Download Intravenous regional conduction anesthesia

Intravenous regional conduction anesthesia:
A technique and literature review-Part I
CHARLES A. REESE, CRNA, PhD, CDR, NC, USN
Portsmouth, Virginia
In the first of a two part series on
intravenous regional anesthesia (IVRA),
the author reviews the history and
development of the Bier block
technique. He discusses the various
intravenous devices and their placement,
and investigates the use of tourniquets,
as well as the site and mode of action of
IVRA.
In the wave of enthusiasm and experimentation
which followed Koeller's introduction of cocaine
as a local anesthetic agent in 1884, a number of
regional nerve block techniques were advanced.1
Corning reported experiments with subcutaneous
cocaine while Conway advocated the injection of
4% cocaine directly into fracture sites.2 8
Perhaps the first record of cutaneous analgesia as a result of chemicals injected intravascularly is that of Alms, who in 1886 demonstrated
the loss of sensation along the course of an artery
into which a cocaine solution had been instilled.4
Interestingly, no mention was made of whether
intravenous injection was attempted.
The duration of action of cocaine was brief
and numerous reports appeared describing "poisoning" or shock following the injudicious use of the
drug. In 1892, Schleich, hoping to decrease the
incidence of toxic reactions, introduced the massive
infiltration of dilute cocaine solutions for literally
August/1981
all types of surgical procedures. 5 Similarly, the use
of the Esmarch bandage as a type of vascular
tourniquet became widely used to prolong the
duration of cocaine and to lessen its systemic toxic
effects. 0 It was not until 1901 however, that Braun
suggested the addition of dilute epinephrine to
infiltration solutions in order to slow circulatory
uptake of the drug.7
By the late 1890s, Halstead and Crile had
reported their techniques of regional anesthesia
for the upper extremity. 8s- Their approach apparently was not popular as it required the surgical
exposure of the brachial plexus and direct injection of cocaine into the nerve roots.
The Bier block
By the time August Bier introduced his now
famous venous anesthesia in 1908, Einhorn had
synthesized and Braun had popularized a new,
less toxic chemical local anesthetic agent-procaine. 10
1,12
.
It comes as no surprise to learn that
Bier's work was a direct outgrowth of his interest
in "cocainization" of nerves and use of the tourniquet to decrease blood loss during extremity
surgery.'l He was so excited by the success of his
new technique that he published his work in no
less than five separate journals and was able to
report on over 100 cases without a single misadventure.
A number of anecdotal reports followed Bier's
papers but added little new information other
357
than expanding the list of surgical operations for
which intravenous regional anesthesia (IVRA)
had been shown to be successful. 14, 1 In 1911,
Hirschel and Kulenkampff introduced their percutaneous auxiliary and supraclavicular brachial
plexus blocks, respectively.'6 17 The apparent popularity of these techniques and the development
of safer general anesthetic agents overshadowed
Bier's intravenous block. With only a few exceptions, it did not receive further attention in the
professional literature for more than half a century.
As the popularity of regional conduction anesthesia increased, the complexity, and hence the
duration of surgical procedures, required the development of new local anesthetic agents of longer
action and lower systemic toxicity. From this demand came Lofgren's development and introduction of lidocaine hydrochloride in 1946, the first
of a series of long-acting amide local anesthetic
agents. 8s
In 1963, Holmes reintroduced IVRA and included several modifications based on the newer
technology of intravenous therapy and pneumatic
tourniquets.'" In addition, he suggested the use
of lidocaine HC1, an idea which is still very
popular today.
Following Holmes' paper, a plethora of research articles and additional anecdotal accounts
glutted the surgical and anesthesia literature. Most
have praised the value of IVRA while others have
warned of its potential shortcomings or considered
it frankly dangerous. In 1965, an editorial in the
Journal of the American Medical Association
openly condemned the technique. 20
At least two major symposia have explored
the state of the art in IVRA. Interestingly, the
findings of the first symposium in 1969, which
were to have been published as a text, were
clouded by the U.S. Federal Drug Administration's denial to approve lidocaine HCI as an intravenous anesthetic. 21 These important papers were
subsequently published in Acta Anesthesiologica
Scandinavica-Supplementum XXXVI (1969). Reports of the second conference held in 1978, sponsored by the American Society of Regional Anesthesia, appear in their official publication Regional
Anesthesia, (Volume #4 Number 1).
An interesting historical aside, it was not until
1970, that Colbern suggested the now popular
eponymous name Bier Block for the technique of
IVRA. 22
Since its inception, and more particularly, its
reintroduction, considerable controversy has surrounded several aspects of the IVRA technique.
358
These include conflicting opinions about anatomic
placement of injection sites, exsanguination of the
extremity, and use of various tourniquet devices.
Each of these will be discussed in this article, as
well as the role of premedication. A review of the
literature regarding the pharmacokinetics of local
anesthetics in IVRA will be included in Part II
(to be featured in the October AANA Journal).
Premedication for the IVRA technique
The choice of preanesthetic medication for
patients who will receive IVRA does not differ
significantly from that chosen for any patient receiving other forms of regional anesthesia. Al-
though personal preferences may vary widely, the
goal of any premedication regimen should consider the following.
Analgesia for the patient in pain preoperatively: Narcotics are presently the agents of
choice, however, the recently introduced agonistantagonist analgesic combinations may find an increasing role in the near future. A number of these
drugs are available, each with its distinctive advantages as well as disadvantages. One should not
consider the technique of IVRA (placement of an
intravenous cannula and tourniquet) as indication
alone for preanesthetic analgesics.
Protection from harmful reflexes: Vagus
nerve-induced bradycardia, the so-called vaso-vagal
response, is clearly not desirable. The clinical incidence of this event would seem too infrequent
to warrant the routine use of vagolytic doses of
the parasympatholytic drugs such as atropine sulfate or glycopyrrolate to patients receiving IVRA.
Sedation/tranquilization:Egbert has suggested
that an informative preoperative visit by the anesthetist who will provide the anesthesia care may
significantly reduce the need for preoperative sedative medications.2 3 Such visits are highly recommended, even when minor surgery is planned.
Occasionally, the anesthetist will encounter
an extraordinarily apprehensive patient who is not
sufficiently calmed by the preoperative visit alone.
The patient's desire to be "asleep" may in itself
cause him to resist conduction anesthesia techniques, thus certain considerations should be made.
Sedative-hypnotics or tranquilizers may be used to
decrease the emotional reactions some patients
may experience when confronted with anesthesia
and surgery.
In addition to their psychotropic effects, a
number of these agents have been shown to protect the central nervous system from the higher
blood levels of local anesthetic agents encountered
Journal of the American Association of Nurse Anesthetists
with large volume regional conduction anesthesia
techniques.
Some authors advocate parenteral barbiturates
(pentobarbital) for prophylaxis against local anesthetic-induced seizures. 24 , 25 It should be appreciated, however, that approximately 70 mg/kg of
this medication must be given in this situation, a
dosage certainly not without its own complications.26
During the early 1970s, a number of authors
demonstrated that equipotent seizure prophylaxis
with diazepam produced fewer undesirable cardiovascular and respiratory side effects than barbiturates. 2 730 In spite of the fact that the exact mechanism of this protection is not clearly understood,
diazepam has subsequently enjoyed considerable
popularity as a sedative-prophylactic premedication for patients receiving large dose regional
anesthetic techniques.
Munson demonstrated that lidocaine-induced
seizures could be successfully aborted by the intravenous infusion of diazepam 0.1 mg/kg with a
minimum of cardiovascular and respiratory effects.
In a study of primates, De Jong found that 60
minutes following an intramuscular (thigh) dose
of diazepam 0.25 mg/kg, the amount of intravenous lidocaine required to cause seizure activity
was increased by two-thirds (12.8 mg/kg to 21.1
mg/kg) .32 Unfortunately, the study did not attempt a correlation between plasma diazepam
levels and degree of safety provided.
Route of diazepam administration
Assuming that there may indeed be some correlation of plasma diazepam levels and the degree
of local anesthetic-induced seizure protection, the
anesthetist should make every attempt to have the
patient receive diazepam at a time and in such a
manner as to provide high plasma diazepam levels
which will coincide with the peak plasma levels of
local anesthetic agents. While it is difficult to extrapolate the exact plasma levels of diazepam necessary to provide antiseizure protection, it is known
that numerous factors influence its uptake and distribution characteristics, including the route of
administration.
Kortilla showed that while intramuscular
(deltoid) diazepam produced a faster onset (20-30
min) of subjective symptoms of drowsiness than
did oral doses, patients reported no perceivable
differences at 60 minutes. 33 Plasma levels rose more
quickly with the intramuscular injection than with
the oral route, but at 60 minutes, the oral dosage
had produced higher plasma levels (190 mcg/cc)
than did intramuscular (153 mcg/cc).
August/1981
The discomfort associated with intramuscular
injection and the high incidence of diazepamrelated thrombophlebitis following intravenous administration, apparently caused by its solvent propylene glycol, have favorably influenced the popularity of the oral route.3 4
When advocating the oral administration of
diazepam it should be remembered that the rate
of dissolution and gastric activity can markedly influence its absorption. Gamble has shown that intramuscular morphine, meperidine or atropine
administered concurrently with oral diazepam will
prolong the peak absorption time of diazepam
from a control of 60 minutes to 90 minutes. It
will also decrease the peak blood level attained
from a control of 200 mcg/cc to 105 mcg/cc, 135
mcg/cc and 144 mcg/cc, respectively. 85
Gamble's work also suggests that drugs which
enhance gastric emptying such as metoclopramide
will decrease diazepam's peak absorption rate to
less than 30 minutes and increase the peak blood
levels attained to 244 mcg/cc.
The efficacious, routine use of antacids as preanesthetic medication is well reviewed in the
literature, and is commonly used in many anesthetists' practices. Recent work has shown that, in
addition to lowering the gastric pH to levels less
harmful should aspiration occur, absorption dynamics of concurrently administered oral medications may be favorably altered.
Sturdee has demonstrated both a markedly increased uptake and increased plasma diazepam
level (120 mcg/cc versus 70 mcg/cc at 30 minutes)
when diazepam 5 mg was given orally along with
an oral antacid (magnesium trisilicate) .8 It should
be noted that at 30 minutes, this surpasses levels
obtained by the administration of 10 mg by either
the intramuscular or oral routes without antacids. 3"
Sturdee postulates that this is due more to decreased gastric emptying time than to a direct effect
of the change in stomach pH.
In contrast, Nair states that one would expect
any antacid which raises stomach pH to near that
of the pKa of diazepam (3.3) to enhance absorption of the drug from the stomach.3 7 He found
that the concomitant administration of magnesium
trisilicate slowed uptake and decreased the clinical
soporific effect of diazepam. The use of sodium
citrate or aluminum hydroxide hastened this effect.
Patients in the aluminum hydroxide group had
significantly higher degrees of absorption resulting
in higher plasma levels by 60 minutes.
To further confuse the issue, Gamble found
that the addition of aluminum hydroxide will indeed hasten the absorption of diazepam but that
359
at 60 minutes, diazepam administered alone and
orally will produce higher plasma levels. 85
Depending upon your interpretation of this
data, it would seem that if the prophylactic effects
of diazepam are desired, the drug should be administered approximately 60 minutes prior to the
expected administration IVRA. Of course, keeping
in mind the incidence of discomfort and vascular
thrombotic activity involved, the intravenous administration of diazepam immediately prior to
initiating IVRA might be considered.
Finally, some would advocate no prophylactic
coverage, favoring instead to use this important
agent only when CNS symptoms are observed.
Moore feels that ventilation with oxygen alone is
sufficient should systemic symptoms be noted. 38 He
believes that hypoxia and hypercarbia play a significant role in the manifestation of seizure activity
and since such activity is short lived, the post-ictal
state is worsened by administration of sedative
drugs.
Regardless of the clinical data presented, preblock therapy with these medications cannot be
considered a guarantee against drug induced
seizures, nor should their administration be considered a substitute for proper technique.
Intravenous devices and their placement
As mentioned earlier, Bier's original technique
remained essentially dormant for more than 50
years following its introduction in 1908. In defense
of this, it must be remembered that his technique
must have been considered cumbersome as it re-
quired two separate tourniquets and an operative
procedure (venous cutdown) for placement of the
intravenous cannula (Figure 1) .10 It was not until
1931 that percutaneous venipuncture was advocated, thus making the technique more practical.89
The site of cannula placement is another
matter altogether. Bier suggested the injection be
made into vessels located in the antecubital fossa,
possibly because it was more accessible for surgical
exposure, and that the cannula be directed distally
in order to force the liquid toward the hand (presumably the surgical site). Such direction of injection is interesting as the presence of valves in
the extremity's superficial venous system would
seem to create an obstruction to distal flow. Indeed research by Fleming more than half a century
later, using radiopaque solutions to study the site
of action of intravenous local anesthetics, demonstrated that venous valvular competency could
cause retrograde flow, even to the point of leakage
beneath a pneumatic tourniquet. From this, there
appears to be no advantage in directing an intravenous device distally when performing IVRA.
Present concepts of anatomical preference for
percutaneous intravenous devices are closely related to the proposed site of action of IVRA. Those
who subscribe to the theory that IVRA works by
simple diffusion of liquid agents from the intravenous space into the soft tissues, thereby anesthetizing the nerve endings at the tissue level, advocate the placement of the injection site as close
to the site of injury or proposed surgery as prac40 44
tical, usually a vein on the dorsum of the hand.
Figure 1
August Bier's original technique of Intravenous Regional Anesthesia. Placement of a metal cannula required a surgical
procedure which no doubt deterred from its ready acceptance. Of interest is the use of both a distal and proximal
tourniquet to isolate the surgical site and to lessen the total volume of injectate.
(From Flagg, P.J. The Art of Anesthesia, J. B. Lippincott Co., Philadelphia, Pa. 1932, With Permission.)
Proximal
Sbandage
Distal
bandae
Esmarch
SKIN MARKING OF NOW ISCHEMIC VEIN
--
360
Journal of the American Association of Nurse Anesthetists
Advocates of the opposing view, which is that
IVRA works at the major nerve trunks in a manner similar to traditional peripheral nerve block
techniques, have promulgated the practice of placing the injection site in close proximity to these
structures, such as in superficial veins in the antecubital fossa. 46 47 Caution should be taken, however, when injecting at the antecubital fossa as
competent valves in the veins may prevent retrograde flow. This would cause injection pressure to
surpass that created by the tourniquet, thus allowing liquid anesthetic agent to flow into the general
circulation (Figure 2).
Sorbie mentions this argument in favor of
placing the intravenous cannula in the hand or
forearm in spite of his belief that the drug works
primarily at the nerve trunk. 47 A slow injection
will lessen the risk of this problem as well as
preventing possible rupture of the vein. Van
Niekerk has reported a similar complication when
Figure 2
Distribution of injection in median cubital vein at
elbow. Note that contrast remains in vessels near the
elbow while no contrast can be seen in the distal third
of the forearm. Onset of analgesia is in the typical
distal to proximal "glove" pattern, the posterior
elbow being last. Note also the presence of contrast
above the tourniquet, presumably due to excessive
pressure during injection. Such drug enters systemic
circulation and may result in symptoms of toxicity.
(From Raj, P.P. et al 1972 "The Site of Action of Intravenous Regional Anesthesia," Anesthesia and Analgesia
51:776-781. With Permission.)
a long cannula device was placed at the antecubital
fossa and threaded to a point proximal to the
tourniquet, with resultant systemic injection. 48
Raj has shown that within five minutes of
injection, regardless of the site, the majority of
liquid injectate concentrates in the large superficial veins of the antecubital fossa (Figure 3) .4
Regardless of the site preferred, the selection
of the percutaneous indwelling intravenous device
should be made with due care. The technical development of numerous highly flexible cannula
devices would seem to antiquate the further use of
inflexible metallic needles. Such cannulae are
available in virtually all sizes (25-12 gauge) and
a myriad of adaptations. It is recommended that
a small bore (22-25 gauge) be used as this will
reduce the size of rent remaining in the vein when
the device is removed and will lessen extravasation
of local anesthetic agent into the subcutaneous
tissue or out through the skin.
By attaching a sterile intravenous extension
tubing and syringe of local anesthetic agent, a
sterile closed system can be achieved which allows
considerable flexibility during exsanguination of
the extremity (Figure 4) without fear of dislodgement or infiltration into the subcutaneous tissue.
Brown suggests leaving such a system intact during
a case in order to conduct a continuous technique. 49
One may wish to employ an indwelling cannula which accommodates a tight fitting obturator
stylet or a Heparin-Lok® device (Figure 5) as these
will remain in the vein during exsanguination and
are less cumbersome to use than the syringe-tubing
arrangement.
Exsanguination
In the years following Holmes' popularization
of IVRA, a number of papers appeared which
anecdotally described modifications of Bier's original work. Among these were reports exploring the
efficacy of exsanguination prior to inflation of
the tourniquet. In modern practice this issue is
only academic as most surgeons desire a "bloodless
field" in which to work, thus requiring careful
exsanguination prior to tourniquet inflation. Additionally, the present concept of the site of action
of IVRA, which is detailed later, mandates conscientious and complete vascular exsanguination.
In current practice a latex Esmarch bandage,
an elastic wrap such as an Ace® bandage or a
Crepe bandage"0 is wrapped snugly around the
extremity from the fingers toward the shoulder.
Occasionally this practice is impractical due to
pain or an open wound. In such cases a pneumatic
August/1981
Figure 3
(A) Distribution of 5cc injected into median cubital veins. Note preferential filling of superficial veins around elbow.
(B) Distribution of 15cc injected into dorsum of hand with second tourniquet added to obstruct cephalad spread. Note
drug has reached the median and cephalic cubital veins via communicating perforating veins but does not reach the
phalanges or extravasate into hand tissue.
(From Raj, P.P. et al 1972 'The Site of Action of Intravenous Regional Anesthesia," Anesthesia and Analgesia, 51:776-781. With Permission.)
A
B
orthopedic splint or 3-5 minutes of gravity drain4 .
age may be used. 47, 51, 52,
Care must he taken when utilizing the Esmarch or elastic bandage as excessive shearing forces (up to 1000 mmHg) may be produced particularly on previously traumatized areas, or exquisitely
sensitive skin as found in elderly or cachectic
patients. 53 ~"4 Pulmonary embolism has been reported following this type of exsanguination when
used for delayed internal fixation of long bone
fractures. 55
A number of authors have presented convincing arguments favoring exsanguination with
IVRA. 46.1 6.57 Adams has determined the venous
volume of the upper extremity below a midhumerus tourniquet to be approximately 170 cc.
If this volume were not exsanguinated, the injection of a small volume (40 cc) of a local anesthetic agent into this vascular pool would considerably dilute the agent, making it weak and
ineffective.5 8 Atkinson believes this dilution may
prevent or severely retard the spread of agent from
the vascular bed into surrounding tissue thus re-
Figure 4
Closed injection system for Intravenous Regional
Anesthesia. A drug-filled 50cc syringe is attached to
a sterile intravenous extension tube. Drug is injected
into the extension tube and connected to an indwelling intravenous cannulae (22 Ga) and secured.
The extremity and injection system is ready for exsanguination of blood.
Journal of the American Association of Nurse Anesthetists
sulting in a large reservoir of agent available to
enter the systemic circulation when the tourniquet
is released. 57
Furthermore, Adams also feels that the exsanguinated vascular tree plays a significant role
in transport of local anesthetic agents to the nerve
substance. Thus, he strongly favors complete exsanguination prior to injection" 8
Bradford has reported that exsanguination of
a single upper extremity can increase central
venous pressure up to 6 cm H 2 O and advises that
caution be used when exsanguination is considered
in a patient with a history of congestive cardiac
failure. 9
When injecting local anesthetics into the exsanguinated extremity, one will often notice a
blotchy appearance of the skin (cutis marmorata)
caused by residual blood being forced from deep
vessels into small subcutaneous capillaries. 19 This
apparently has no clinical significance and is mentioned only so that the anesthetist is aware of its
possible occurrence.
The anesthetist is reminded that even with
complete exsanguination and tight fitting tour-
niquets, some vascular leakage may occur via the
intramedullary vessels of the humerus and may
appear as "oozing" at the operative site. 60 Again,
other than being an annoyance for the surgeon,
this is apparently of little clinical significance.
The use of tourniquets
It is perhaps obvious that without the use of
a tourniquet, there would not be a technique such
as IVRA. However, the physiologic and pharmacologic effects of this device are perhaps the least
discussed aspects of the technique.
The development of resistive/restrictive tourniquets invariably is linked with the surgical
amputation of extremities. As early as the 16th
century, Pare advocated such a technique to decrease blood loss and thereby ease the surgical
exposure.6 1 In 1718, Petit introduced a screw-type
device and coined the term tourniquet from the
French tourner, to turn. 62
In the 1860s, Lister became the first to use a
tourniquet for a surgical procedure other than
amputation.68 Shortly thereafter, Esmarch introduced his eponymous rubber bandage for the dual
Figure 5
(A) Alternative system of injection for Intravenous Regional Anesthesia. Once placed, a sterile obturator is inserted into
the intravenous cannulae and secured. Following exsanguination the obturator is removed and a drug-filled syringe is
connected to the cannula for injection.
(B) Placement of a "Heparin Lock" device onto the indwelling cannula allows additional mobility during exsanguination of the extremity. Following this, a syringe/needle isplaced inthe device and injection made.
August/1981
purpose of exsanguination and producing ischemia
of the extremities. This was later modified by von
Langenbeck to its present wide band-like form."6
In 1904, Harvey Cushing revolutionized surgical
tourniquets by his development of a pneumatic
device to which a manometer and tank of compressed air could be attached, thus creating a controllable constant pressure in the tourniquet. 65
Cushing's idea apparently went unnoticed, at
least relative to IVRA, as Bier's original works
utilized only the Esmarch bandage. Indeed, even
Holmes' work in 1963 mentioned only the application of a single Riva-Rocca type blood pressure
cuff as a tourniquet for performing IVRA. 19 In
1964, apparently unaware of Herreros' earlier
work, Hoyle introduced a specially designed two66
compartment pneumatic tourniquet for IVRA. *
His suggestion was that the proximal compartment
be inflated first and IVRA be carried out as usual.
After 15-20 minutes, the distal compartment was
to be inflated over what was now anesthetized
tissues, and the proximal compartment deflated.
This concept and device found many ardent advocates and is widely practiced today.
Despite the widespread clinical use of pneumatic tourniquets, there is a paucity of experimental and clinical data establishing the duration
of ischemia which may be considered safe and the
optimum pressure at which a tourniquet should be
maintained.
In common practice, two hours is often stated
as the maximum time a tourniquet can be safely
left inflated. This empirical limit apparently dates
from Bruner's work in 1951, and has survived
essentially unchallenged to date. 68
Prolonged ischemia of an extremity is obviously contrary to physiologic well-being. Following
two hours of tourniquet induced ischemia, the
venous pH falls in a linear fashion from a normal
of 7.4 to 6.9. Venous pO2 falls from a normal of
45 mmHg to a low of 4 mmHg while venous pCO 2
rises from a normal of 35 mmHg to 104 mmHg. 69
Miller has shown that after 60 minutes of tourniquet induced ischemia, tissue pO2 levels are significantly lower than venous oxygen tensions taken
at the same interval. 70 Additionally, following release of the tourniquet, tissue gas tensions and pH
return to normal levels much more slowly than do
venous values.
While the clinical application of such data is
inconclusive, Adams has shown that irreversible
muscle fatigue develops at two hours of ischemia. 1
Webb has demonstrated evidence of cell damage
in striated muscle which results in marked increases in capillary permeability to fluid and pro-
67
364
tein. 72 That this fluid loss may be clinically significant is supported by Fine's report of acute
renal failure and circulatory shock following release of an extremity tourniquet. 78 Although
modern practice of aggressive perioperative systemic fluid therapy generally precludes such disasters, the large shift of protein and fluids following
tourniquet ischemia cannot be discounted. The
importance of this phenomenon at the microscopic
level has only recently been suggested as a course
of post-tourniquet sequelae.
Miller's work suggests increased interstitial
pressure resulting from such edema may be
hazardous, particularly when it occurs in muscles
which are highly compartmentalized by fascial
sheaths, preventing adequate perfusion of these
tissues.70 His finding that a six-fold increase in interstitial pressure may persist as long as 24 hours
following only one hour of tourniquet ischemia
should be noted. Fowler demonstrated nerve conduction delays which he attributed to intramyelin
and periaxonal edema which resulted in swelling
of the myelin sheath. 74 The somatic and nervous
complications resulting from such insults such as
the post ischemic hand syndrome have long been
recognized by surgeons and should be considered
by anesthetists any time a tourniquet has been
employed. 7
In contrast to the concept of ischemia related
sequelae, another popular opinion is that direct
compression of tissues beneath a tourniquet may
play a significant role in such complications. In
1954, Moldaver inferred that the decrease in the
number of reports of tourniquet-related nerve
damage was due to the increased use of the pneumatic tourniquet, the popular rubber tube style
of that period. 76 He noted that even with the
pneumatic tourniquet, some residual damage did
occasionally occur. He described a tourniquet
paralysis syndrome which was manifest as functional disturbances in the neural distribution distal to the site of compression which could not be
explained on the basis of ischemia alone.
Ochoa supports this concept with his demonstration of localized edema in the myelin layer of
the compressed segment. 77 Lundborg also demonstrated marked changes in the epithelium of infrafunicular capillaries located beneath the cuff site,
more so than nerves in the ischemic limb distal to
the compression.78
From the data reviewed, it is difficult to
identify a singular causative situation. Quite probably, neural sequelae are a result of a combination
of compression and ischemia; changes from com-
Journal of the American Association of Nurse Anesthetists
pression begin immediately with inflation of the
device while ischemic changes develop later.
It would be evident that the majority of tourniquet related complications can be avoided by
careful attention to technical details. Certainly,
misapplied pneumatic tourniquets can produce
undue pressure on a concentrated site. When a
tourniquet is initially applied too loosely, the fabric cuff may restrict lateral expansion of the rubber bladder, thus narrowing the pressure band as
much as 75%. 71 There is no simple direct relationship between the pressure applied at the skin surface and that realized in the interior of the limb. 54
Lundberg has shown that the sciatic nerve
may realize a pressure of only 110 mmHg when
700 mmHg is applied over the thigh. Stewart suggests that a tourniquet be applied at the point
of maximum circumference, thereby compressing
nerves and vessels within the bulk of periosteous
muscle rather than direct compression of these vital
structures over honey prominences.s8 In this regard, it is generally advised that a tourniquet not
be utilized distal to the elbow or knee.el
Prior to application of the tourniquet, it is
recommended that orthopedic wool (Webrill®)
be wrapped circumferentially around the extrem-
ity so as to completely cover the area beneath and
approximately one inch to either side of the device
(Figure 6). 81 The imprint wrinkle which is usually
present following deflation and removal of the
tourniquet apparently is of little clinical significance. Ecchymosis or blistering of the skin is the
most common complication observed following the
use of an unpadded tourniquet. 71 Additionally,
care should be taken to prevent prepping solutions
from pooling under the tourniquet or its padding,
82 84
as serious chemical burns may result. The recommended inflation pressure of a
pneumatic tourniquet remains an illusive subject.
Such pressures will depend in part on the site of
application, size of the limb involved and the
patient's systemic blood pressure. Cuff pressures in
the range of 250-300 mmHg for the upper extremity and 450-500 mmHg for the lower extremity
are widely published and practiced. The derivation
of these figures is, however, unclear. Nobel has
demonstrated that in the arm, a cuff pressure of
250 mmHg will totally occlude intraneural as well
as superficial vasculature in the compressed segment.85
Sanders suggests that arbitrary inflation pressures should not be used. He favors instead a min-
Figure 6
Prior to application of the tourniquet a layer of cotton wool (Webrill*) should be placed circumferencially beneath the
tourniquet to extend approximately one inch beyond the tourniquet's margins. Care should be taken during the preparation of the extremity not to saturate the padding with antiseptic solutions.
August/1981
imum effective pressure (MEP), achieved by adjusting the tourniquet pressure, regardless of the
indicated gauge pressure, until distal pulses are no
longer felt in the extremity. 86 It must be remembered, however, that systemic arterial pressures
may change, often as much as 70-100 torr, particularly if any discomfort is felt. Therefore, some advocate that the MEP be identified and an additional 100 mmHg be added to the tourniquet
gauge pressure. 87 This technique has been found
clinically satisfactory by the author with no known
complications after several hundred procedures.
A properly functioning tourniquet is a necessity. This should consist of a double compartment
cuff and switching device which is inflation-tested
prior to each application (Figure 7) . Additionally,
the rubber bladders should be removed from the
fabric binder and inspected periodically for deterioration. If there is any question as to their condition, new bladders should be obtained.
Before purchasing an inflation device, one
must be sure that it will totally satisfy its intended
purpose. While numerous styles are available, the
author prefers a compressed air or oxygen powered
model which includes a constant read pressure
gauge and minute timer to remind the user of
elapsed time. Portable models are available which
will allow patients to be transferred (for example,
to the radiology department) with the IVRA
intact.
Pressure gauges should be tested against a
liquid mercury manometer prior to each application and the inflated tourniquet squeezed while
observing for a deflection or "bounce" on the
pressure gauge. This latter maneuver is done to
observe patency of the delivery line and to insure
that a "flap valve" effect is not present in the
lumen of the delivery tube. Mullick has reported
a case in which a pressure gauge displayed 350
mmHg while the tourniquet was pressurized to
over 1200 mmHg.88
Prior to initiating IVRA, the anesthetist is
advised to consult the surgeon as to projected
operative time. If this time plus preparation exceeds two hours, an alternative form of anesthesia
is suggested such as brachial plexus block. When
employing IVRA, the judicious utilization of time
is imperative. The anesthetist should request the
surgeon to make any necessary skin marks with an
indelible marker prior to the block technique and
that he time his scrub and gowning to coincide
with the termination of the patient's skin prep.
Accordingly, the anesthetist should make sure that
a technician is available to commence the skin
prep immediately following the injection of local
anesthesia. Conservation of this precious time will
make a significant contribution toward successful
IVRA.
The technique of tourniquet deflation plays
a significant role in the uptake and distribution
Figure 7
(A) Double-cuff tourniquet recommended
B
for Intravenous Regional
Anesthesia. Note that two compartments are combined within one
strap, each compartment having a separate inflation nipple. Luer-Lock®
fittings are highly recommended to prevent disconnects. Single valving
system from which either tourniquet compartment can be individually
regulated. With this device a single pressure source (02. compressed air,
nitrogen, etc.) can be utilized.
3000
un lus"
iMamuNI
(B) Pressure regulator and gauge. Gauges on such devices must be
checked against a mercury manometer prior to each use. Inaccurate
gauges may result in patient injury.
A
/i;~
*
~
:
Journal of the American Association of Nurse Anesthetists
of local anesthetic agents following IVRA and will
be discussed in Part II of this article.
Tourniquet pain
Of all complications associated with the use
of pneumatic tourniquets for IVRA, the most
common and least clearly understood is the occurrence of tourniquet pain.
The application of tourniquet compression of
approximately 250 mmHg over the upper aspect
of an extremity will invariably result in some
degree of discomfort after 30-45 minutes. This
pain has been attributed to the direct compression
of tissues, including nerves and muscle. 89, 90 Subjectively, this pain may vary among patients but is
most often intolerable after one hour. While
systemic analgesics and hypnotics may attenuate
the intensity temporarily, some degree of basal
narcosis is often required to make completion of
surgery possible. This pain may even be noted
during inhalation or intravenous general anesthesia
as a narrowing of pulse pressure and a gradual
rise in mean blood pressure and pulse rate.
August/1981
In order to better understand this phenomenon, the somatic distribution of the upper arm is
illustrated in Figure 8. The lower lateral and
posterior cutaneous nerves arise from within the
brachial plexus and innervate the anterior, lateral
and posterior aspects of the upper arm whereas
the intercostobrachialis, which innervates the
medial aspect, is formed by branches of the second
thoracic nerve (T2).
Sorbie postulates that the terminal branches
of these nerves possess a minimum of vasculature
at this point, therefore, their axons are exposed to
a minimum of local anesthetic agent when utilizing
conventional techniques of IVRA. 47 Expanding
this concept, Haas has suggested a second wrap
modification wherein the extremity is exsanguinated as usual, the proximal cuff of a double
tourniquet is inflated and the Esmarch bandage
or elastic wrap is removed."' A local anesthetic
agent of choice is injected intravenously and the
extremity is then rewrapped in the same manner
as the initial exsanguination. The premise of this
maneuver is that it will force the liquid injectate
into the smaller vasculature, thus exposing the
terminal branches of the proximal nerves to the
agent, particularly those innervating the skin beneath the distal tourniquet.
As these nerves become subcutaneous proximal to the site of an upper arm tourniquet, an
effective and technically simple method is a subcutaneous wheal of local anesthetic agent placed
around the circumference of the arm just proximal
19 ,
to the tourniquet. 92
Exploring further the physiology or origin of
tourniquet pain, Kuntz had demonstrated that
some afferent (somatic) spinal nerve fibers traverse the white communicating rami and are
associated with the sympathetic trunk as it enters
the dorsal roots of the spinal cord. 93 These afferent
fibers are not normally considered in the same
functional category as the somatic fibers of the
integument and are not found distributed in the
skin or muscle.
Threadgill has shown that direct noxious
stimulation of blood vessels distal to the site of
mechanical or chemical somatic disruption will
result in afferent conduction of pain. 9 ' From this
he hypothesized that small somatic afferent fibers
travel in concert with the sympathetic nerves from
the vasculature of the extremities. Further, it is
known that sympathetic vasomotor nerves play a
significant role in pain associated with ischemic
extremities. Such pain stimulates an increase in
vasomotor tone which in turn results in still further painful ischemia. Chemical or surgical sym-
367
pathectomy has been recognized as therapeutic in
resolving this unfortunate situation.
From this information the combination of
ischemia and chronic compression of vascular innervation is thought to contribute to the afferent
transmission of the discomfort known as tourniquet
pain.
Site and mode of action of local agents
The site of action of intravenously injected local
anesthetic agents is perhaps the most thoroughly
studied but least clearly understood aspect of
IVRA. A number of explanations have been advanced in recent years, however, the subject is very
abstract and highly vulnerable to statistical manipulation of data for the sake of emphasizing a
particular point of view.
The proposed sites of action generally emphasize one anatomical location or a combination
of locations: (1) peripheral sensory nerve endings;
(2) neuromuscular junctions; and (3) major
nerve trunks. In addition, a dual mechanism is
considered.
Peripheral nerve endings: tissue level
Bier, using procaine stained with methylene
blue, demonstrated that injectate dispersed rapidly
throughout the extremity, including the substance
of major nerves. 95 He felt that this dispersion was
facilitated by the rich vasculature and absence of
valves in small vessels (less than 2 mm in diameter) which emerge along the course of the
major nerves. From this he concluded that local
anesthetics injected intravenously worked at the
"end apparatus of the nerves."
Using radioisotope labeled lidocaine, Knapp
demonstrated that the drug rapidly enters the
extracellular fluid and reaches a state of equilibrium within the muscle mass.9"
Atkinson suggests that the rapid injection-toonset and tourniquet deflation-to-resolution times
and the anatomical pattern of analgesia distribution favor the vascular perfusion of peripheral
tissue and sensory nerve endings as the site of
action. 7, 97 He suggests that one would not expect
to effectively block nerve trunks with the dilute
solutions of lidocaine (0.5%) which are clinically
employed. He further postulates that the superimposition of acidosis resulting from ischemia
may potentiate this effect, thus mimicking a true
nerve block. Mazzee suggests that this acidosis increases capillary and venule permeability to the
small lidocaine molecule, allowing it to easily
escape into the surrounding extracellular fluid
and tissue."
368
Atkinson supports this concept with a case
report in which IVRA was incomplete in a finger
on which the skin and muscle had been avulsed.
He felt this indicated that the interruption in
vascular flow precluded exposure of these tissues
57
to the local anesthetic agent. ' 97
Using electrophysiologic nerve conduction
studies, Miles showed that while a 66% increase
in latency of action potential in sensory nerves
can be attributed to ischemia alone, there was a
180% increase with the addition of lidocaine."8
Interestingly, the rate of conduction in motor
nerves was not affected by ischemia or the combination of ischemia and lidocaine. From this he
concluded that intravenously injected local anesthetic agents acted at the sensory nerve ending and
not major nerve trunks. Though unclear to what
degree, ischemia certainly plays some contributing
role in the establishment and maintenance of
IVRA.
Referring to perfusion studies using radiopaque anesthetic solutions, Fleming implied a
strong correlation between the onset and pattern
of sensory loss and distribution of opacity in the
soft tissues of the arm. 40 She thus proposed the
site of action to be at the tissue level. In similar
studies, Sorbie and Raj came to quite the opposite
conclusion.,
5
47
Allen found a localization of agent 6-8 times
greater in traumatized tissue than in normal tissue.
He felt this was due to easier diffusion of agent
via broken capillaries. 99
The neuromuscular junction
The neurophysiological studies by Miles
yielded interesting muscle response data similar
to that found when patients received a nondepolarizing muscle relaxant. It was demonstrated
that with lidocaine, a point could be reached at
which nerve stimulation failed to generate a
muscle response while direct muscle stimulation
could still elicit muscle contraction. Unlike the
non-depolarizing block, administration of neostigmine to patients blocked with lidocaine did not
alter the muscle responses. Considering this and
similar results reported earlier by Harvey and
Jaco, Miles concluded that lidocaine inhibited
production of acetylcholine and opposed its action
98
01
at the neuromuscular junction. , 100oo,
To demonstrate the anatomical distribution
of intravenously injected drugs, Atkinson used a
dilute solution (0.1 mg/cc) of d-Tubocurarine
and found profound relaxation of the muscles
below the tourniquet. 7 7
Using elaborate electrophysiologic experi-
Journal of the American Association of Nurse Anesthetists
ments, Fujita demonstrated post-tetanic facilitation during IVRA, especially with procaine and
suggests that local anesthetic agents vary in their
anticholinesterase activity. He feels that agents are
carried via the vessels to the myoneural junction
where there is "direct competition between acetylcholine and the local anesthetic agent to occupy
the receptor site on the postjunctional membrane."
While these demonstrations do not adequately
explain the profound analgesia obtained with
dilute local anesthetic solutions, the clinical observation of undesirable volitional motor movement during hand surgery has prompted the author to adopt the addition of dilute solutions of
a non-depolarizing muscle relaxant (d-Tubocurarine 0.1 mg/cc). This mixture has proven adequate to block all motor activity below the tourniquet and is of little clinical significance when
released into systemic circulation following completion of the technique.
Nerve Trunks
A number of authors have suggested the site
of action to be the major nerve trunks as they
traverse the tissue distal to the tourniquet. In his
original description of IVRA, Bier noted the
delayed onset of analgesia in tissue distal to the injection site and isolated by a second tourniquet. 10
He concluded this delay in onset represented
block of nerve trunks.
Atkinson noted a paresthesia when utilizing
IVRA and attributed this to forceful perfusion of
intraneural vessels. 57 Using nerve conduction
studies to identify the role of ischemia and radiographic studies to determine the vascular distribution of injectates, Sorbie felt that the effects of
lidocaine were due to direct contact of the drug
with the large nerve trunks. 47 He too implicated
the intraneural vasculature as a possible site of
this important interface. Using radioisotope-tagged
lidocaine to study tissue distribution of IVRA,
Cotev found that shortly following injection the
concentration in nerve tissue was four times that
0s 104
of muscle or skin.
In nerve conduction studies performed by
Shanks, motor and sensory conduction velocity
delays were attributed to effects of local anesthetics
at the nerve trunks. 10' This is in opposition to the
conclusion drawn by Miles who felt similar findings
were primarily the result of tourniquet ischemia."
Combined site of action
Bier was the first to suggest a dual mechanism
of action for IVRA, stating, "The direct anesthesia
in the area between the two tourniquets occurs
immediately if one uses Novocain® in sufficient
A ugust/1981
amounts. The indirect anesthesia distal to the peri-
pheral tourniquet needs some time to develop." 10
His implication was that the direct anesthesia is
due to block of peripheral nerve endings in the
tissues saturated by local anesthesia agents while
the indirect anesthesia distal to the distal tourniquet results from block of the large nerve trunks
as they traverse the proximal tissue.
Using a combination of clinical investigation
techniques, Raj derived convincing documentation for the bi-phasic theory. 45 Following the injection of only 5 cc of radiopaque stained lidocaine (0.5%) solution into a dorsal hand vein,
contrast material can be noted in the large superficial veins of the forearm: radial, ulnar and
median antebrachial (Figure 3) . Of particular
note, even with this small volume, is the presence
of contrast in the basilic, cephalic and median
cubital veins at the elbow. Additionally, no contrast material is noted distal to the injection site,
presumably blocked by venous valves. Only following injection of 30 cc could contrast be noted
distally and then only as far as the second set
of venous valves at the first proximal phalanx
(Figure 9).
Figure 9
Distribution of 30cc injected into dorsum of hand.
Note that drug has spread distally only as far as the
first proximal phalanx. Loss of sensation begins in
the digits and travels proximally.
(From Raj, P.P., at al 1972 "The Site of Action of Intravenous Regional Anesthesia," Anesthesia and Analgesia
51:776-786. With Permission.)
The onset of sensory loss was immediate,
beginning first in the digits and traveling proximally toward the anterior and medial aspects of
the forearm in a "glovelike" fashion, finally reaching the posterior aspect of the elbow. A total of
10-15 minutes elapsed before any contrast was
noted to have extravasated into muscle tissue
(Figure 10).
When this experiment was repeated with a
rubber band-tourniquet occluding the midforearm, the 5 cc volume again passed proximally,
presumably via the perforating and interosseous
veins, to the level of the elbow (Figure 11). With
15 cc, the majority of contrast was again found at
the elbow with only a small amount having extravasated into the hand and wrist.
In a similar experiment, injection was made
into the medial cubital vein at the elbow. A
similar filling pattern and onset of anesthesia was
noted as before (Figure 2), with good filling of
vessels around the elbow. Virtually no contrast
was seen in the distal one-third of the forearm.
The presence of contrast intravascularly above
the mid-humerus was of particular interest. It is
postulated that injection pressure exceeded the
tourniquet pressure, allowing proximal flow of
Figure 10
local anesthetic into systemic circulation. Transient
CNS symptoms were noted in this patient. Similar
leakage of solution during forceful injection was
40
radiographically documented by Fleming.
In experiments using radioisotope-tagged local
anesthetic agents, Adams estimated the intravascular volume of the upper extremity to be 170 cc."'
Instillation of 40 cc of local anesthetic will not
produce any significant hydrostatic pressure, thus,
it will seek the path of least resistance, the large
superficial veins. Along with radiographic documentation indicating that contrast does not significantly leave the vascular system for approximately
15 minutes following injection, this must be taken
as strong evidence against the concept of localization at the peripheral nerve endings, at least in the
early stages of the technique. This does not preclude such a site of action later in the technique.
It is interesting to note that regardless of the
injection site used, the pattern of onset was the
same. This gives rise to further questions concerning the peripheral nerve ending as the site of
action.
By investigating the microvascularity of peripheral nerves, the proposed site of action can be
clarified. DeJong has shown that the fibers which
Figure 11
Distribution of 5cc injected into dorsum of hand
with occlusive tourniquets on forearm. Note that
Distribution of spread 15 minutes following injection of 40cc into dorsum of hand. Note diffusion of
drug into the muscle tissue of forearm. Anesthesia of
arm was complete within 5 minutes of injection.
drug has passed proximally to the elbow via interosseous and perforating veins.
(From Raj, P.P., et al 1972 "The Site of Action of Intravenous Regional Anesthesia," Anesthesia and Analgesia
51:776-786. With Permission.)
(From Raj, P.P., et al 1972 "The Site of Action of Intravenous Regional Anesthesia," Anesthesia and Analgesia
51:776-786. With Permission.)
Journal of the American Association of Nurse Anesthetists
serve the distal extremity are located primarily
in the middle or core of major nerve trunks
while those which serve the proximal tissues are
around the mantle or periphery of the trunk
(Figure 12) . 10 7 Figures 13 and 14 demonstrate the
microvascularity of such a peripheral nerve trunk.
The majority of the larger intraneural vessels are
located near the "core". Raj postulates that immediately following injection of local anesthetic
agent into the exsanguinated and isolated vessels
of the extremity, these vascular channels carry the
agent to the nerve trunks in the vicinity of the
elbow. From there, the fluid flows into the intraneural vessels near the core of the trunk and
diffuses into the nerve fibrils due to a concentration gradient. Ten to 15 minutes later, diffusion
of the local anesthetic agent into the extracellular
fluid of muscle tissue ensues and continues until
an equilibrium with the intravascular drug is
approached.
Sensory perception returns in a similar pattern, proximal to distal, and is similarly explained.
When circulation is restored, the drug is first
washed from the nerve core, thus restoring the
distal sensory distribution. This is followed by
removal from the mantle, restoring the proximal
segments. Eventually, circulation in the muscle
mass will reduce the concentration of the peripheral nerve endings. As these events are telescoped into a 5-15 minute time frame, this obscures
the discrimination of events and it is impossible
Figure 12
Axons located in the nerve's "mantle" innervate
proximal regions, those in the "core" distal regions.
Onset of anesthesia is related to the distribution of
nerve exposed to local anesthesia agents.
Nerve trunk
August/1981
to clinically ascertain the differentiation of these
two mechanisms.
This direct intraneural exposure of the drug
also explains why relatively small volumes of very
dilute agents can produce profound sensory loss.
If applied directly to the outside of a major nerve
trunk, the equivalent drug would produce little
effect whatsoever.
Regardless of the site of action, the onset of
analgesia is immediate and generally complete
within 5-10 minutes, thus coinciding with completion of the presurgical skin preparation and
draping.
Part II will focus on local anesthetic agents
and principles of pharmcokinetics. It will also investigate complications and contraindications of
IVRA as well as special considerations for its use.
REFERENCES
(1) Koeller C. 1884. The Use of Local Anesthesia on the Eye,
Preliminary Report. Rostock Universitiits-Buchdruckeri von
Adler's Erben, Translation in Foundations of Anesthesiology by
Faulconer and Keys, pp. 773-775, Volume 2.
(2) Corning JL. 1885. On the Prolongation of the Anaesthetic
Effects of the Hydrochlorate of Cocaine when Subcutaneously
Injected. New York Medical Journal 42:317.
Conway JR. 1885. Cocaine as an Anaesthetic in Fractures
(3)
and Dislocations. New York Medical Journal 42:632.
(4) Alms H. 1886. Die Wirkung des Cocains auf die peripherischen Nerven. Arch. Physiol. Suppl. Bd. p. 293.
(5) Schleich KL. 1892. A New Method of Local Anaesthesia
(Infiltration Anaesthesia) . International Clinics (5th series),
2:177-192.
(6) Esmarch JFA. 1878. The Surgeons Handbook on the
Treatment of Wounded in War, English translation by H.H.
Cluton. London: Sampson Low, Marston, Searle & Rivington,
p. 127.
(7) Braun H. 1901. The Addition of Epinepherine to Cocaine
for Local Anesthesia. Archiv fur klinische Chirugie 96:541-591,
(Translated in Foundations of Anesthesiology by Faulconer and
Keys, Volume 2, pp. 834-842).
(8) Halstead WS. 1885. Practical Comments on the Use and
Abuse of Cocaine; Suggested by Its Invariably Successful Employment in More Than A Thousand Minor Surgical Operations, New York Medical Journal 42:294-295.
(9) Crile GW. 1897. Anesthesia of Nerve Roots with Cocaine.
Cleveland Med. ]., 2:355.
(10.) Bier A. 1908. Concerning a New Method of Local Anesthesia of the Extremities. Arch Klin Chir 86:1007-1016, (Translated by C.S. Hellijas in Survey of Anesthesiology-Classical File,
11:294-300).
(11)
Einhorn A. 1899. On the Chemistry of Local Anesthetics.
Munchen medicinische Wochenscrift 46:1218-1220, (Translated
in Faulconer and Keys, pp. 801-807).
Braun H. 1905. Several New Local Anesthetic Agents.
(12)
Deutsche medizinishe Wochenschrift, 2:1667-1671, (Translated
in Faulconer and Keys, pp. 842-847) .
Bier A. 1899. Versuche iiber Cocainisrung des Riicken(13)
markes. Dtsch. 7. Chir, 51:361.
Hirtel F. 1909. Die Technik der Veneanlisthesie. Wien
(14)
med WVschr, 35:1999.
Hitzrot JM. 1909. Intravenous I.ocal Anaesthesia. Ann
(15)
Surg 50:782.
Hirschel G. 1911. Die Anisthesierung des Plexus Brachialis
(16)
bei Operationen an der oberen Extremitit, Munchen Med
Wschr 58:1555.
371
(17)
Kulenkampff D.
1911.
brachialis, Zbl Chir 38:1337.
Die
Anasthesierung
des
Plesus
(18)
Loifgren N. 1948. Studies on Local Anaesthetics. Xylocaine,
a new Synthetic Drug. Stockholm: Ivar Haeggstroms.
(19)
Holmes C. 1963. Intravenous Regional Analgesia-A Useful Method of Producing Analgesia of the Limbs, Lancet 1:245247 (Feb 2).
(20.)
Editorial,
1965. Regional
Intravenous Anesthesia.
JAMA
193:120 (Jul-Sept) .
(21)
Steinhaus j. 1973. Regional Intravenous Anesthesia. Audio
Digest-Anesthesiology Vol. 15 #5.
(22)
Colbern EC. 1970. The Bier Block for Intravenous Regional Anesthesia: Technic and Literature Review. Anesthesia
and Analgesia 49:935-940.
(23)
Eghert LD, Battit GE, Turndorff H. et al. 1963. The
Value of the Pre-Operative Visit by an Anesthetist. JAMA 185:
553-555.
(24)
Tatum AL, Atkinson AJ, Collins KH. 1925. Acute Cocaine Poisoning: Its Prophylaxis and Treatment in Laboratory
Animals. J. Pharmacol. 7'her. 26:325-335.
(25)
Mazzee RI, Dunbar RW. 1969. Intravenous Regional
Anesthesia-A Report of 47 Cases With a Toxicity Study. Acta.
Anes. Scandinarv., Supp. XXXVI, p. 27-34.
(26)
Tatum
AL, Collins KH.
and Its Treatment
(27)
Feinstein,
in
MB,
1926. Acute Cocaine
the Monkey. Arci
Lenard
W,
Poisoning
Intern Med 38:405-409.
Mathias
J.
1970.
The
an-
tagonism of local anesthetic induced convulsions by the benzodiazepine derivative diazepain. Arch Int
Pharinacodyn 187:144154.
(28)
Aldrete JA, Daniel W. 1971. Evaluation of Premedicants
as Protective Agents Again Convulsive (LD5O) Doses of Local
Anesthetic Agents in Rats Anesth. Analg. 50:127-130.
(29)
DeJong RH, Heavner JE. 1971. Diazepam Prevents Local
Anesthetic Seizures. Anest hesiology 34:523-531.
(30)
DeJong RH, Heavner JE. 1972. Local Anesthetic Seizure
Prevention:
Diazepam
versus
Pentobarbital.
Anesthesiology
36:449-457.
(31)
Local
Munson ES, Wagman I. 1972. Diazepam Treatment of
Anesthetic-Induced Seizures. Anest/hesiology 37:523-528.
(32)
DeJong RH, Heavner JE. 1974. Diazepam Prevents and
Aborts Lidocaine Convulsions in Monkeys. Anesthesiology 41:
226-230.
(33)
Kortilla K, Linnoila M. 1975. Absorption and Sedative
Effects of Diazepam after Oral Administration and Intramuscular Administration into the Vastus Lateralis muscle and the I)eltoid Muscle. Br. J. Anaesth, 47:857-861.
(34)
Langdon DE, Harlan JR, Bailey RL. 1973. Thrombophlebitis with diazepam used Intravenously. JAMA 223:184-185.
(35)
Gamble JAS, Gaston JH, Nair SG, and Dundee JW.
1976. Soine Pharmacological Factors Influencing the Absorption of
Diazepam Following Oral Administration. Br. J. Anaesth, 48:10911095.
(36)
Sturdee DW. 1976. Diazepam: Routes of Administration
and Rate of Absorption (A Study of Women with Pre-Eclampsia) , Br. J. Anaesth, 48:1091-1095.
(37)
Nair SC, Gamble JAS, Dundee JW, Howard PJ.
1976.
The Influence of Three Antacids on the Absorption and Clinical
Action of Oral Diazepam" Br. J. Anaesth, 48:1175-1179.
(38)
Moore DC, Bridenbaugh LD. 1960. Oxygen: the antidote
for systemic toxic reactions from local anesthetic drugs. JAMA,
174:182-847.
(39)
Morrison JT. 1931. Intravenous Local Anesthesia, British
Journalof Surgery, 18:642-647.
(40) Fleming SA. Viega-Pires JA, McCutheon RM, et al.
1966. A Demonstration of the site of action of intravenous hignocaine. Can. Anaesthe. Soc. 1. 13:21-27.
(41)
Ong RT, Kortis HI. 1965. Experiences with Intravenous
Regional Anesthesia For Upper Extremity Surgery. Jornaifl of
the Newark Bet/i israel Hospital, 16:87-92.
(42) Manthey FA. 1965. Intravenous Regional Anesthesia of
the Upper Extremnity. Anesthesiology, 26:827-828.
(43)
Cox JMR. 1964. Intravenous Regional Anesthesia. Cant.
Anaes. Soc. . 11:03-508.
372
(44)
Dunbar RW, Mazzee RI. 1967. Intravenous Regional
Anesthesia-Experience With 779 Cases. Anesthesia and Analgesia,
46:806-813.
(45) Raj PP, Garcia CE, Burleson JW, Jenkins MT. 1972.
The Site of Action of Intravenous Regional Anesthesia. Anesthesia and Analgesia 51 (5): 776-786.
(46) Adams JP, Albert S. 1964. Intravenous Regional Anesthesia in Hand Surgery. Journal of Bone and Joint Surgery 46-A
4, (June) p. 8 1 1 - 8 1 6 .
(47) Sorbie C, Chacha P. 1965. Regional Anaesthesia by Intravenous Route. Br. J. Med. 5440:957-960.
(48) Van Niekerk JP, De V. Tonkin, PA. 1966. Intravenous
Regional Analgesia, S. Afr. Med. j. 40:165-169.
(49) Brown EM.
1966, Prolonged Intravenous Regional Anesthesia. Anesthesia and Analgesia, 45:319-321.
(50)
Pygros NM. Argyopoulos EL., Pygos VN. 1977. The Use
of Intravenous Regional Anesthesia for the Reduction of Colles
Fractures. Resuscitation (Casualty Surgeons Association Papers)
5:59-63.
(51)
Finlay H. 1977. A Modification of Bier's Intravenous
Analgesia-Use of the Pneumatic Splint. Anaesthesia 32:357-358.
(52) Dawkins OS. 1964. Intravenous Regional Anaesthesia.
Can. Anaes. Soc. J. 11:243-246.
(53) Middleton RWD, Varian JP. 1973. Tourniquet Paralysis,
Journal of Bone and joint Surgery. 55B:432.
(54)
Griffiths JC., Heywood OB. 1973. Biochemical Aspects of
the Tourniquet. Hand 5:113-118.
(55)
Austin M. 1963. The Esmarch Bandage and Pulmonary
Embolism. Journal of Bone and Joint Surgery 45-B:384-385.
(56) Bell HM. Slater EM. Harris HH. 1963. Regional Anesthesia with Intravenous I.idocaine. JAMA 186:544-549.
(57)
Atkinson DI, Modell J, Moya F. 1965. Intravenous Regional Anesthesia, Anesthesia and Analgesia 44:313-317.
(58)
Adams JP, Albert S. 1962. The Blood Volume in the
Lower Extremities: A Technique for its letermination utilizing
Cr 5 ' tagged red cells. Journal of Bone and Joint Surgery 44A:
489-493.
(59)
Bradford EMW. 1969. Haemodynamic changes associated
with the application of lower leg tourniquets. Anaesthesia 24:
190-197.
(60)
Furlow I.T. 1971. Cause and Prevention of Tourniquet
Ooze. Surg Gynecol Obstet 132:1069-1072.
(61)
Klenerman L. 1962. The Tourniluet in Surgery. Journal
of Bone and Joint Surgery 44B: 937-943.
(62)
Thompson CJS. 1942. Th/,e History andl Evolution of Surgical Instruments, Schumans Pub. Co. pg. 85.
(63)
I.ister J. 1909. Collected Papers Volume I, Oxford: Clarendon Press, pg. 176.
(64) Von Esmarch, JFA. 1873. Ucher kiinstliche Blutleere bei
Operationetn. Sanim
lug
Klinischcr VortrYge in Verhindung mit
Detschen Klinikern. Chirurgie 19(58):373.
(65)
Cashing H. 1904. Pneumatic Tourniquets: with Especial
Reference to their use in Craniotomies, Medical Neus 84:577580.
(66) Herreros LG. 1946. Regional Anesthesia by the Intravenous Route (Slight Modication of Bier's Method) Anesthesiology 7:558-560.
(67) Hoyle JR. 1964. "Tourniquet for Intravenous Regional
Anlalgesia. Anaestesia 19:294-295.
(68) Bruner JM. 1951. Safety Factors in the use of the pneurmatic tourniquet for hemostasis in sur~ery of the hand, Jourrnal
of Bone and Joit Srry 33A221-224.
(69)
Wilis EFS. 1971. Ob~servations on the effects of tourniquect ischenia, Joutrnal of Bone ndr Joint SurRPY 53A: 1343-1346.
(70)
Miller SH. I~ung RJ, et al. 1978. The Acute Effects of
Tourniquet
Ischeia on Tissue and Blood Gas Tensions in the
Primate I.imnb, I. Hnd SJrery 3(1) :11-20.
(71) Aams JP. Wilia EFS. 1971. Observation of the effects of
tourniqut ischemia, Joucrnl of Bone and Joint Srgery
5,3A:
1346.
(72)
Web~b WR. 19)6.
ioloic Foundations of Srery, Surery Cliics of Northi Aerca 45:267-287.
(73)
Fine J, Frank HA, Seliman
AM. 1944. Tramatic Shock
Journal of the American Association of Nurse Anesthetists
VIII. Studies in the Therapy and Hemodynamics of Tourniquet
Shock. Journal of Clinical Investigation, 23:731.
(74) Fowler TJ, Danta G, Gilliatt RW. 1972. Recovery of
Nerve Conduction After a Pneumatic Tourniquet: Observations
on the Hind-limb of the Baboon, J. Neurol. Neurosurg. Psychiat.
35:638.
(75) Bruner JM. 1973. Time, Pressure, and Temperature Factors in the Safe Use of the Tourniquet, Hand 5:39-42.
(76) Moldaver J. 1954. Tourniquet Paralysis Syndrome, Arch.
Surg., 68:136-144.
(77) Ochoa J, Fowler TJ, Gilliat RW. 1972. Anatomical
Changes in Peripheral Nerves Compressed by a Pneumatic
Tourniquet, J. Anatomy 113:433.
(78) Lundborg G. 1970. Ischemic Nerve Injury: Experimental
Studies on Intraneuronal Microvascular Pathophysiology and
Nerve Function in a Limb Subjected to Temporary Circulatory
Arrest: Scand. J. Plastic Reconstr. Surg. 4 (Supp 6):91-106.
Thomassen EH. 1978. An Improved Method of Applica(79)
tion of the Pneumatic Tourniquet on Extremities, Clinical Orthopaedics and Related Research 103:99-100.
(80) Stewart JDM. 1975. Tourniquets, In: Traction and Orthopaedic Appliances, Churchill Livingstone, New York, p. 181.
(81)
Mullick S. 1977. Low leg Tourniquet, West Ind. Med. J.,
26:182.
(82) Flatt AE. 172. Tourniquet Time in Hand Surgery, Arch
Surg. 104:190-192.
(83) Flewellen EH, Jarem B. 1978. Pneumatic Tourniquets,
Anesthesiology Review 5:31-34.
(84) Smith H. 1971. Surgical Technique, In: Campbell's Operative Orthopaedics.5th ed. Vol. 1, C.V. Mosby Co., St. Louis p. 19.
(85)
Nobel W, Black D, Johnson P, Kase C. 1974. Effect of
Chronic Compression on the Microcirculation and Function of
Peripheral Nerves. Proceedings of the International Symposium,
Berlin, Sept. 1973, ed. J. Cervos-Navarra. Walter de Gruyter,
New York, p. 483.
(86) Sanders R. 1973. The Tourniquet. Instrument or Weapon?
Hand 5(2) :119-123.
(87)
Thorn-Alquist AM. 1971. Intravenous Regional Anaesthesia: A Seven-Year Survey. Acta. Anaesth. Scandinav. 15:23-32.
(88) Mullick S. 1978. The Tourniquet in Operations upon the
Extremities. Surg. Gynecol. Obstet. 146:823-826.
(89) Giesecke H. 1976. Anesthesia for the Surgery of Trauma,
F.A. Davis Co., Philadelphia, p. 52-53.
(90) Cole F. 1952. Tourniquet Pain, Anesthesia and Analgesia
31:63-64.
(91)
Haas LM, Lnadeen FH. 1979. Improved Intravenous Regional Anesthesia for Surgery of the Hand, Wrist, and Forearm:
The Second Wrap Technique, J. Hand Surgery 3 (2) :194-195.
(92) Rousso M. Wexler MR, Weinberg H, et al. 1978. Subcutaneous Ring Anaesthesia in the Prevention of Tourniquet
Pain in Hand Surgery, J. Hand Surgery 10(3) :317-320.
(93) Kuntz A. 1951. Afferent Innervation of Peripheral Blood
Vessels Through Sympathetic Trunks, Southern Medical Journal
44 (8) :673-678.
(94) Threadgill FD, Solnitzky O. 1949. Anatomical Studies of
Afferency Within the Lumbosacral Sympathetic Ganglia. Anat.
Rec. 103:96.
(95) Bier A. 1901. Ueber Venenanaesthesie Berlinger klin
Wochenschr. 46:477.
(96) Knapp RB, Weinberg M. 1969. Distribution of Radioactive Local Anesthetics Following Intravenous Regional Anesthesia, Acta. Anaes. Scandinav. Supplementum XXXVI pg. 121-126.
(97) Atkinson DL. 1969. The Mode of Action of Intravenous
Regional Anesthetics. Acta. Anaes. Scandinav. Supplementum
XXXVI p. 131-134.
August/1981
(98) Miles DW, James JL, Clark DE. et al. 1964. Site of action
of Intravenous Regional Anesthesia. J. Neurol. Neurosurg. Psychiatry 27:574-576.
(99) Allen FM, Crossman LW, Lyons LV. 1946. Intravenous
Procaine Analgesia, Anesthesia and Analgesia 25:1-9.
(100)
Harvey A. 1939. The Actions of Procaine on Neuromuscular Transmission, Bull. Johns Hopkins Hospital 65:223-238.
(101)
Jaco NT, Wood DR. 1944. The Interaction between
Procaine, Cocaine, Adrenaline and Prostigmine on Skeletal
Muscle, J. Pharmacol.Exp. Ther, 82:63-73.
(102)
Fujita T, Miyazaki M. 1968. A Comparative Study of
Various Local Anesthetic Agents in Intravenous Regional Anesthesia, Anesthesia and Analgesia 47(5): 575-586.
(103) Cotev S. 1966. Experimental Studies On Intravenous
Regional Anaesthesia Using Radioactive Lignocaine. Br. J. Anaesthesia 38:936-939.
(104)
Cotev S, Robin GC. 1969. Experimental Studies on Intravenous Regional Using Radioactive Lidocaine. Acta. Anaes.
Scandinav.-Supplementum XXXVI p. 127-130.
(105) Shanks CA. 1970. Nerve Conduction Studies in Regional
Intravenous Analgesia Using 1 Per Cent Lignocaine, Br. J.
Anaesthesia 42:1060-1065.
(106) DeJong R. 1970. Physiology and Pharmacology of Local
Anesthesia, Charles C Thomas Co., Springfield, Ill.
(107)
Collins VJ. 1979. Principles of Anesthesiology, 2nd Ed.
Lea and Febiger, Philadelphia, p. 877, 873.
AUTHOR
Commander Charles A. Reese, CRNA, PhD, USN, received his
BSN from the University of Oklahoma and his BS in Nurse Anesthesia from George Washington University in Washington, DC. He
received his MBA in Health Services Management from the National
University in San Diego, California, and his PhD in Hospital/Health
Services Administration from California Pacific University in San
Diego.
Dr. Reese has published extensively on the subject of regional
anesthesia, and he has made numerous presentations on clinical anesthesia care. At the present time, he serves as the sole anesthetist
aboard the nuclear aircraft carrier USS Nimitz, which is currently
deployed in the Mediterranean Sea. Prior to his present assignment,
Dr. Reese served on the AANA Continuing Education and Education Committees. He is currently a member of the AANA Journal's
Editorial Advisory Board.
This article was written while Dr. Reese was the Clinical Coordinator of the U.S. Navy Nurse Corps Anesthesia School at the
Naval Regional Medical Center in Portsmouth, Virginia.
The author wishes to state that the opinions or assertions contained in his article are his private views and are not to be construed
as official and/or reflecting the views of the Department of Anesthesia, USS Nimitz, the Navy Nurse Corps, the Department of the
Navy, or the Department of Defense.