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
Faculty of Medicine, Cairo University
Assist.Prof.Dr. Enas Mohamed Samir Assistant professor of anesthesiology
Faculty of medicine, Cairo University
Dr. Ahmad RagabAbd Elhakim Lecturer of anesthesiology
Faculty of Medicine, Cairo University
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).
Review of Literature
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).
Review of Literature
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)
Review of Literature
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).
Review of Literature
11
Figure 3: Ligaments of Vertebral Column(12)
Figure 4: Sagittal Section of Vertebral column(12)
Review of Literature
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
Review of Literature
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
Review of Literature
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).
Review of Literature
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)
Review of Literature
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).
Review of Literature
17
Figure 6: Midline Sagittal View of the Lumbar Spine (18)
Chapter 2: Physiologic Changes during
Pregnancy
Review of Literature
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
Review of Literature
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).
Review of Literature
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
Review of Literature
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.
Review of Literature
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).
Review of Literature
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
Review of Literature
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).
Review of Literature
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.
Review of Literature
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.
Review of Literature
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
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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
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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,
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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.
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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).
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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).
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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).
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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
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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
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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).
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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).
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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
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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.
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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).
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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
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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.
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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
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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).
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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.
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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
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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
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.
Patients and Methods
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
Patients and Methods
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.
Patients and Methods
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
Data are expressed as number, mean and standard deviation.
Sitting(n=20) Lateral(n=20) P-value
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*
*= statistically significant. (P-value of statistical significance ≤ 0.05)
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
Data are expressed as number, mean and standard deviation.
Sitting(n=20) Lateral(n=20) P-value
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
Data are expressed as number, mean and standard deviation.
Sitting(n=20) Lateral(n=20) P-value
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*
*= statistically significant. (P-value of statistical significance ≤ 0.05)
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
Sitting(n=20) Lateral(n=20) P-value
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
Sitting(n=20) Lateral(n=20) P-value
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
امللخص العرىب
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
امللخص العرىب
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
القاهرة جامعة , الطب آلية
سمير محمد إيناس/ الدآتور األستاذ التخدير مساعد أستاذ
القاهرة جامعة , الطب آلية
الحكيم عبد رجب أحمد/ الدآتور التخدير مدرس
القاهرة جامعة , الطب آلية
٢٠١٢