristic curvatures: the anterior convexity of the sacrum, the lumbar

lordosis, the thoracic kyphosis, and the cervical lordosis. In the supine

patient, the lumbar spine has its highest point at L4 and the thoracic spine

has its lowest point at T4. In the lumbar area, the spinous processes project

directly posteriorly whereas in the thoracic area, the spinous processes

project posteriorly and more inferiorly until they reach their steepest

downward angulation at the mid-thoracic level where they overlap with the

lamina of the vertebra immediately inferior. This overlap can make the

midline approach to the epidural space difficult or impossible at the T5-T9

levels. At higher thoracic levels, the spinous processes angle elevated again

to become nearly horizontal at C7. The spinal canal is enclosed by the

vertebral bodies anteriorly, the pedicles laterally, and the ligament flava

and the laminae posteriorly. The canal ends superiorly in the foramen

magnum and inferiorly in the sacral hiatus (12).


8

Figure 1: Vertebral Column (12)

Anatomical Consideration of the Vertebrae:

Typical vertebra has an anterior body and a posterior neural arch which

forms the boundaries of the vertebral foramen (spinal canal). As the

column descends, the bodies increase in size to accommodate the

proportional increase in body weight that passes through them. The

vertebrae are separated from each other by the intervertebral discs and the

neural arch of the vertebra is connected anteriorly to the body via 2 bars of

bones called pedicles. These pedicles tend to be attached towards the

superior poles of the bodies resulting in 2 notches of uneven depth. When

two vertebrae articulate with each other, an intervertebral foramen is

formed through which passes the roots of the spinal nerves and the vascular

structures supplying the spinal cord (12).


9

The neural arch has a single midline spinous process which projects

posteriorly, and paired transverse processes which passes laterally. These

processes are connected by laminae on each side (12).

Figure 2: vertebra(12)


10

Ligaments:

The supraspinous ligament runs along the tips of the spinous processes

and blends with the ligamentum nuchae at its superior end. In elderly

individuals and in persons who engage in heavy physical activity, the

ligament can become ossified, making a midline approach to the epidural

space impossible. The interspinous ligament stretches vertically from the

inferior border of each spinous process to the superior border of the spinous

process below, except in the cervical spine, where it is absent. Dorsally, the

interspinous ligament blends with the supraspinous ligament. Ventrally, it

fuses with the ligament flava and the laminae. The laminae slope

posteriorly and inferiorly so that their ventral surfaces are in close contact

with the dura(12). The ligamentum flavum is a tough elastic ligament that

attaches to the ventral surface of the superior lamina and the dorsal surface

of the inferior lamina. Laterally, the ligament thins as it blends with the

joint capsule of the articular processes. Within the spinal canal, the

posterior longitudinal ligament runs along the dorsal surface of the

vertebral bodies, adherent to the anterior dura and The anterior longitudinal

ligament joins the vertebral bodies along their anterior surface (12).


11

Figure 3: Ligaments of Vertebral Column(12)

Figure 4: Sagittal Section of Vertebral column(12)


12

Spinal Meninges

The Dura Mater

The dura mater is a tough fibrous membrane that envelopes the

arachnoid mater, cerebrospinal fluid, pia mater, spinal nerves, spinal cord

and brain. Within the cranium, the dura is composed of an outer endosteal

component that lies against the bone of the cranium and an inner meningeal

component. These two layers are tightly adherent except where they divide

to form the venous sinuses. At the foramen magnum, the endosteal layer

divides from the meningeal layer and lines the spinal canal as the

endosteum of the vertebral bodies. The meningeal layer continues caudally

as the dural sac, and ends at the S2 level in adults. The attachment of the

meningeal dura to the endosteal dura at the foramen magnum anatomically

isolates the cranial vault from the epidural space of the spinal canal (13).

The spinal dura mater is a tube extending from the foramen magnum to

the second segment of the sacrum. It contains the spinal cord and nerve

roots that pierce it, the dura mater is a dense, connective tissue layer made

up of collagen and elastic fibers and the classical description of the spinal

dura mater is of collagen fibers running in a longitudinal direction (14). This

had been supported by histological studies of the dura mater (15). Clinical

teaching based upon this view of the dura recommends that a cutting spinal

needle be orientated parallel rather than at right angles to these longitudinal

dural fibers. Orientating the needle at right angles to the parallel fibers, it

was said would cut more fibers. The cut dural fibers, previously under

tension, would then tend to retract and increase the longitudinal dimensions


13

of the dural perforation, increasing the likelihood of a post spinal headache.

Clinical studies had confirmed that post dural puncture headache was more

likely when the cutting spinal needle was directed perpendicular on the

direction of the dural fibers.

However, light and electron microscopic studies of human dura mater

have confirmed this classical description of the anatomy of the dura mater (16).

Other studies also describe the dura mater as consisting of collagen

fibers arranged in several layers parallel to the surface. Each layer or

lamellae consists of both collagen and elastic fibers that do not demonstrate

specific orientation (17).The outer or epidural surface may indeed have dural

fibers arranged in a longitudinal direction, but this pattern is not repeated

through successive dural layers. Recent measurements of dural thickness

have also demonstrated that the posterior dura varies in thickness, and that

the thickness of the dura at a particular spinal level is not predictable within

an individual or between individuals (16). Dural perforation in a thick area of

dura may be less likely to lead to a CSF leak than a perforation in a thin

area, and may explain the unpredictable consequences of a dural

perforation.

The Arachnoid Mater

The arachnoid mater is a thin metabolically active membrane that loosely

adheres to the dural sac and contains the brain and spinal cord bathed in

CSF. Between the arachnoid and the dura lies the subdural space, a


14

potential space through which local anesthetics can distribute via a

misplaced spinal needle or epidural catheter. Connective tissue trabeculae

extend from the arachnoid to the pial surface of the spinal cord to secure

the cord in the CSF. Arachnoid granulations ranging from microscopic to 3

mm in diameter cluster around the nerve roots in the dural cuff region.

These granulations emerge through the dura and press into surrounding

veins and epidural fat. By transcellular vacuolar transport, the granulations

clear the CSF of foreign particulate material, likely by emptying directly

into the epidural venous plexus or into the epidural connective tissue, for

subsequent removal by lymphatic drainage (13).

The Pia Mater and Spinal Cord:

The pia mater is a thin highly vascular membrane composed of flat

epithelial cells and tightly adherent to the spinal cord. A long filamentous

extension of the pia, the filum terminale, pierces the caudal end of the dural

sac and blends with the periosteum of the coccyx to secure the spinal cord

within the sac. The spinal cord ends at the L1-2 level in adults. The spinal

roots continue caudally to the intervertebral foramina of the lower lumbar

and sacral levels as the cauda equina(13).


15

Anatomy of the Epidural Space

The epidural space surrounds the dural sac and is bounded by the

posterior longitudinal ligament anteriorly, the ligament flava and the

periosteum of the laminae posteriorly, and the pedicles of the spinal

column and the intervertebral foramina containing their neural elements

laterally. The space communicates freely with the paravertebral space

through the intervertebral foramina. Superiorly, the space is anatomically

closed at the foramen magnum where the spinal dura attaches with the

endosteal dura of the cranium. Functionally, however, local anesthetics can

diffuse intracranially during excessively high epidural block. Caudally, the

epidural space ends at the sacral hiatus which is closed by the

sacrococcygeal ligament.

Figure 5: Cross Section of spinal cord (13)


16

The epidural space contains loose areolar connective tissue, semi liquid

fat, lymphatics, arteries, an extensive plexus of veins, and the spinal nerve

roots as they exit the dural sac and pass through the intervertebral

foramina(18).

Epidural Veins

The epidural venous plexus is a valveless system that communicates

with the basivertebral vein, the intracranial sigmoid, occipital, and basilar

venous sinuses, and the azygous system. Drugs, air, or other material

injected into the epidural space can potentially reach the heart or brain

directly through this route. Abdominal and thoracic veins connect with the

venous plexus through the intervertebral foramina, and transmit intra-

abdominal and intra-thoracic pressure to the epidural space. Inferiorly, the

venous plexus connects with the iliac veins through the sacral venous

plexus.

Chronically increased intra-abdominal pressure or obstruction of the

inferior vena cava (as in late trimester pregnancy or in the presence of a

large intra-abdominal tumor) can distend the epidural venous plexus, with

important implications for epidural anesthesia. This increases the risk of

intravascular cannulation with an epidural catheter. It effectively decreases

epidural space volume, allowing local anesthetics to distribute more widely

with resulting greater degrees of block. Exposure to greater vascular

surface area also potentially increases the risk for local anesthetic toxicity

due to absorption from the epidural space (19).


17

Figure 6: Midline Sagittal View of the Lumbar Spine (18)

Chapter 2: Physiologic Changes during

Pregnancy


19

Maternal physiologic changes in pregnancy occur as a result of hormonal

alterations, mechanical effects of the gravid uterus, increased metabolic and

oxygen requirements, metabolic demands of the fetoplacental unit, and

hemodynamic alterations associated with the placental circulation. Such

changes become more significant as pregnancy progresses, and they have

major implications for anesthetic management, especially in high-risk

parturient (20).

Central Nervous System:

Pregnant women demonstrate increased sensitivity to both regional and

general anesthetics. From early stages, when neuraxial anesthesia is

administered, pregnant women require less local anesthetic than non-

pregnant women do to reach a given dermatomal sensory level. The

minimum alveolar concentrations of halothane and isoflurane are reduced

by 25% and 40%, respectively, during pregnancy (21). The underlying

mechanism of the decreased anesthetic requirements remains unclear.

Furthermore, reduced local anesthetic requirements predate the mechanical

effects of the gravid uterus (22). In addition, the increased concentrations of

endorphins and dynorphins found in pregnant rats may be related to altered

pain thresholds (23) (24). Obviously a multifactorial explanation for the

decreased anesthetic requirements is likely.

Cardiovascular System:

The cardiovascular system adjusts throughout pregnancy to meet the

changes that occur. Hemodynamic and maternal cardiovascular changes in

pregnancy are outlined in Table (1) (25). Although the physiologic changes


20

in the cardiovascular system appear to begin in the first trimester, these

changes continue into the second and third trimesters, when cardiac output

increases by approximately 40% of non-pregnant values. Cardiac output

increases from the fifth week of pregnancy and reaches its maximum levels

at approximately 32 weeks, after which there is only a slight increase until

labor, delivery, and the postpartum period (26).

Changes in heart rate are extremely difficult to reliably quantify, but it is

thought that the approximately 20% increase in heart rate is present by the

fourth week of pregnancy.

Although the normal variability in heart rate does not change in

pregnancy, there does appear to be a reduction in the sympathetic

component (27).Tachyarrhythmias are more common, especially later in

pregnancy as a result of both hormonal and autonomic factors (28).


21

Table 1-- Cardiovascular Changes in Pregnancy (25)

Parameter Change Amount (%)

Heart rate Increased 20-30

Stroke volume Increased 20-50

Cardiac output Increased 30-50

Contractility Variable ±10

Central venous pressure Unchanged

Pulmonary capillary wedge

pressure

Unchanged

Systemic vascular

resistance

Decreased 20

Systemic blood pressure Slight

decrease

Mid-trimester 10-15 mm

Hg, then rises

Pulmonary vascular

resistance

Decreased 30

Pulmonary artery pressure Slight

decrease

Because of the decrease in peripheral vascular resistance, arterial blood

pressure does not change in a normal pregnant woman. Cardiac output

decreases during the third trimester due to effects of the supine position in

the patient at term (29). Ueland and colleagues found that the decrease in

cardiac output was due to obstruction of the inferior vena cava by the

gravid uterus, which did not occur when women were placed in the lateral

position (30). Despite the increase in blood volume and cardiac output,

parturient at term are susceptible to hypotension, especially when in the


22

supine position. This phenomenon has been termed the syndrome of supine

hypotension. To compensate, collateral routes of venous return develop,

including the paravertebral veins to the azygos vein. Unlike compression of

the vena cava, compression of the aorta is generally not associated with

maternal symptoms in a healthy parturient but it may be associated with

decreased utero-placental perfusion (31). Anesthetics and drugs that cause

vasodilation or anesthetic techniques that cause sympathectomy (e.g.,

neuraxial techniques) may exacerbate the impact of aortocaval

compression. In the operating room, a small pillow or “wedge” should be

used to provide left uterine displacement of 15 to 20 degrees (20).

Hematologic System:

Maternal blood volume begins to increase early in pregnancy as a result

of changes in osmoregulation and the renin-angiotensin system, causing

sodium retention and increasing total body water to 8.5 L (32). By term,

blood volume increases by up to 45% whereas red cell volume increases by

only 30%. This differential increase leads to the “physiologic anemia” of

pregnancy with an average hemoglobin and hematocrit of 11.6 g/dL and

35.5%, respectively (33). However, oxygen transport is not impaired by this

relative anemia because the mother's body compensates for it by increased

cardiac output, increased PaO2, and a rightward shift in the oxy-

hemoglobin dissociation curve (20).

A state of hypercoagulability exists in pregnancy, with increased levels

of most coagulation factors (Table 2) (34). Fibrinogen and factor VII are

markedly increased, whereas the other factors increase to a lesser extent.


23

This increase in coagulation factors has been verified by

thromboelastography (35) and is probably a protective adaptation to lessen

the risks associated with the acute hemorrhage that occurs at delivery. This

hypercoagulable state, however, may lead to thromboembolism, which

remains a leading cause of maternal mortality.

The platelet count remains unchanged throughout most of pregnancy, but

it may be slightly reduced in the third trimester with increased activity in

vivo (20). The platelet count increases in the postpartum period, probably

because of activation of hemostasis at the time of delivery. The incidence

of low platelet counts in normal pregnancy is approximately 8 %( 36).

However, thrombocytopenia during the latter part of pregnancy is not

associated with adverse sequelae. Obstetric management of parturient with

stable platelet counts above 50,000 × 109/L should be no different from that

of normal parturient (37). In addition, although the cutoff for initiation of

neuraxial blocks was considered to be 100,000 × 109/L in the past, this

level is no longer considered absolute. Currently, most anesthesiologists

feel comfortable initiating a regional technique with platelet counts above

75,000 × 109/L and with counts between 50,000 and 75,000 if the level is

stable and clinical laboratory abnormalities or signs of a coagulopathic

state are absent (20).


24

Table 2-- Coagulation Factors in Pregnancy (34)

Factor Change

II Unchanged

VII Increased +++

VIII, IX, X, XII Increased

XI Reduced

Fibrinogen Increased +++

Platelets Stable

Respiratory System:

To accommodate the increased oxygen demand and requirement for

carbon dioxide elimination, pregnancy is associated with an increase in the

respiratory minute volume and work of breathing. Because of difficulties in

performing clinical research on pregnant women, few investigations of

respiratory changes in pregnancy have been conducted (38).

The most impressive change in maternal lung dynamics is a decrease in

functional residual capacity (FRC), which at term may have changed by as

much as 20% of pre-pregnancy values. Minute ventilation increases by

45%, primarily as a result of an increase in tidal volume because the

respiratory rate is essentially unchanged (20).

Hormonal changes and an increase in the rate of carbon dioxide

production are responsible for the increase in ventilation. Progesterone

sensitizes the respiratory center to carbon dioxide. PaCO2 falls to

approximately 30 mm Hg by the 12th week of gestation, and it remains at


25

this level for the remainder of pregnancy. Tidal volume increases by 50%,

with half of this increase occurring during the first trimester. The parturient

breathing pattern changes; it becomes more diaphragmatic as pregnancy

progresses because of the effects of the gravid uterus and limitation of

thoracic cage movement. Closing capacity (CC), however, remains

unchanged. The resulting decrease in the FRC/CC ratio causes faster small-

airway closure when lung volume is reduced; thus, parturient can

desaturate at a much faster rate as compared with non-pregnant women.

The rapid development of hypoxia as a result of decreased FRC, increased

oxygen consumption, and airway closure may be minimized by

administration of 100% oxygen for 3 to 5 minutes before the induction of

anesthesia. In an emergency setting, four maximal capacity breaths with

100% oxygen should be sufficient (20).

Other changes in the respiratory tract and oropharynx during pregnancy

may have profound anesthetic implications. Capillary engorgement of the

mucosa and edema of the oropharynx, larynx, and trachea may result in a

difficult intubation. Any manipulation of the upper airway such as

suctioning, insertion of airways, or laryngoscopy may cause edema,

bleeding, and upper airway trauma. Because of the particularly friable

mucosa of the nasopharynx, instrumentation of the nose should be avoided

if at all possible. In performing intubation of a pregnant patient, a smaller

than usual endotracheal tube (size 6.0 to 7.0) should be used and repeated

attempts at laryngoscopy minimized (20).


26

Gastrointestinal System:

Gastrointestinal function in pregnancy and during labor is a topic that

continues to be controversial. However, there is no doubt that the

gastrointestinal tract undergoes significant anatomic and physiologic

changes that increase the risk of aspiration associated with general

anesthesia. Progesterone relaxes smooth muscle; consequently, it impairs

esophageal and intestinal motility during pregnancy. The fact that gastric

emptying is delayed during pregnancy is controversial. Wong and

coworkers suggest that the ingestion of 300 mL of water may actually

enhance gastric emptying in healthy, term, non-obese, non-laboring

parturient (39).

However, the risk of pulmonary aspiration of gastric contents remains

real in parturient, especially when undergoing an emergency cesarean

delivery under general anesthesia. Even if gastrointestinal motility has not

been affected during pregnancy, established labor and the administration of

parenteral opioids delay gastric emptying (40)(41).

Epidural analgesia using local anesthetics without opioids does not affect

gastric emptying, and the use of small doses of epidural fentanyl also has

no effect on gastric function(42)(43)(44). Large doses of fentanyl, however,

may slow gastric emptying.

The pain of labor, however, may delay gastric emptying and promote

emesis. These changes may be caused by the effects of placentally derived

gastrin (45). Because of the gastrointestinal alterations associated with

pregnancy, the use of endotracheal intubation is warranted to reduce the

risk of aspiration of gastric contents if general anesthesia is required.


27

Renal System:

The renal system undergoes major changes in pregnant patients, mainly

because of the effects of progesterone and the mechanical effects of

compression of the enlarging uterus. Urea, creatinine, and uric acid

clearance all rise in pregnancy (as illustrated in Table 3) (46). Renal plasma

flow and the glomerular filtration rate (GFR) both increase rapidly in

pregnancy as a result of the increase in cardiac output. The GFR rises by

almost 50%; this increase, accompanied by the dilutional effect of plasma

volume expansion, accounts for the decrease in plasma creatinine and urea.

Hence, “normal” renal indices in pregnancy are lower than in the non-

pregnant state.

Therefore, blood urea nitrogen and creatinine levels that would be

considered marginally elevated in pre-pregnant patients are usually

indicative of severe renal impairment in parturient. The increase in GFR

generally precedes the expansion of blood volume and is considered to be a

marker of pregnancy-induced vasodilation (47). Glycosuria is a common

finding that is attributable to the increase in GFR and reduced renal tubular

resorption capacity.


28

Table 3-- Values for Renal Function (46) Parameter Pregnant Non-pregnant Creatinine clearance

140-160 mL/min 90-110 mL/min

Urea

2.0-4.5 mmol/L 6-7 mmol/L

Creatinine

25-75 µmol/L 100 µmol/L

Uric acid

0.2 mmol/L 0.35 mmol/L

pH

7.44 7.40

Bicarbonate

18-22 mmol/L 23-26 mmol/L

Chapter 3:

Post Dural Puncture Headache


30

Pathophysiology Of Dural Puncture

Cerebrospinal Fluid

CSF production occurs mainly in the choroid plexus, but there is some

evidence of extra-choroidal production. About 500 ml of CSF is produced

daily (0.35 ml/ min), its volume in the adult is approximately 150 ml, of

which half is within the cranial cavity, and its pressure in the lumbar region

in the horizontal position is between 5 and 15 cm H2O.On assuming the

erect posture, this increases to over 40 cm H2O.The pressure of the CSF in

children rises with age, and maybe little more than a few cm H2O in early

life (48).

Consequences Of Dural Puncture

Puncture of the dura has the potential to allow the development of

excessive leakage of CSF. Excess loss of CSF leads to intracranial

hypotension and a demonstrable reduction in CSF volume (14). The adult

subarachnoid pressure of 5–15 cm H2O is reduced to 4.0 cm H2O or less (49). The rate of CSF loss through the dural perforation, (50)(0.084–

4.5 ml/sec) is generally greater than the rate of CSF production

(0.35 ml/min), particularly with needle sizes larger than 25G (51).

Although the loss of CSF and lowering of CSF pressure is not disputed,

the actual mechanism producing the headache is unclear. There are two

possible explanations. First, the lowering of CSF pressure causes traction

on the intracranial structures in the upright position. These structures are

pain sensitive, leading to the characteristic headache. Secondly, the loss of

CSF produces a compensatory venodilatation vis-à-vis the Monro–Kellie


31

doctrine (14).The Monro–Kellie doctrine, or hypothesis, states that the sum

of volumes of the brain, CSF, and intracranial blood is constant.

The consequence of a decrease in CSF volume is a compensatory increase

in blood volume. The venodilatation is then responsible for the headache.

Factors Contributing To The Development Of Headache After

Lumbar Puncture:

The following factors contribute to the development of headache after

lumbar puncture:

1. Needle Size:

The size of the dural tear is directly proportionate to the amount of CSF

leakage. As a smaller needle diameter produces a smaller tear in the dura,

there is less potential for leakage and incidence of headache after lumbar

puncture. The incidence of headache is 70% if the needle size is between

16 and 19G, 40% if the needle size is between 20 and 22G and 12% if the

needle size is between 24 and 27G(52).

2. Direction Of Bevel:

As the collagen fibers in the dura matter run in a longitudinal direction,

parallel to the long or vertical axis of the spine, the incidence of headache

after lumbar puncture is less if the needle is inserted with the bevel parallel

to the dural fibers, rather than perpendicular (53). This ‘‘separates’’ the

fibers rather than cutting them, thus facilitating closure of the hole on

needle withdrawal. If the needle is at right angles to the collagen fibers, the

cut in the dural fibers, previously under tension, would then tend to retract,


32

resulting in a bigger dural tear, thus increasing the likelihood of CSF

leakage and the incidence of headache after lumbar puncture (53).Clinical

studies had confirmed that post dural puncture headache was more likely

when the cutting spinal needle was directed perpendicular on the direction

of the dural fibers (16).

3. Needle Design:

Types of Needles (54): a- Quincke Needle

b- Whitacre Needle (Pencil-Point)

c- Sprotte Spinal Needle

Figure 7: Spinal Needles (54)

There is convincing evidence in the anesthesia literature that headache

after lumbar puncture is reduced using non-cutting (Atraumatic) needles (55). These atraumatic needles have a diamond shaped tip and the orifice is

situated up to 0.5 mm from the needle tip.


33

As these needles cause temporary separation rather than cutting the

elastic fibers, which then recoil after removal of the needle, the damage to

the dura is less with atraumatic needles (53). This considerably reduces the

incidence of headache and the need for medical intervention. As the tip has

to be passed at least 0.5 mm into the subarachnoid space before the orifice

enters into it, some patients may develop paraesthesia owing to the possible

impingement on the stretched cauda equina by the tip of the needle (56).

4. Replacement Of The Stylet:

The standard procedure is to replace the stylet before withdrawing the

needle when a non-cutting needle is used. In a study of 600 patient (57). The

incidence of headache was 5% in patients whose stylet was replaced as

compared with 16% in the patients whose stylet was not reinserted. It is

thought that the higher incidence in the second group is due to a strand of

arachnoid that may enter the needle with the CSF and when the needle is

removed the strand could be threaded back through the dural defect and

produce prolonged CSF leakage.

5. Number Of Lumbar Puncture Attempts:

As the number of dural punctures directly relates to the size of the dural

damage, making fewer attempts at dural puncture could be associated with

lesser incidence of headache after lumbar puncture. However, recent study

states that therewere no statistically significant associations among post-

dural puncture headache and the number of lumbar punctures (58).


34

6. Age And Sex Of The Patient:

Certain patient population is at an increased risk for development of

post dural puncture headache. Patients age 20-40 years are most

susceptible whereas the lowest incidence occurs after fifth decades (59) (60).

Women are more likely to be affected than men when risk is adjusted for

age. In the series reported by Vandane and Dripps women had twice the

incidence i.e., 14% of PDPH compared with men i.e. 7 %( 61).

Incidence

This alarmingly high incidence of post-spinal headache was likely

attributable to the use of large gauge, medium bevel, cutting spinal needles

(Figure7). In 1956, with the introduction of 22G and 24G needles, the

incidence was estimated to be 11% (63).

Today the use of fine gauge pencil-point needles, such as the Whitacre

and Sprotte® has produced a greater reduction in the incidence of post-

dural puncture headache, which varies with the type of procedure and

patients involved. It is related to the size and design of the spinal needle

used, the experience of the personnel performing the dural puncture, and

the age and sex of the patient (64) (65).

Presentation Of Dural Puncture Headache

Onset

Headache and backache are the dominant symptoms that develop after

accidental dural puncture. Ninety per cent of headaches will occur within 3

days of the procedure(66)and 66% start within the first 48 h(67).


35

Symptoms

Headache is the predominant, but not ubiquitous presenting complaint (68). The headache is described as severe, searing and spreading like hot

metal(69). The common distribution is over the frontal and occipital areas

radiating to the neck and shoulders. The temporal, vertex and nuchal areas

are reported less commonly as the site of discomfort, although neck

stiffness may be present. The pain is exacerbated by head movement, and

adoption of the upright posture, and relieved by lying down.

Diagnosis

The history of accidental or deliberate dural puncture and symptoms of a

postural headache, neck ache and the presence of neurological signs,

usually guide the diagnosis. Where there is doubt regarding the diagnosis

of post-dural puncture headache, additional tests may confirm the clinical

findings. A diagnostic lumbar puncture may demonstrate a low CSF

opening pressure or a ‘dry tap’, a slightly raised CSF protein, and a rise in

CSF lymphocyte count. An MRI may demonstrate: diffuse dural

enhancement, with evidence of a sagging brain; descent of the brain, optic

chiasm, and brain stem; obliteration of the basilar cisterns; and enlargement

of the pituitary gland (70)(Figure 8) (71).


36

Figure 8: MRI showing diffuse dural enhancement (71)

Differential Diagnosis

The diagnosis of post-dural puncture headache is frequently clear from

the history of dural puncture and the presence of a severe postural

headache. However, it is important to consider alternative diagnoses as

serious intracranial pathology may masquerade as a post-dural puncture

headache. Clinicians should remember that intracranial hypotension can

lead to intracranial hemorrhage through tearing of bridging dural veins (72)

and a delay in diagnosis and treatment can be dangerous. Diagnoses that

may masquerade as post-dural puncture headache include intracranial

tumors(73), intracranial hematoma(74), pituitary apoplexy (75), cerebral


37

venous thrombosis (76) (77), migraine, chemical or infective meningitis (78)

and non-specific headache. It has been estimated that 39% of parturient

report symptoms of a headache unrelated to dural puncture following

delivery (79).

Duration

The largest follow-up of post-dural puncture headache is still that of

Vandam and Dripps in 1956 (63). They reported that 72% of headaches

resolved within 7 days, and 87% had resolved in 6 months (Table 4). In a

minority of patients the headache can persist (69).Indeed, case reports have

described the persistence of headache for as long as 1–8 yr after dural

puncture (80).

It is interesting to note that even post-dural puncture headaches of this

duration have been successfully treated with an epidural blood patch (67).

Table 4: Estimated rate of spontaneous recovery from post-dural

puncture Headache (81).

Duration Percentage recovery %

1±2 days 24 3±4 days 29 5±7 days 19 8±14 days 8 3±6 weeks 5 3±6 months 2 7±12 months 4


38

Prevention And Treatment Of PDPH

The aim of management of post-dural puncture headache is to:

(I)Replace the lost CSF.

(II) Seal the puncture site.

(III) Control the cerebral vasodilatation.

Overview

The literature regarding the treatment of post dural puncture headache

often involves small numbers of patients, or uses inappropriate statistical

analysis. Studies observing the effects of treatments in post-dural puncture

headache often fail to recognize that, with no treatment, over 85% of post-

dural puncture headaches will resolve within 6 weeks (Table 4) (81).

A- Psychological

Patients who develop post-dural puncture headache may reveal a wide

range of emotional responses from misery and tears to anger and panic. It is

important both from a clinical and medico-legal point of view, to discuss

the possibility of headache before a procedure is undertaken that has a risk

of this complication. Obstetric patients are particularly unfortunate should

they develop this complication, as they expect to feel well and happy and to

be able to look after their new baby. It is important to give the mother a

thorough explanation of the reason for the headache, the expected time

course, and the therapeutic options available (69).


39

B- Simple

Spriggs DA et al. found that bed rest has been shown to be of no benefit (82). Supportive therapy such as rehydration, acetaminophen, non-steroidal

anti-inflammatory drugs, opioids, and anti-emetics may control the

symptoms and so reduce the need for more aggressive therapy (83)but do

not provide complete relief (84).

C- Posture

If a patient develops a headache, they should be encouraged to lie in a

comfortable position. The patient will often have identified this, without

the intervention of an anesthetist. The prone position has been advocated,

but it is not a comfortable position for the post-partum patient. The prone

position according to Handler CE et al. raises the intra-abdominal pressure,

which is transmitted to the epidural space and may alleviate the headache.

A clinical trial of the prone position following dural puncture failed to

demonstrate a reduction in post-dural puncture headache (85).

D- Abdominal Binder

A tight abdominal binder raises the intra-abdominal pressure. The

elevated intra-abdominal pressure is transmitted to the epidural space and

may relieve the headache (85).


40

E- Haydration : There is no evidence supporting the use of increased fluids to prevent

post-LP headache (86). The only prospective study of this intervention

involved oral hydration. Dieterich and Brandt performed a prospective

study of 100 age-matched, randomly allocated neurologic patients and

found no correlation between the incidence of post lumber puncture

headache and the amount of fluid intake (87).

F- Pharmacological Treatment

A number of therapeutic agents have been suggested for the management

of post-dural puncture headache.

The main problem in choosing the most appropriate one is the lack of

large, randomized, controlled clinical trials.

a) Desmopressin Acetate And Adrenocortico trophic Hormone

Regarding desmopressin acetate, intramuscular administration before

lumbar puncture was not shown to reduce the incidence of post-dural

puncture headache (88). ACTH (adreno-cortico-trophic-hormone) has been

administered as an infusion (1.5 µg/kg),but inadequate statistical analysis

prevents assessment of the value of ACTH (89).

b) Caffeine

Caffeine is a central nervous system stimulant that amongst other

properties produces cerebral vasoconstriction. It is available in an oral and

I.V. form. The oral form is well absorbed with peak levels reached in


41

30 min. Caffeine crosses the blood–brain barrier and the long half-life of 3–

7.5 h allows for infrequent dosing schedules.

Dose

The dose now recommended for the treatment of post-dural puncture

headache is 300–500 mg of oral or I.V. caffeine once or twice daily (90).

One cup of coffee contains about 50–100 mg of caffeine and soft drinks

contain 35–50 mg.

Mode Of Action

It is assumed that caffeine acts through vasoconstriction of dilated

cerebral vessels (53). If cerebral vasodilatation were the source of the pain,

cerebral vasoconstriction might limit the pain experienced. Indeed, it has

been demonstrated that caffeine causes a reduction in cerebral blood flow, (91)but this effect is not sustained. However, the effects of caffeine on post-

dural puncture headache seem, at best, temporary (90). In addition, caffeine

is not a therapy without complications(92)and does not restore normal CSF

dynamics, thus leaving the patient at risk from the serious complications

associated with low CSF pressure(92).

c) Sumatriptan

The treatment for migranous headaches has focused on modification of

cerebral vascular tone. Sumatriptan is a 5-HT1D receptor agonist that

promotes cerebral vasoconstriction, in a similar way to caffeine (93).

Sumatriptan is advocated for the management of migraine and for post-

dural puncture headache.


42

However, a controlled trial found no evidence of benefit from Sumatriptan

for the conservative management of post-dural puncture headache (94).

d) Gabapentin

Gabapentin is an antiepileptic drug (AED) with analgesic properties. The

mechanism by which gabapentin exerts its analgesic action is unknown.

Gabapentin is structurally related to the neurotransmitter GABA (gamma-

aminobutyric acid) but it does not modify GABA (A) or GABA (B) radio-

ligand binding, it is not converted metabolically into GABA or a GABA

agonist, and it is not an inhibitor of GABA uptake or degradation.

Advantages And Disadvantages:

Potential advantages of gabapentin include lack of cardiovascular or

respiratory adverse effects, very good tolerability, lack of hepatic

metabolism, lack of liver and enzyme-inducing or –inhibiting effects, less

monitoring of laboratory tests. Gabapentin may have an advantage in

patients taking medications (e.g., antiretroviral agents for HIV infection)

that may result in clinically important interactions when taken concurrently

with enzyme-inducing or –inhibiting drugs. In addition, acute oral

overdoses of gabapentin tend to produce non–life-threatening symptoms

(e.g., ataxia, diarrhea, diplopia, drowsiness, lethargy, and slurred speech).

A potential drawback to gabapentin is a delay in response due to need for

dosage titration. Dosage adjustment is required in patients with renal

impairment (95).


43

Gabapentin has been reported to be effective in prophylaxis and treatment

of PDPH. After treatment with gabapentin 400 mg three times daily, PDPH

was relieved remarkably in 24 hr(96).

G- Epidural Blood Patch

History

After the observation that ‘bloody taps’ were associated with a reduced

headache rate the concept of the epidural blood patch has developed. The

theory is that the blood, once introduced into the epidural space, will clot

and occlude the perforation, preventing further CSF leak. The high success

rateand the low incidence of complications have established the epidural

blood patch as the standard against which to evaluate alternative methods

to treat post-dural puncture headache (97).

The Mechanism of Action

Using either radiolabelled red cells (98) or an MRI scan (99)several studies

have reported the degree of spread of the epidural blood patch. After

injection, blood is distributed caudally and cephalad regardless of the

direction of the bevel of the Tuohy needle. The blood also passes

circumferentially around to the anterior epidural space. In addition, the

blood passes out of the intervertebral foramina and into the paravertebral

space. The mean spread of 14 ml of blood is six spinal segments cephalad

and three segments caudal. Compression of the thecal space for the first 3

h, and a presumed elevation of subarachnoid pressure, may explain the


44

rapid resolution of the headache. Compression of the thecal sac is not,

however, sustained and maintenance of the therapeutic effect is likely to be

attributable to the presence of the clot eliminating the CSF leak. It has been

observed that CSF acts as a procoagulant, accelerating the clotting process (98). At 7–13 h, there is clot resolution leaving a thick layer of mature clot

over the dorsal part of the thecal sac. Animal studies have demonstrated

that 7 days after the administration of an epidural blood patch, there is

widespread fibroblastic activity and collagen formation. Fortunately, the

presence of blood does not initiate an inflammatory process and there is no

evidence of axonal edema, necrosis or demyelination (100)(101).

Technique

The presences of fever, infection on the back, coagulopathy, or patient

refusal are contraindications to the performance of an epidural blood patch

(102). As a precautionary measure, a sample of the subject’s blood should

be sent to microbiology for culture (103). With the patient in the lateral

position, the epidural space is located with a Tuohy needle at the level of

the supposed dural puncture or an intervertebral space lower. The operator

should be prepared for the presence of CSF within the epidural space. Up

to 30 ml of blood is then taken from the patient’s arm and injecting slowly

through the Tuohy needle. There is no consensus as to the precise volume

of blood required. Most practitioners now recognize that the 2–3 ml of

blood originally described by Gormley is inadequate, and that 20–30 ml of

blood is more likely to guarantee success (103). Larger volumes, up to

60 ml, (104) have been used successfully in cases of spontaneous intracranial

hypotension. At the conclusion of the procedure, the patient is asked to lie

still for one (102) or, preferably, 2 h (105) and is then allowed to walk.


45

Outcome

The technique has a success rate of 70–98% if carried out more than 24 h

after the dural puncture. If an epidural blood patch fails to resolve the

headache, repeating the blood patch has a similar success rate. Failure of

the second patch and repeating the patch for a third or fourth time has been

reported. However, in the presence of persistent severe headache, an

alternative cause should be considered (106).

Complications

Immediate exacerbation of symptoms and radicular pain has been

described (107). These symptoms do not persist and resolve with the

administration of simple pain killers. Long-term complications of epidural

blood patch are rare. A single case report of an inadvertent subdural

epidural blood patch described non-postural, persistent headache and lower

extremity discomfort (108).

Prophylactic Epidural Blood Patch

Where the known incidence of post-dural puncture headache is high, such

as in the parturient, the use of a prophylactic epidural blood patch after

accidental dural puncture, that is blood patching before the onset of

symptoms, is an attractive option. Prophylactic patching has generally been

dismissed as ineffective, but the evidence is conflicting. A controlled trial

in post-myelogram headaches (109) and one after spinal anesthesia and after

unintentional dural puncture with an epidural needle (110) have confirmed

the benefit of prophylactic patching. Those studies that have not supported


46

the use of prophylactic patching may have used insufficient blood for the

patch (110).

The pressure gradient between the thecal and epidural space may be high

immediately after dural puncture and lead to patch separation from the site

of the perforation. Blood patching at that time may therefore need a greater

volume of blood to produce a successful patch compared with a late patch,

where the CSF pressure may be lower (111).

H- Epidural saline

Concerns have been expressed about the potential danger of an

autologous epidural blood patch for the treatment of post-dural puncture

headache. The immediate resolution of the headache with a blood patch is

attributable to thecal compression raising the CSF pressure. An epidural

injection of saline would, in theory, produce the same mass effect, and

restore normal CSF dynamics. As saline is a relatively inert and sterile

solution, epidural saline bolus or infusion appears to be an attractive

alternative. Regimens that have been advocated include:

(i) 1.0–1.5 liter of epidural Hartmanns solution over 24 h, starting

on the first day after dural puncture (112).

(ii) Up to 35 ml/h of epidural saline or Hartmanns solution for 24–

48 h, or after development of the headache (113).

(iii) A single 30 ml bolus of epidural saline after development of

headache (114).

(iv) 10–120 ml of saline injected as a bolus via the caudal epidural

space (115).


47

Advocates of an epidural saline bolus or infusion maintain that the

lumbar injection of saline raises epidural and intra-thecal pressure.

Reduction in the leak would allow the dura to repair.

However, observations of the pressures produced in the subarachnoid

and epidural space show that, despite a large rise in epidural pressure, the

consequent rise in subarachnoid pressure maintains the differential pressure

across the dura. The pressure rise is also not sustained and is dissipated

within 10 min (116). The saline may induce an inflammatory reaction within

the epidural space, promoting closure of the dural perforation.

I- Epidural Dextran

Despite the paucity of evidence to support epidural saline, some

observers have considered the epidural administration of Dextran 40 (117).

Those studies that recommend Dextran 40, either as an infusion or as a

bolus, conclude that the high molecular weight and viscosity of Dextran 40

slows its removal from the epidural space. The sustained tamponade around

the dural perforation allows spontaneous closure. However, it is unlikely

that Dextran 40 will act any differently to saline in the epidural space. Any

pressure rise within the subarachnoid space would, like saline, be only

transient. Histological inspection of the epidural space after administration

of Dextran 40 (100), does not demonstrate any inflammatory response that

would promote the healing process. The evidence for the administration of

epidural Dextran to treat post-dural puncture headache is not proven and

the theoretical argument to justify its use is poor.


48

J- Epidural, Intrathecal And Parenteral Opioids

A number of authors have advocated the use of epidural (118), intra-

thecal (119) or parenteral morphine (120) the majority of these reports are

either case reports or inadequately controlled trials.

Some of the studies used epidural morphine after the onset of headache;

others used epidural or intra-thecal morphine as prophylaxis or in

combination with an intra-thecal catheter (119). A controlled trial of intra-

thecal fentanyl as prophylaxis found no evidence of a reduction in the

incidence of post-spinal headache after dural puncture with a 25-gauge

spinal needle (121).

K- Fibrin Glue

Alternative agents to blood, such as fibrinous glue, have been proposed

to repair spinal dural perforations (122). Cranial dural perforations are

frequently repaired successfully with it. In the case of lumbar dural

perforation, the fibrin glue may be placed blindly or using CT-guided

percutaneous injection (123). There is, however, a risk of the development of

aseptic meningitis with this procedure (124).

L- Intrathecal Catheters

After accidental dural perforation with a Tuohy needle, it has been

suggested that placement of a spinal catheter through the perforation may

provoke an inflammatory reaction that will seal the hole. Evidence to

support this claim is conflicting (125). The mean age of the patients in some


49

of the trials has been >50 yr, where the rate of post-dural puncture

headache is low. Some trials have used spinal microcatheters, 26G–32G;

others have placed 20G epidural catheters through an 18G Tuohy needle (126).

Histopathological studies in animals and humans with long-term intra-

thecal catheters confirm the presence of an inflammatory reaction at the site

of the catheter. Comparison between the effects of a catheter left in situ for

24 h and for several days or weeks would seem inappropriate (127).

If, after accidental dural puncture with a Tuohy needle, the insertion of an

intra-thecal catheter reduced the post-dural puncture headache rate, then it

would be worth considering. However, neurological complications, such as

cauda equina syndrome and infection, should preclude the use of intra-

thecal catheters (128).

M- Surgery

There are case reports of persistent CSF leaks that are unresponsive to

other therapies, being treated successfully by surgical closure of the dural

perforation(129). This is clearly a last resort treatment.

Patients and Methods


51

After approval by the Ethical Committee and written informed patient

consent, 40 adult ASA physical status I parturients at full-term gestation

and presenting for elective cesarean delivery were enrolled in this

prospective, randomized study. Women suffering from preeclampsia,

hypertension, diabetes, obesity, or ante-partum hemorrhage were excluded.

On arrival to the operating room basic monitoring was applied for each

patient in the form of electrocardiogram (ECG), pulse oximetry and blood

pressure. Two wide bore cannulae (18G) were inserted after application of

EMLA® cream at site of cannulation.

Before initiation the of the block, each patient received 500 mL of

Ringer Acetate solution within 10-15 minute and placed in the supine

position with a 15° left lateral tilt then patients were randomized into one of

two groups. Group (A) in the sitting position (n=20) and group (B) in the

right lateral decubitus position (n=20).

After obtaining baseline recordings (Time 1) (T 1) for Blood pressure

(Systolic, Diastolic, Mean arterial blood pressure (MAP)), Heart rate (HR)

and O2 saturation anesthesia was given in the sitting position (Group A)

where a stool can be provided as a footrest and a pillow placed in the lap.

The assistant then maintains the patient in a vertical plane while flexing the

patient’s neck and arms over the pillow to open up the lumbar vertebral

space. While in the right lateral position(Group B) the patients were placed

with their back parallel to the edge of the operating table nearest the

anesthesiologist, their thighs flexed on their abdomen, and their neck flexed

to allow the forehead to bias close as possible to the knees.


52

After sterilization of patient back with povidone-iodine (Betadine), the

L3-4 or L4-5 interspace is identified and using 25G Quincke`s spinal

needle inserted in the defined space. After obtaining clear cerebrospinal

fluid, 2 ml of hyperbaric bupivacaine (Bucain 0.5% Hyperbar®) + 25 mcg

Fentanyl were slowly injected. After removal of spinal needle, patients

were placed in the supine position with a 15° left lateral tilt. The height of

sensory block measured with alcohol swabs and the degree of motor

impairment using the Bromage scale were evaluated every 2 min which

described on Table (5) (130 ). Surgery was allowed to start when at least the

T4 dermatome was anesthetized.

Table (5): Bromage scale (130)

Grade Criteria Degree of block

I Free movement of legs and feet Nil (0%)

II Just able to flex knees with free movement of feet Partial (33%)

III Unable to flex knees, but with free movement of

feet

Almost complete

(66%)

IV Unable to move legs or feet Complete (100%)

Intra-operative blood pressure, heart rate and O2 saturation were

monitored every 5 min and systolic blood pressure, HR, O2 saturation were

recorded before induction of anesthesia as mentioned before (T 1), after

induction (T 2), after stabilization of the sensory level ( T 3) and by the end

of operation (T 4) . Ephedrine in increments of 5 mg was given IV to treat

hypotension, defined in this study as a maternal systolic blood pressure


53

below 70-80% of baseline recordings and/or an absolute value of < 90 -

100mmHg. In addition, bradycardia with heart rate less than 60 beats/min.

was treated was atropine 0.5 mg. Other side effects such as nausea or

vomiting were recorded throughout the intraoperative period and treated

accordingly.

Follow up of PDPH within 48 hours of the end of operation and all

participants informed to lie flat in bed after the procedure, to have adequate

hydration and in case of developing headache to have Paracetamol 500 mg

+ Caffeine 50 mg(Panadol Extra®) /6 hours.


54

Statistical Analysis:

Continuous variables were analyzed statistically using analysis of variance

and Scheffé’spost hoc test or unpaired Student’s t-testing whenever

appropriate. Categorical data were analyzed using the Fisher’s exact test

and χ2 analysis. A P value < 0.05 was considered statistically significant.

RESULTS

Results

56

There were no differences in patient demographics with respect to age,

weight, height and the operative time (Table 6). Baseline systolic blood

pressures (Time 1)(T1) were almost similar in both groups (120.05 ± 6.84

mm Hg versus 117.70 ± 7.45 mm Hg in the sitting and lateral group,

respectively; (P =0.376)( Table 7).

In the lateral group, 3 (15%) patients became hypotensive as compared

with 1 (5%) in the sitting group in the reading after induction (T2). This

difference did not achieve statistical significance (P = 0.292) (Table 8).

Hypotension was also noticed later after stabilization of sensory level (T3)

in the lateral group, 11 (55%) more than in the sitting group, 4 (20%). This

difference achieve statistical significance (P = 0.022) (Table 8). There was

no difference in HR, O2 Saturation (Table 9) (Table 10) respectively. There

was increased incidence of nausea/vomiting in lateral group; 8 (40%)

versus 2 (10%) in sitting group, (P =0.028) (Table 11).

All patients had a sensory block reaching at least T4, but the maximal

spread of the sensory block was more cephalad with the lateral position and

this group also had more sensory blocks that reached higher than the T3

dermatome (80% versus 35%, P = 0.004) (Table 12). Regarding PDPH; In

the lateral group, 11 (55%) patients developed PDPH within 48 hours post-

operative versus 2 (10%) patients in the sitting group ;( P = 0.002) (Table

13).

Results

57

Table (6) Demographic data and Operative time of patients during study

Data are expressed as number, mean and standard deviation.

Sitting(n=20) Lateral(n=20) P-value

Age (years)

24.55±2.65 25.05±2.54 0.546

Weight (kg)

75.00±6.28 74.75±6.1 0.900

Height (cm)

162.25 ± 3.02 160.5 ± 3.94 0.123

Operative Time (min.)

65.25 ± 6.78 65.25 ± 6.78 1.000

Results

58

Table 7: Systolic Blood Pressure of patients during study



T1

120.05 ± 6.84 117.70 ± 7.45 0.376

T2

111.75 ± 8.93 104.40 ± 5.46 0.003*

T3

102.00 ± 5.54 96.75 ± 5.44 0.004*

T4

115.50 ± 7.42 111.30 ± 6.08 0.054

*= statistically significant. (P-value of statistical significance ≤ 0.05)

Figure (9): Systolic Blood Pressure of patients during study

Results

59

Table 8: Systolic Blood Pressure less than 100 mmHg of patients during study

Data are expressed as number and percentage.

Sitting (n=20) Lateral (n=20) P-value

T2

1 (5%) 3 (15%) 0.292

T3

4 (20%) 11 (55%) 0.022*


Figure (10): Systolic Blood Pressure less than 100 mmHg of patients during study in T3

Results

60

Table 9: Heart Rate (HR) of patients during study



T 1

92.40±9.56 91.65±9.52 0.805

T 2

92.55±9.57 96.85±10.30 0.180

T 3

91.15±8.61 96.20±11.54 0.125

T 4

91.50±8.60 92.25±8.87 0.788

Table 10: O2 Saturation of patients during study



T 1

99.00±0.56 98.75±0.96 0.32

T 2

99.05±0.51 98.80±0.83 0.26

T 3

99.20±0.61 99.05±0.05 0.58

T 4

99.45±0.51 99.25±0.78 0.35

Results

61

Table 11: Incidence of Nausea and Vomiting of patients during study

Data are expressed as number and percentage within group.

Sitting(n=20) Lateral(n=20) P-value N&V

2 (10%) 8 (40%) 0.028*


Figure (11): Incidence of Nausea and Vomiting of patients during study

Results

62

Table 12: Level of Sensory Block of patients during study

Data are expressed as number and percentage within group


T4

13 (65%) 4 (20%) 0.004*

T2

7 (35%) 16 (80%) 0.004*

*= statistically significant.

Figure (12): Level of Sensory Block of patients during study

Results

63

Table 13: Incidence of PDPH within 48 hours of patients during study

Data are expressed as number and percentage within group


PDPH

2 (10%) 11 (55%) 0.002*

*= statistically significant.

Figure (13): Incidence of PDPH within 48 hours of patients during study

Discussion

Discussion

65

Since, regional anesthesia became of choice in obstetric patients for its

characteristics in providing almost rapid onset of anesthesia, allowing the

mother to immediately interact with her baby; it is safer for mother than

general anesthesia. So, the complications following regional anesthesia

became of great interest either to the anesthesiologist or to the parturient

(1) (2).Complications of spinal or epidural block are either acute in the form

of pain on injection, high (total) spinal anesthesia and hypotension or

postoperative complications as backache, Post Dural Puncture Headache

(PDPH), urine retention, meningitis and nerve injury(3).

During pregnancy, Maternal physiologic changes occur as a result of

hormonal alterations, mechanical effects of the gravid uterus, increased

metabolic and oxygen requirements, metabolic demands of the feto-

placental unit, and hemodynamic alterations associated with the placental

circulation. Such changes become more significant as pregnancy

progresses, and they have major implications for anesthetic management,

especially in high-risk parturient (20).

PDPH presents one of the major complications of spinal and epidural

block annoying to the patients especially parturient(4)(5)(6). The incidence

of post-dural puncture headache was 66% in 1998 (62). Ninety per cent of

headaches will occur within 3 days of the procedure (66), 66% start within

the first 48 h (67) and rarely, the headache develops between 5 and 14 days

after the procedure. The headache is described as severe, searing and

spreading like hot metal (69). The common distribution is over the frontal

and occipital areas radiating to the neck and shoulders. The pain is

exacerbated by head movement, and adoption of the upright posture, and

relieved by lying down. The largest follow-up of post-dural puncture

Discussion

66

headache is still that of Vandam and Dripps in 1956 (63). They reported

that 72% of headaches resolved within 7 days.

Many studies implementing incidence of PDPH following different

techniques like median and para-median approach or usage of different

sizes and types of spinal needles. The outcome of these studies revealed

increased incidence with para-median technique in young patients and

decrease incidence while using smaller sizes spinal needles(7)(8).

In our study we studied the effect of placing parturient either in sitting

position or right lateral position during induction of spinal anesthesia on

severity of hypotension, level of sensory block, incidence of nausea and

vomiting and development of PDPH within 48 hours post-operative.

Twenty patients in each group were assessed. The right lateral group

showed more hypotension and more cephaled spread than in the sitting

group.

In our study there were no statistically significant differences in patient

demographics with respect to age, weight, height and the operative time.

Baseline systolic blood pressures (T1) were almost similar in both groups

(120.05 ± 6.84 mm Hg versus 117.70 ± 7.45 mm Hg in the sitting and

lateral group, respectively; P = 0.376). In the lateral group, 3 (15%)

patients became hypotensive as compared with 1 (5%) in the sitting group

in the reading after induction (T2). This difference did not achieve

statistical significance (P = 0.292). Hypotension was also noticed later

after stabilization of sensory level (T3) in the lateral group, 11 (55%)

more than in the sitting group, 4 (20%). This difference achieve statistical

significance (P = 0.022). There was no difference in HR, O2 Sat. There

was increased incidence of nausea/vomiting in lateral group; 8 (40%)

versus 2 (10%) in sitting group, (P =0.028).

Discussion

67

All patients had a sensory block reaching at least T4, but the maximal

spread of the sensory block was more cephalad with the lateral position

and this group also had more sensory blocks that reached higher than the

T3 dermatome (80% versus 35%, P = 0.004).

Regarding PDPH; in the lateral group, 11 (55%) patients developed

PDPH within 48 hours post-operative versus 2 (10%) patients in the

sitting group; (P = 0.002).

Studies comparing the left and right lateral position were unable to find

a final preference. The first investigators evaluating the sitting versus the

lateral position during induction of spinal anesthesia placed patients back

in the supine position immediately after a single-dose intra-thecal

injection (131)(132). Because of the extremely short interval between

injection and resuming the supine position, it is not surprising that the

block characteristics did not differ significantly but Inglis A et al. found

that there was a faster onset of sensory block to a higher level in right

lateral group and in turn required more ephedrine in the first 10 m after

siting the spinal (132). These results are on the side of more hypotension

that developed with lateral group in our study which in turn required

ephedrine supplementation early post induction but in our study we found

even after stabilization of sensory level there was characteristic difference

in level of sensory block between sitting and right lateral group.

Similar to our study Hilde C. Coppejans et al.(11)evaluated whether

the sitting position during initiation of small-dose combined spinal-

epidural anesthesia (CSE) would induce less hypotension as compared

with the lateral position , their findings are in accordance with our result

as respect more severe hypotension , more cephaled spread and increase

incidence of nausea and vomiting with right lateral group more than with

Discussion

68

the sitting group in spite of they used combined spinal epidural technique

using small dose of local anesthetic and in turn they needed epidural

supplementation more in sitting group.

Patel et al. found that the slower and more limited cephalad spread of

sensory block may explain the reduced incidence and/or severity of

hypotension (133) and these results are consistent with our results as seen in

the sitting position versus in the right lateral position which showed more

cephaled spread.

Rucklidge MW et al. made a comparison of the lateral, oxford and

sitting positions for performing combined spinal-epidural anesthesia for

elective caesarean section(134) and there result are in accordance with our

results as regarding higher dermatomal level in the lateral group more

than in the sitting group.

Studies reporting incidence of PDPH used different techniques like

median and para-median approach or usage of different sizes and types of

spinal needles (7) (8) other than implementing incidence after using

different positions for induction of regional anesthesia are not as plenty as

we mentioned regarding severity of hypotension or level of sensory block

and in turn incidence of nausea and vomiting and ephedrine

supplementation.

Siamak Afshin Majd et al. evaluated the occurrence of post lumbar

puncture headache in 125 patients undergoing lumbar puncture with a21

gauge Quincke`s needle(135), divided randomly into sitting and lateral

decubitus groups in the following five days and they found lumbar

puncture in sitting position could produce more post lumbar puncture

headache in comparison with lateral decubitus position. this was in

Discussion

69

contrast to our study as we found that incidence of PDPH was more in

lateral group but we must take in consideration that we use 25 gauge

Quincke`s needle and the mean of the patients’ age in their study was

50.96 ± 13.15 while in our study was 24.55±2.65 and 25.05±2.54 in

sitting and lateral group respectively.

Another study implemented by R. J. Chilvers et al. noted the frequent

incidence of Post dural puncture headache (PDPH), particularly with the

25- gauge Quincke`s needle(136 ) which used in our study but also they

found that even for the 25-gauge Whitacre needle the PDPH rate was

more than 3% which may assume that type of needle may not present an

actual predictor for development of PDPH.

Hans Lybecker et al. reported that age was significant predictors of

PDPH (53) as he evaluated a wide range of age in his study and this is not

in accordance with our study as age was insignificant between right

lateral group and sitting group as regarding females in child bearing

period.

In the current study incidence of PDPH was higher in the right lateral

group than in the sitting group. There are no studies reported why

incidence of PDPH may be high in right lateral position and if there is a

relation between high sensory level block and more severe hypotension

that develop with right lateral position and incidence of PDPH. Incidence

of PDPH in current study being high in lateral position may be

misestimated due to small number of cases in the study so, it is important

in to implement similar studies on larger number of patient to be more

efficient and conclusive. Also, it should be taken into consideration to

make more studies regarding this aspect in different age groups for good

estimation of the results.

Conclusion

70

Conclusion

Performing spinal anesthesia in caesarian section in the sitting position

is more technically easier and induces less severe hypotension, less

cephaled spread and less post dural puncture headache than in the right

lateral group.

Summary

Summary

72

Internationally, obstetric anesthesia guidelines recommend spinal and

epidural over general anesthesia (GA) for most caesarean sections.

The primary reason for recommending regional blocks is the risk of

failed endotracheal intubation and aspiration of gastric contents in pregnant

women who undergo general anesthesia (GA), while there is evidence that

GA is associated with an increased need for neonatal resuscitation.

The anesthetic plan for cesarean delivery should take into account the

well-being of two patients: the mother and the fetus. Regional anesthesia is

the most common method of anesthesia for delivery because it allows the

mother to be awake and immediately interact with her baby. It is also safer

for the mother than general anesthesia.

Regional anesthesia is used for 95% of planned cesarean deliveries in the

United States. The use of spinal anesthesia for cesarean delivery was

facilitated by the popularization of pencil-point needles, which dramatically

reduced the incidence of post dural puncture headache.

The question posed regarding the effect of sitting versus lateral position

approach for spinal anesthesia on severity of hypotension, block

characteristics, incidence of nausea and vomiting and incidence of PDPH is

an interesting one. This subject has been studied by many investigators

over the years. Most of theses studies found there were more hypotension,

more cephaled spread and increased incidence of nausea and vomiting with

lateral group. Regarding PDPH, incidence of its occurrence was evaluated

in a lot of studies either following different techniques like median and

para-median approach or usage of different sizes and types of spinal

needles also as regarding position of patient either in sitting or lateral

approach.

Summary

73

A total of 40 consecutive women with uncomplicated singleton

pregnancies at term and scheduled to undergo elective CS participated in

this prospective study .The women were divided into 2 groups of equal

size (each 20) , Sitting group (A) and right lateral group (B).

Women who had uncomplicated pregnancies were delivered electively

by Caesarean section at Kasr El-Aini hospital.

Measured variable

‐ Vital Signs recordings every 5 minutes (Blood Pressure, oxygen saturation and pulse)

‐ Incidence of nausea and vomiting ‐ Level of Sensory Block ‐ Development of PDPH within 48 hours

There was statistically significant differences between the 2 groups as

regarding severity of hypotension , where with right lateral group there was

more hypotension after induction if spinal anesthesia and after stabilization

of sensory level than with sitting group.

There was a statistically significant difference between the 2 groups as

regarding level of sensory block and incidence of nausea and vomiting,

where with right lateral group there was more cepaled spread following

spinal anesthesia than with sitting group and also increased incidence of

nausea and vomiting with lateral group.

Patients in right lateral group developed more PDPH compared to

patients in sitting group.

Summary

74

There was no statistical difference of medical importance between the 2

groups as regarding demographic data, operative time, HR and O2

saturation.

Conclusion:

Performing spinal anesthesia in caesarian section in the sitting position is

more technically easier and induce less severe hypotension, less cephaled

spread and less post dural puncture headache than in the right lateral group.

.

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الملخص العربي

امللخص العرىب

ب

على الصعيد الدولي،نجد أن التخدير في الوالده القيصريه بإستخدام التخدير النصفي مع

.قيصريةالالتخدير فوق األم الجافيه هوأآثر شيوعآ من التخدير الكلي في معظم أقسام الوالدة

في هو إزدياد مخاطرإرتجاع محتويات المعده ودخولها السبب الرئيسي للتوصية بالتخدير النص

في الجهاز التنفسي في النساء الحوامل الالتي يخضعن للتخدير الكلي، باإلضافه إلي أنه هناك أدلة

.على إرتباط التخدير الكلي مع إزدياد الحاجة إلنعاش الوليد

ي االعتبار سالمة إثنين من يجب على طبيب التخدير أثناء الوالدة القيصرية أن يأخذ ف

التخدير النصفي هو األسلوب األآثر شيوعا من التخدير الكلي ألنه يسمح . األم والجنين: المرضى

بل هو أيضا أآثر أمانا لألم من . لألم أن تكون مستيقظه وتتفاعل مباشرة مع طفلها بعد والدته

.التخدير الكلي

وقد . المئة من الوالدات القيصريه في الواليات المتحدة في ٩٥يتم استخدام التخدير النصفي ل

إنتشر التخدير النصفي للوالدة القيصرية بإستخدام اإلبر الشبيهه بالقلم الرصاص والتي خفضت

.بشكل آبير من حاالت الصداع الذي يأتي عقب ثقب األم الجافيه

التخدير النصفي عليى فى الوضع الجانب مقابل وضع الجلوسالسؤال المطروح بشأن تأثير

ومستوى فقد اإلحساس الحسى و نسبة حدوث الغثيان و القئ و نسبة مستوى الهبوط بضغط الدم

وقد تمت دراسة هذا الموضوع من قبل . هو أمرمثير لالهتمامحدوث صداع ما بعد ثقب األم الجافية

يوجد هبوط أآثر بضغط الدم الدراسات أنه معظموقد أظهرت . لعديد من الباحثين على مر السنينا

و . فى الوضع الجانبىنسبة حدوث الغثيان و القئزيادة وإرتفاع بمستوى فقد اإلحساس الحسى و

بالنسبة لصداع ما بعد ثقب األم الجافية فقد تمت دراسة نسبة حدوثه فى آثير من الدراسات منها ما

نبيه و دراسات أخرى تستخدم أنواع و بعد اعطاء البنج النصفى بمنتصف العمود الفقرى أو على جا

.دراسات فى وضع الجلوس و الوضع الجانبىأحجام مختلفة من إبر البنج النصفى و أيضا

إمرأه حامل في طفل واحد والحمل خالي من أي ٤٠بحثنا هو دراسه رصديه تتضمن

،وهي ) ٢٠آل مجوعه (حيث تم تقسيمهم إلى مجموعتين متساويتن في الحجم . فاتمضاع


ت

الحوامل الالتي لديهم حاالت الحمل ).ب( الوضع الجانبىومجموعة ) أ (وضع الجلوس مجموعة

. القصر العينيمستشفىخاليه من المضاعفات يخضعون لوالده قيصريه غير طارئه في

:المقاسةالمتغيرات

دقائق٥ آل ثمالعمليةقبل وتشبع األآسجين و النبض تم قياس البيانات الخاصة بالضغط •

.حتى نهاية العملية

. نسبة حدوث الغثيان و القئتم قياس •

. بمستوى فقد اإلحساس الحسىتم قياس •

. نسبة نسبة حدوث صداع ما بعد ثقب األم الجافيةتم قياس •

، بمستوى الهبوط بضغط الدمهناك فروق ذات داللة إحصائية بين المجموعتين فيما يتعلق

هبوط بضغط الدم بعد إعطاء البنج النصفى بالوضع الجانبى ينتج عنهج للتخدير حيث وجد أن النتائ

.و بعد إستقرار مستوى فقد اإلحساس الحسى أآثر من وضع الجلوس

بمستوى فقد اإلحساس آان هناك فروق ذات داللة إحصائية بين المجموعتين فيما يتعلق

بالوضع الجانبى ينتج عنهأن النتائج للتخدير حيث وجد ،الحسى و نسبة حدوث الغثيان و القئ

إرتفاع أعلى بمستوى فقد اإلحساس الحسى أآثر من وضع الجلوس و أيضا إرتفاع نسبة حدوث

.الغثيان و القئ فى الوضع الجانبى

الوضع الجانبى تعرضوا لصداع ما بعد ثقب األم الجافية أآثر من وضع المرضى في مجموعة

.الجلوس

و البيانات الديموغرافيةب اك فرق إحصائي ذات أهمية طبية بين المجموعتين ، فيما يتعلقلم يكن هن

. وتشبع األآسجين وقت العملية و النبض


ث

:والخالصة

ينتج و وضع الجلوس أسهل من حيث التقنية معفى الوالدة القيصرية أن التخدير النصفي

وصداع ما بعد ثقب االم الجافية فقد اإلحساس الحسى إرتفاع بمستوى وعنه هبوط فى ضغط الدم

.أقل مما ينتج عن الوضع الجانبى

الوضع و الجلوس وضع بين مقارنة: القيصرية الوالدة فى النصفى خديرالت الجانبى

المرآزة الرعاية و التخدير فى الماجستير درجة على للحصول توطئة مقدمة بحثية رسالةاأللم عالج و الجراحية

من مقدمة

عليق يوسف محمد أحمد محمد الجراحة و الطب بكالوريوس

القاهرة جامعة , الطب آلية

إشراف تحت

الخولى محمود منار/ الدآتور األستاذ التخدير أستاذ


سمير محمد إيناس/ الدآتور األستاذ التخدير مساعد أستاذ


الحكيم عبد رجب أحمد/ الدآتور التخدير مدرس


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prof.dr. manar mahmoud elkholy assist.prof.dr. enas...

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