Brit. J. Anaesth.

(1964), 36, 438

ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS

BY

JOHN H. STEVENS
Department of Anaesthetics, Welsh National School of Medicine, Cardiff, Wales

SUMMARY

The problems of anaesthetizing ill patients with intestinal obstruction arise from the
possibility of aspirating stomach contents, and from attempts to produce adequate
abdominal muscular relaxation. The hazards and mechanisms of both vomiting and
regurgitation are discussed in detail. On this basis, the rationale of preventing aspira-
tion is described. For the production of adequate abdominal relaxation, the muscle
relaxants appear to be the method of choice, despite occasional abnormal responses
in these patients. The nature of these responses and methods of rendering them even
less common are discussed in detail.

One of the constantly recurring problems which patient soon becomes gravely ill from dehydration
anaesthetists have to face is the patient who and electrolyte loss. The electrolyte content of the
requires operation for the relief of intestinal fluid lost depends on whether the small bowel
obstruction. Some of these patients are compara- obstruction is high or low. If it is high, a large
tively fit, but others are so gravely ill that they proportion of the fluid lost is gastric juice (contain-
present anaesthetic problems demanding a degree ing H+ ions) and its loss produces a metabolic
of care and skill which only great experience alkalosis, whereas if the obstruction is low, a
can provide. These problems have been grouped much greater loss of pancreatic and intestinal
under two main headings, the aspiration of secretions (containing HCOj ions) produces a
stomach contents and the provision of adequate metabolic acidosis. The intestinal secretions also
surgical access in the abdomen. The purpose of contain potassium in a concentration similar to
this paper is to discuss these in the light of recent that of plasma, and its loss has important effects
contributions to the literature. also (vide infra). The changes associated with
In the pre-operative period there is also a group dehydration and electrolyte loss are not marked in
of problems which, although not the direct con- the majority of cases, because the obstruction is
cern of the anaesthetist, have an important usually diagnosed and treated early. In the gravely
bearing on his work and they will be mentioned ill patient, however, these changes have an
first briefly. important bearing on the survival of the patient
and on the action of muscle relaxants} and they
PRE-OPERATIVE PROBLEMS will be discussed later.
Fluid and electrolyte loss. The accumulation of fluid and gas in the bowel
Normally, about 8 litres of digestive juices are causes abdominal distension and the rise in intra-
secreted every 24 hours, most of which is re- luminal pressure impairs the blood supply to the
absorbed in the colon. If there is an obstruction bowel wall. This occurs to an appreciable extent,
proximal to the colon, large volumes of gas even without strangulation, and is a cause of the
(mainly nitrogen) and fluid accumulate above it. toxaemia seen in intestinal obstruction of any
Small bowel obstruction presents a more urgent duration.
problem than large bowel obstruction because the Strangulation occurs when the blood supply to
the bowel wall is cut off. It gives rise to an
Present address: Department of Anesthesiology, intensely toxic peritoneal fluid (Barnett and
University of Washington School of Medicine, Seattle,
U.S.A. Doyle, 1958; Barnett, 1959a, b; Fine, 1961), the
438
ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS
absorption of which endangers life, and the
toxicity of which increases progressively the
farther down the alimentary tract the site of
strangulation is from the stomach. In addition,
great congestion of the bowel is caused because
the veins are usually occluded first. This results
in the extravasation of plasma or whole blood
into the bowel wall and lumen, and the loss may
be so great as to require transfusion (Crawford
and Nemir, 1960; Savage, 1960).
The replacement of fluid and electrolyte
deficiencies is usually undertaken by the surgical
team and will not be discussed here. The anaes-
thetist must be able to recognize such deficiencies,
however, and must be able to treat them ade-
quately, for he will have to institute or supervise
such treatment himself on occasions.
Pre-operative medication.
When the patient's general condition is poor,
narcotics, which are depressant, should be given
sparingly if at aU. Ill and elderly people readily
aspirate material into the lower air passages
without evoking any protective response. Mor-
phine and its analogues also depress this response
in these patients, with the same results (Pontop-
pidan and Beecher, 1960). If such drugs are re-
quired in hypotensive patients, they should not
be given hypodermically, but intravenously
because of the danger of rapid absorption later
when the blood pressure is restored. If atropine
is felt to be necessary for dehydrated patients, it
is kinder to inject it intravenously at the induction
of anaesthesia.
The timing of the operation.
Prompt diagnosis and early operation both re-
duce the mortality of intestinal obstruction.
However, a proportion of patients arrive in hos-
pital in very poor general condition, and such
patients should not be taken to the operating
theatre too soon (Burdette and Stevens, 1961;
Marcus, 1962). There is much to be said for
allowing adequate time (2-4 hours) for replace-
ment of fluid and electrolyte deficiencies, reduc-
ing abdominal distension, and ensuring that the
stomach is kept empty. The aim is to improve
the operative risk by getting the patient into the
best possible condition for surgery. [The mor-
tality is 12 per cent rising to 50 per cent in
439
patients over 70 years old (Savage, 1960; Scott,
1961).] Once the "drip-and-suck" regime has been
instituted the patient's general condition will not
deteriorate, provided strangulation is not present.
If there is any doubt, however, the patient must
be treated as if strangulation is present and
operation is mandatory as soon as the patient can
tolerate it [When strangulation has caused
gangrene of the small bowel, the mortality is
30 per cent, rising to 90 per cent in patients over
70 years old (Savage, I960).]
Much work has been done recently on "low
flow states" of the peripheral circulation, associ-
ated with prolonged hypotension, Le. intestinal
obstruction of some duration. As a result of the
low flow rate of blood in the peripheral vascula-
ture red blood cells form aggregates, causing
post-capillary occlusion (Gelin, 1961; Gelin and
Zederfeldt, 1961; Moore, 1963; Lancet, 1964).
This leads to further reductions in tissue per-
fusion, increasing the metabolic acidosis already
caused by hypotension. It leads to micro-infarc-
tion of parenchymatous organs such as the kidney
where, in addition, the glomeruli may be blocked
by aggregations of red blood cells causing
oliguria.
Restoration of the blood pressure may not
necessarily abolish these changes, which are due
to an increase in the viscosity of the blood at low
flow rates and a decrease in the suspension
stability of the blood. However, the administration
of low molecular weight dextran (m.w. 40,000;
not the dextran used as a plasma expander)
appears to improve the peripheral bloodflow
considerably (Bergentz et al., 1961). Metabolic
acidosis and ':low flow states" have an important
bearing on the action of muscle relaxants and will
be discussed later.
With the fluid and electrolyte deficits replaced
and the peripheral circulation restored, a con-
siderable improvement occurs in the patient's
general condition. The extremities are no longer
cyanosed and cold but pink and warm; the blood
pressure rises to about 100 mm Hg or more and
there is reasonable filling of the veins on the
back of the hand. As soon as these changes have
taken place, the patient should be taken to the
operating theatre.
440
ASPIRATION OF STOMACH CONTENTS IN
INTESTINAL OBSTRUCTION
Airway complications, such as aspiration and
atelectasis, are supplanting shock, electrolyte
imbalance and renal failure as the leading causes
of death in surgical patients (Simenstad, Galway
and MacClean, 1962). The incidence of aspira-
tion in intestinal obstruction is unknown, but in
several series of unselected cases undergoing
"elective" surgery, aspiration of detectable,
although inconsequential, amounts of stomach
contents occurred in about 17 per cent of patients
(Weiss, 1950; Culver, Makel and Beecher, 1951;
Berson and Adriani, 1954). It must be assumed
that in patients with intestinal obstruction this
incidence will be much higher unless preventive
measures are taken. It is worth noting that ap-
proximately 8 per cent of all surgical deaths are
due to aspiration of stomach contents in patients
with intestinal obstruction (Edwards et al., 1956;
Collins, 1960; Clifton and Hotten, 1963).
Clinical
When aspiration into the lungs occurs in quan-
tity, the patient may die almost immediately from
drowning or from profound anoxia following laryn-
geal spasm, bronchospasm or other airway obstruc-
tion. He may also die from reflex cardiac arrest
mediated via the vagi, though this calamity is
rare. Fortunately, the patient usually survives the
immediate crisis. Small amounts of acid material
cause coughing and laryngospasm, but larger
quantities give rise to an intense bronchospasm
and pneumonias—Mendelson's syndrome (Men- (I) Vomiting.
delson, 1946; Lancet, 1962). The course is acute
and critical, and again the patient may die.
Treatment includes restoring the patient's
oxygenation (Morton and Wylie, 1951), placing
\ stomachs are not empty. It is a highly integrated
him in a head-down position, applying tracheo-
bronchial suction and lavage (Bannister and
Satillaro, 1962; Simenstad, Galway and MacClean,
1962), and administration of antibiotics and
hydrocortisone (Dines, Baker and Scantland,
1961). The best treatment of the aspiration of
stomach contents, however, is prevention.
PREVENTION OF ASPIRATION
Aspiration can be prevented by: emptying the
stomach; preventing gastric contents leaving the
BRITISH JOURNAL OF ANAESTHESIA
stomach; preventing gastric contents reaching the
pharynx, either by vomiting or regurgitation
(these are separate and distinct mechanisms);
positioning the patient so that aspiration is
impossible; sealing off the airway by means of a
cuffed endotracheal tube, thereby separating the
pharynx from the lower air passages; and
avoiding general anaesthesia.
Emptying the Stomach.
A wide-bore oesophageal tube, such as a Levine's
tube, must be passed and the stomach emptied.
(A Ryle's tube is quite inadequate for this pur-
pose.) Even after apparent success, the anaesthe-
tist must proceed on the assumption that the
stomach is not completely empty.
Preventing Gastric Contents leaving
the Stomach.
Interest is periodically revived in this idea, which
was first described 60 years ago (Kausch, 1903).
Basically, a tube is passed into the stomach and
inflation of a cuff blocks the gastro-oesophageal
junction and prevents reflux (Macintosh, 1951;
Fisher, 1953; Guiffrida and Bizzari, 1957). How-
ever, the oesophagus is a very distensible organ
and the pressure from below can dislodge the
tube. Consequently, the method has never been
widely regarded as reliable.
Preventing Gastric Contents reaching
the Pharynx.
Vomiting may be associated with the colicky
abdominal pain of intestinal obstruction, but it
usually occurs during induction with an inhala-
tional agent, particularly in patients whose
act, involving the respiratory centre, the larynx,
•the abdominal muscles, and the musculature of
the stomach and oesophagus (Browns 1963). It
gives ample warning of its onset, and prodromal
signs include salivation, swallowing and irregular
respiration. In early anaesthesia the patient can
still protect his airway by means of coughing or
laryngeal spasm. There are three ways in which
vomiting can be prevented:
The stomach must be as empty as possible at
the actual moment of induction.
ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS
General anaesthesia must be deepened as
smoothly and as rapidly as possible, so that
anaesthesia is deepened to a point where
vomiting does not occur. This may be
achieved with diethyl ether, after increasing
the patient's minute volume by adding
carbon dioxide to the inspired mixture
(Inkster, 1963). The hyperpnoea induced also
helps to prevent vomiting. This technique
requires a certain skill and emphasizes the
point that these cases must not be anaesthe-
tized by a novice. Some anaesthetists prefer
halothane or cyclopropane, adding a liberal
proportion of oxygen to the mixture. Others
achieve deeper anaesthesia rapidly by in-
jecting a carefully calculated dose of thio-
pentone. Here again, experience is essential.
The administration of a paralyzing dose of a
muscle relaxant as soon as the patient loses
consciousness prevents the muscular effort
required for vomiting (Wylie, 1963).
The mechanism of regurgitation is quite dif-
ferent from that of vomiting (Atkinson, 1962) and
in order to understand it, the factors maintaining
gastro-oesophageal competence under normal
conditions will be discussed first.
The competence of the gastro-oesophageal
junction.
The intragastric-oesophageal and pleuro-
peritoneal pressure differences. The greater these
are, the more likely is regurgitation to occur. The
average intragastric pressure required to produce
reflux in a paralyzed anaesthetized patient in whom
the stomach and oesophagus are in normal re-
lationship is 35 cm H , 0 (range, 16-77 cm H3O)
(Greenan, 1961). Clark and Riddoch (1962), using
the same technique, found that an average intra-
gastric pressure of 23 cm H a O caused reflux
(range, 13-28 cm H a O). This compares with an
average resting intragastric pressure in anaes-
thetized subjects of 11 cm H , 0 (Roe, 1962).
The gastro-oesophageal angle. This is thought
to act mechanically as a flap valve, regurgitation
being more likely if the angle is less acute than
normal (Marchand, 1954; Sinclair, 1959;
Greenan, 1961). It is possible, though, that this
factor has been overstressed in the past (Clark
and Riddoch, 1962).
441
The lower end of the oesophagus. Although
there is no anatomical structure to account for it,
the lower 4 cm of the oesophagus acts physio-
logically as a tonically contracted sphincter J
(Atkinson et al., 1957; Fleshier et al., 1958;
Botha, 1959; Robson and Welt, 1959; Ingram,
Respess and Muller, 1959). In proper function-
ing is largely independent of the vagal innervation
(Greenwood et al., 1962; Clark and Riddoch,
1962) and its tone is reduced by distending the
upper oesophagus and by swallowing. This oeso-
phageal segment is only moderately resistant to
reflux but it is assisted by mucosal folds, which
are invariably present and which plug the conical
space where the oesophagus joins the stomach
(Botha, 1958). They are held in apposition by
the active tone of muscularis mucosae (Dornhorst,
Harrison and Pierce3 1954). This tone may be
increased by vagotomy or by atropine (Clark and
Vane, 1961, Clark and Riddoch, 1962). At all
events, both cause an increased resistance to re-
flux. The mucosal folds, too, are normally only
moderately resistant to reflux, but they help to
dissipate the intragastric pressure evenly at the
gastro-oesophageal junction. In this way the
sphincter and the mucosal folds assist each other.
In addition, the oesophagus passes down from
a zone of lower pressure to one of higher pressure
as it pierces the diaphragm. Since the lower
2-3 cm of the oesophagus are intra-abdominal
and its walls are in apposition, this pressure
difference further obliterates the oesophageal
lumen and tends to extrude the oesophagus up
into the thorax. This tendency is resisted by the
phrenico-oesophageal ligament (Brown, 1963).
The diaphragm. This is not directly concerned
with the competence of the gastro-oesophageal
junction (Braasch and Ellis, 1956; Atkinson et al.,
1957; Dornhorst et al., 1954; Botha, 1959).
The "pinchcock" action of the crura may occur
during deep inspiration, but it is precisely in this
phase of respiration that reflux may occur
(Creamer, 1955). The importance of the dia-
phragm (in this context) lies in the fact that it
maintains the normal relationship of the stomach
to the oesophagus and only if this is preserved
does the closing mechanism function properly.
Certain patients with a full stomach do not
regurgitate as anticipated, whilst others, properly
 442
prepared for elective surgery, do regurgitate. In
the second group the patients are often found to
have a hiatus hernia of the short oesophagus type
(Dinnick, 1961). The history and radiological
appearance of the barium swallow are typical of
the condition. The patients are often obese, with
short thick necks, so that they tend to develop
airway obstruction during an inhalational induc-
tion. The short oesophagus type of hiatus hernia
predisposes to regurgitation by diminishing the
gastro-oesophageal angle and by eliminating the
mechanical effect of intra-abdominal pressure
acting on the lower 2-3 cm of oesophagus. Any
airway obstruction enhances these effects (vide
infra).
The situation at the upper end of the oesopha-
gus should be noted also. When partially paralyzed
either by relaxants or deep anaesthesia, the
cricopharyngeal sphincter acts as a valve, allow-
• ing an upward passage but no downward passage
(O'Mullane, 1954). The oesophagus can hold a
considerable volume of fluid and this may appear
in the pharynx if the cricopharyngeal sphincter
» is paralyzed and if an oesophago-pharyngeal
pressure difference exists. Once in the pharynx,
the fluid must spill over into the larynx.
(II) Regurgitation.
This is a passive decanting of stomach contents,
which is much more dangerous than vomiting. It
may occur insidiously and even occasionally with-
out the anaesthetist's knowledge, because there
are no prodromal signs.
Factors predisposing to regurgitation.
Any factor which increases the intragastric-
j oesophageal or pleuro-peritoneal pressure differ-
' ences, or which increases the gastro-oesophageal
angle, predisposes to regurgitation. For example:
(1) A raised intragastric pressure.
(2) A change in the patient's posture, so that
gravity increases an already raised intra-
gastric pressure (as when a steep head-
down tilt is assumed).
(3) A reduction in the capacity of the peri-
toneal cavity, raising the intra-abdominal
pressure (as by distending the bowel).
(4) Obstructed spontaneous respiration, caus-
ing (a) a marked increase in the pleuro-
peritoneal pressure difference during
attempted inspiration, and (b) overaction
BRITISH JOURNAL OF ANAESTHESIA
of the diaphragm, raising the intragastric
pressure.
(5) Pulmonary ventilation of a paralyzed
patient, prior to endotracheal intubation.
The cardia invariably opens when the
pharyngeal pressure exceeds 25 cm HjO,
with consequent insufflation of anaesthetic
gases into the stomach. If the lungs are
ventilated vigorously a high intragastric
pressure is soon produced and this, com-
bined with intermittent opening of the
cardia during ventilation, makes regurgi-
tation very probable. During ventilation
via the nose, the resistance of the nasal
air passages produces a lower pharyngeal
pressure (and hence less risk of gastric
inflation). The pharyngeal pressure (and
the risk of regurgitation) is higher during
ventilation through the mouth with a
pharyngeal airway in position (Ruben and
Ruben, 1962).
(6) The presence of an intragastric tube
renders the gastro-oesophageal junction
less competent than normal, and so may
predispose to regurgitation.
Prevention of regurgitation.
The measures to be taken are now self-evident.
Reduction of the intragastric pressure. The
stomach must be kept empty up to the very
moment of induction, when the tube should be
withdrawn above the gastro-oesophageal junction.
It can be reinserted after the patient has been
intubated.
Reduction of the intra-abdominal pressure.
Although desirable for several reasons, this is
difficult and unsatisfactory. The nitrogen can be
"washed out" of the bowel by giving the patient
oxygen to breathe (Fine, Banks and Hermanson,
1936; Macintosh, Mushin and Epstein, 1958).*
•Recent work indicates that during anaesthesia, due to
the far greater solubility in blood of nitrous oxide than
nitrogen, nitrous oxide diffuses into the bowel lumen
in a closed loop type of obstruction. The bowel is
compliant so that the intraluminal pressure remains
constant but the volume increases. For instance, 50
per cent nitrous oxide in the inspired mixture causes
a volume increase, in such a loop, of 100 per cent,
whereas 70 to 80 per cent nitrous oxide causes a
volume increase of 500 per cent. This can occur within
10-30 minutes (Eger, 1964, personal communication).
The possibility of rendering the abdomen difficult to
close, and postoperative breathing difficult, should be
noted.
ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS
The fluid in the bowel can be removed by means
of a gastro-intestinal tube, for example, a Miller-
Abbott tube. Both these procedures are time-
consuming, often exceeding 6 hours. The passage
of a gastro-intestinal tube is technically difficult,
even requiring radiological control, and it diverts
attention away from the problem of resuscitating
of the patient.
Clearly each case must be judged on its merits,
but as regards the prevention of regurgitation, the
reduction of abdominal distension is usually less
important than the ability of the anaesthetist to
empty the stomach and to keep it empty up to
the moment of induction.
Maintenance of a clear airway. It is hardly
necessary to impress on an anaesthetist embarking
on an inhalational induction, the importance of
avoiding laryngeal spasm and maintaining a clear
airway. Nevertheless, it is clear that the stormier
the induction the higher is the incidence of
regurgitation (Weiss, 1950; Culver, Makel and
Beecher, 1951; Berson and Adriani, 1954). In
other words, this calamity becomes less likely with
increase in the skill and experience of the anaes-
thetist.
Pre-oxygenation. If endotracheal intubation is
to be facilitated by means of a relaxant, the lungs
must not be ventilated until the cuffed endo-
tracheal tube is in place. Pre-oxygenation is there-
fore required in order to tide the apnoeic patient
over the period required for laryngoscopy.
Cricoid pressure. As soon as the patient loses
consciousness, an assistant exerts firm back-
ward pressure on the cricoid cartilage, obliterat-
ing the oesophageal lumen. This prevents regur-
gitated fluids entering the pharynx from below, it
prevents anaesthetic gases entering (and dis-
tending) the stomach from above, and it facili-
tates intubation by pushing the larynx posteriorly.
Cricoid pressure should not be used to prevent
vomiting, however, because the intra-luminal
pressure might rupture the oesophagus (Sellick,
1961).
Positioning the Patient to render
Aspiration impossible.
Head-down tilt.
In this position the patient may vomit or re-
gurgitate, but gastric contents finding their way
into the pharynx tend to flow out of the mouth,
443
rather than flow against gravity up into the
larynx.
There are, however, several difficulties. Al-
though aspiration is prevented, the larynx may
be submerged so that the pharynx must be cleared
rapidly if regurgitation occurs. Furthermore,
gravity increases the intragastric pressure and the
, abdominal contents come to lie on the dia-
. phragm. A greater respiratory effort is re-
quired, increasing the pleuro-peritoneal pressure
difference. Both these factors predispose to re-
gurgitation. However, the risk is not great and
can be minimized by ensuring that the tilt is not
too steep.
The head-down tilt is sometimes combined
with the left lateral position, as an extra precau-
tion. It has been shown that to avoid aspiration
in this posture a tilt of at least 20 degrees is
required. This is very steep. In addition there
must be a clear egress from the mouth to allow
any fluid reaching the pharynx to escape; fur-
thermore, the patient must be endentulous so that
a cuffed endotracheal tube can be inserted with-
out delay (Elliott, 1963). A head-down tilt is
usually combined with an inhalational induction
of anaesthesia.
Head-up tilt.
This posture is usually adopted when intra-
venous induction of anaesthesia is contemplated
(Snow and Nunn, 1959). Vomiting is prevented
by use of a muscle relaxant and this leaves only
the problem of regurgitation to be solved. The
patient is tilted so that the larynx is at such a
vertical height above the gastro-oesophageal
junction that the intra-gastric pressure is unlikely
to exceed this hydrostatic pressure. In these cir-
cumstances, gastric contents, even if forced into
the oesophagus, will not reach the larynx.
There are two serious drawbacks to this
manoeuvre. The intragastric pressure cannot be
estimated (see range of pressures on page 441)
and so the required degree of head-up tilt cannot
be determined. Should stomach contents reach
the pharynx, then the patient is positioned so
that aspiration is bound to occur. Further, gravely
ill patients become markedly hypotensive in the
head-up position, although this can be minimized
by adjusting the operating table to form a "V"
or "N" shape, and by maintaining the position
 444
for only a minute or so during the actual induc-
tion of anaesthesia.
Hypotension may also be produced even by a
small dose of thiopentone, and many anaesthe-
tists prefer to induce anaesthesia with a suitable
mixture of cyclopropane (30-40 per cent) in
oxygen, when the patient is in this position.
Sealing off the Airway.
Aspiration of stomach contents from the pharynx
is prevented by sealing off the airway. This is
achieved by passing a cuffed endotracheal tube
and the patient is in considerable danger from the
moment consciousness is lost until this has been
done. All methods of inducing general anaesthesia
in intestinal obstruction rely on the speedy
insertion of such a tube, and the anaesthetist
must ensure pre-operatively that the patient can,
in fact, be intubated. He should check on incon-
/ veniently spaced teeth, arthritis of the cervical
spine or temporomandibular joint, and on whether
the patient has a short, thick neck, or not.
In patients in whom endotracheal intubation is
likely to be exceedingly difficult, a safer alter-
native is to pass a cuffed endotracheal tube before
the patient is anaesthetized, so that he can pro-
tect his own airway until it has been sealed off.
Unfortunately, it is necessary to depress the pro-
tective laryngeal reflexes with local analgesia, in
order to intubate a conscious patient, so that
much of the safety of the method is thereby lost.
Avoiding General Anaesthesia.
At one time aspiration was so feared that it was
considered safer for the patient to remain con-
scious and in possession of the cough reflex by em-
ploying conduction anaesthesia. The technique
was thought to avoid any deterioration in the
patient's general condition due to "toxic" inhala-
tional agents, and it provided good relaxation.
There are few valid reasons for employing con-
duction anaesthesia today.
Subarachnoid and epidural blocks may diem-
selves cause nausea and vomiting (Moore, 1955)
and patients have died from aspiration of vomitus
whilst a subarachnoid block was being performed
in the sitting position. The retention of con-
sciousness does not necessarily prevent aspiration
(Clark, 1963). Further, if the upper abdominal
BRITISH JOURNAL OF ANAESTHESIA
muscles are affected by a subarachnoid block, the
patient cannot cough effectively although he may
still be able to inspire deeply (Egbert, Tamersoy
and Deas, 1961). This contrasts with a high
epidural block which, by reducing the capacity
for forced expiration only slightly, preserves an
effective cough (Moir, 1963).
Conduction anaesthesia may cause a deteriora-
tion in the patient's general condition by pro-
ducing hypotension. In the elderly this occurs
because the closure of intervertebral foramina
renders an epidural block unpredictable and more
extensive than intended (Mostert, 1960). A
similar result is obtained by administering a sub-
arachnoid block to a dehydrated patient (Lee,
1959). Hypotension may also occur as a result
of handling the bowel at operation, unless the
surgeon can block the vagi (para-oesophageal).
This may be impracticable if he is working in
the lower abdomen.
A field block is unlikely to permit the return
of distended bowel to the peritoneal cavity, so
that either a subarachnoid or an epidural block
is necessary to provide adequate relaxation. Both
will produce hypotension if the required number
of segments are blocked. Both may reduce the
respiratory tidal volume, and if the patient is
hypoventilating from any other cause, such as
pre-existing respiratory disease or splinting of the
diaphragm by abdominal distension, he will
become hypoxic. The combination of hypotension
and hypoxia is lethal and must be avoided
(Mushin, 1942; Edwards et al., 1956; Bonica et
al., 1957; Lund, Cwik and Quinn, 1961). In fact,
ill patients with intestinal obstruction fare better
with a properly administered general anaesthetic
(Bonica, 1958).
To summarize, it appears to the writer that
both thiopentone and a head-up tilt are inherently
dangerous in these patients, and that probably
the greatest safety here lies in an inhalational
induction with the patient in the head-down
position. Aspiration is very unlikely in such a
posture and some reflex activity is preserved
almost into the stage of surgical anaesthesia.
Furthermore, with inhalational anaesthesia from
the start, the anaesthetist can observe and control
the patient's progress. This is not the case with
an intravenous induction.
ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS
It is not always appreciated that the patient
is in danger of aspirating gastric contents in the
immediate postoperative period also. Conse-
quently, the anaesthetic technique should allow a
rapid return of consciousness with protective
reflexes and it must avoid, as far as possible,
agents likely to cause postoperative vomiting. The
patient should recover in the lateral (tonsil) posi-
tion under skilled supervision as in a recovery
room. Further consideration of the postoperative
period leads to the other major problem, which is
that the effect of any agent used to provide good
surgical relaxation may persist into the post-
operative period, causing hypoxia and inactive
protective reflexes, and thereby endangering the
patient's life.
THE PROBLEM OF SURGICAL ACCESS
Inadequate muscular relaxation may render the
surgical procedure a near-impossibility in a
patient with a distended bowel. It is, therefore, in
the patient's best interests for the anaesthetist to
provide adequate relaxation of the anterior
abdominal wall. Such relaxation can be achieved
by the use of conduction anaesthesia, inhalational
agents or muscle relaxants.
Conduction anaesthesia, although capable of
providing good relaxation, is contraindicated in
cases of intestinal obstruction as already stated.
The use of an inhalational agent ensures that
when the agent is exhaled at the end of the
operation the tissue concentration falls and
muscle tone and power return. Unfortunately, the
depth of anaesthesia required in order to produce
the desired relaxation often causes respiratory
depression and results in cardiovascular depres-
sion with hypotension. Recovery of both con-
sciousness and protective reflexes in the imme-
diate postoperative period is delayed. In view of
these drawbacks, inhalational agents have only a
limited place in providing adequate relaxation
in cases of intestinal obstruction in adults.
The anaesthetist's armamentarium still con-
tains the muscle relaxants, however. They possess
several advantages in that the dose used can be
controlled accurately, only a light general anaes-
thetic is required, and their action is readily
reversed after operation, so that the patient
awakens quickly and is able to protect his airway.
445
The Relaxants.
Depolarizing agents—suxamethonium.
This provides optimal relaxation so that the
trachea can be intubated rapidly, minimizing the
time that the airway is at risk. However, suxame-
thonium occasionally increases the intragastric
pressure (Roe, 1962; Andersen, 1962), due to
contraction of the abdominal musculature and
abnormal movements, caused by muscle fascicu-
lation. This is yet another reason for ensuring
that the stomach is empty at the moment of induc-
tion.
If the anaesthetist intends to use a longer
acting non-depolarizing relaxant during the
operation, it is wise to wait until the effect of
the suxamethonium is wearing off before giving
the non-depolarizing drug, otherwise a prolonged
neuromuscular block may follow. The practice
of administering two different types of relaxants
in the same anaesthetic sequence is better
avoided, however, especially in cases of intestinal
obstruction.
If suxamethonium is used throughout a laparo-
tomy, the Likelihood of some neuromuscular block
persisting into the postoperative period depends
on the method of administration, the total dosage
and the rate of hydrolysis.
The production of continuous adequate relaxa-
tion is difficult using intermittent doses of suxa-
methonium, though the method ensures that the
previous dose is hydrolyzed before the next is
given. The rate of hydrolysis depends on the level
of the plasma cholinesterase (pseudocholinester-
ase), but the plasma level is usually normal in
intestinal obstruction, provided there is little
inflammation or sepsis (Vorhaus and Kark, 1953).
Recently, suxamethonium has been used in
reduced dosage, its rate of hydrolysis being
slowed by tetrahydroaminacrine, an anticholines-
terase (Barrow and Smethurst, 1963; Kenton,
1963). The safety of this interesting approach
remains to be seen, but the initial reports in
ill patients with obstruction are encouraging.
Catabolic protein loss is maximal about one
week after Laparotomy (Wilkinson et al., 1950) and
the plasma cholinesterase is around the lower
level of normal at this time (Burnett, 1960).
Should the bowel become obstructed, due to
adhesions, about a week after laporatomy, the
446
anaesthetist should be wary of using suxame-
thonium during the second operation.
Non-depolarizing agents—tubocurarine and
gallamine.
Patients with fluid and electrolyte deficiencies
usually have an increased sensitivity to muscle
relaxants, especially of the non-depolarizing type.
This is probably due to an increase in the ratio
of intracellular to extracellular potassium, a re-
duction in the volume of the extracellular fluid,
and a reduction in the volume of urine excreted
(Foldes, 1957a, 1960).
The acute loss of extracellular potassium in the
intestinal secretions is aggravated by the lack of
potassium intake from nausea and vomiting. In
severe dehydration, intracellular potassium is lost
also. Although oliguria tends to maintain the ratio
of intracellular to extracellular potassium
j ^ - ) , re-hydration of the patient with saline
only will increase the ratio. This causes the cell
membrane to be hyperpolarized and refractory
to depolarization, so that the myoneural junction
becomes more susceptible to non-depolarizing
relaxants (Feldman, 1963). Consequently, potas-
sium replacement should be considered in these
patients (Taylor, 1963).
After intravenous injection of a relaxant, its
plasma level and its concentration at the myo-
neural junction come into equilibrium, and the
maintenance of the neuromuscular block depends
on the plasma level. In turn this depends on the
redistribution of the relaxant into the extracellular
fluid. If the volume of extracellular fluid is re-
duced, a particular dose of relaxant results in a
higher plasma level than usual.
The plasma level of a relaxant also depends on
the rate of excretion in the urine. If the volume
of urine being excreted is small, then the plasma
level will fall slowly and a given dose of relaxant
will have a longer effect than normal. Gallamine
is completely, and tubocurarine partly, excreted
in the urine.
There are several possible causes for persis-
tence of the action of non-polarizing agents into
the postoperative period.
Overdosage. The anaesthetist should not ad-
minister such a dose of gallamine or tubocur-
BRITISH JOURNAL OF ANAESTHESIA
arine that the effect cannot be reversed by a
reasonable dose of neostigmine at the end of
operation. To prevent overdosage it is essential
that both the anaesthetist and the surgeon differ-
entiate between any difficulty due to distended
bowel on the one hand, and inadequate muscular
relaxation on the other.
A poor peripheral bloodflow. Muscle bloodflow
is very important in the production of a neuro-
muscular block (Churchill-Davidson and Richard-
son, 1952). Cases of intestinal obstruction often
have a poor peripheral circulation ("low flow
state"), and this slows down considerably both
the onset of paralysis and the subsequent recovery
of normal muscle power and tone. The neuro-
muscular block may be prolonged in these
patients. Such a situation may be avoided by
pre-operative restoration of the blood volume and
hence the blood pressure, but the peripheral
bloodflow is probably best improved by the
administration, in addition, of low molecular
weight dextran (m.w. 40,000).
Intraperitoneal antibiotics. The antibiotics
streptomycin, neomycin, polymixin and kana-
mycin all have curare-like properties (Sabawala
and Dillon, 1959). They lower the blood calcium
and thus affect the membrane potential of the
muscle endplates (Corrado, 1963). Cases have
been reported in which large intraperitoneal doses
of these antibiotics reinforced the residual neuro-
muscular block after the use of non-depolarizing
relaxants to such an extent that respiratory
insufficiency resulted postoperatively (Pridgen,
1956; Webber, 1957). Such antibiotics are fre-
quently given by this route at the end of an
operation for intestinal obstruction, especially if
strangulation is present, so the anaesthetist should
be on bis guard. A slow intravenous injection of
10 per cent calcium gluconate reverses the block
and is more effective than neostigmine (Pittinger,
Long and Miller, 1958; Jones, 1959; Pandey,
Kumar and Badola, 1964).
Re-curarization. Although rarely encountered
in practice, it is (at least theoretically) possible
for a patient to become re-curarized. There are
three possible reasons for this. Firstly, urinary
excretion is much reduced in dehydrated or hy-
potensive patients, and relaxants which are
eliminated by the kidneys may still be acting
ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS 447

after the effect of neostigmine has worn off bonate. Subsequently, a similar group of patients,
(Jenkins, 1961). Secondly, in the postoperative in whom the acidosis was treated, did not die.
period water passes from the extracellular fluid Patients with intestinal obstruction often
into the intracellular fluid. This increases the con-present for surgery with a base deficit and with
centration of relaxant at the neuromuscular a "low flow state" of the peripheral circulation.
junction (Foldes, 1957b). Thirdly, if a patient Both produce metabolic acidosis, which is aggra-
vated by anaesthesia and by any hypoxia or
whose I -=^-1 ratio is only being maintained by
\JM>/ hypotension or by massive transfusions of
stored blood. Metabolic acidosis causes depres-
oliguria (vide supra) is given a non-depolarizing
sion of the central nervous system, producing
relaxant before being re-hydrated with saline only, drowsiness or unconsciousness; depression of the
=pi I ratio respiratory centre, with inadequate ventilation
will intensify any myoneural block still present. producing hypercarbia and hypoxia; and depres-
The patient will thus appear to have become re- sion of the cardiovascular system (Bunker, 1962).
curarized (Feldman, 1959, 1963). These effects Tracheal tug is also thought to be due to acidosis
should seldom be seen provided that overdosage (Scurr and Feldman, 1962). In severe acidosis
with relaxants is avoided, and that fluid and (pH<7.0), the ventricular contractile force of the
electrolyte deficiencies are corrected pre- heart weakens (Thrower, Darby and Aldringer,
operatively. 1961), and this causes hypotension and peripheral
Neostigmine-resistant curarization. The term cyanosis. All these effects may be ascribed to
is unsatisfactory because non-depolarizing relax- dehydration or blood loss, and metabolic acidosis
ants have never been directly implicated. The is not suspected.
syndrome was reported in six ill elderly and The blood pH should be restored to normal
dilapidated patients, suffering from intestinal by means of a buffer, such as a solution of sodium
obstruction (Hunter, 1956). Anaesthesia was in- bicarbonate [approximately 1.3 m.equiv/kg
duced in all patients with thiopentone and, after (Brooks and Feldman, 1962), approximately 6
intubation by means of suxamethonium, was m.equiv/kg (Thrower, Darby and Aldinger,
maintained using nitrous oxide, oxygen and 1961)], or a new organic buffer such as THAM
pethidine, with muscular relaxation obtained using [trishydroxymethylaminomethane (Nahas, 1959)].
tubocurarine or gallamine after the effects of This procedure should be carried out under bio-
suxamethonium had worn cff. Postoperatively, chemical control whenever possible. The adminis-
they were unrousable and their paralysis was tration of a buffer does not of itself reverse the
never completely reversed clinically. The patient state of "shock", but it allows time for the usual
had tracheal tug, peripheral cyanosis and methods of resuscitation to become effective.
inadequate tidal volumes. The fundamental It is not known whether this explanation covers
point is that they all died, not from respiratory all cases of "neostigmine-resistant curarization",
insufficiency but from circulatory failure. In but it seems that metabolic acidosis is one cause
spite of a long and involved correspondence in the of the syndrome. Consequently, the pre-operative
journals, the aetiology of the condition remained correction of fluid and electrolyte deficiencies
obscure until recently. It has now been suggested should prevent its occurrence postoperatively.
by Brooks and Feldman (1962), that the under- The causes of persistent relaxant action have
lying cause is a metabolic acidosis. They reported been emphasized, for reasons already mentioned,
five cases, presenting the typical clinical picture because of its seriousness and because its inci-
with apparent "curarization" (e.g. tracheal tug dence is somewhat increased in cases of intestinal
and inadequate respirations), cardiovascular de- obstruction. It must be remembered, however,
pression with hypotension and peripheral cyan- that its overall incidence is low and it would be
osis, and a fatal outcome. All these cases were still rarer if the pre-operative preparation of the
found to have a marked metabolic acidosis, with patient and the administration of relaxants were
a low arterial blood pH and a low plasma bicar- invariably carried out correctly. With these
448
provisos, the writer considers the use of muscle
relaxants to be the method of choice for pro-
viding adequate surgical access in cases of intes-
tinal obstruction.
ACKNOWLEDGMENT
I wish to thank Professor W. W. Mushin for his con-
structive criticism.
REFERENCES
Andersen, N. (1962). Changes in intragastric pressure
following the administration of suxamethonium.
Brit. J. Anaesth., 34. 363.
Atkinson, M. (1962). Mechanisms protecting against
gastro-oesophageal reflux. Gut, 3, 1.
Edwards, D. A. W., Honour, A. J., and Row-
lands, E. N. (1957). Comparison of cardiac and
pyloric sphincters. Lancet, 2, 918.
Bannister, W. K., and Satillaro, A. J. (1962). Vomiting
and aspiration during anesthesia. Anesthesiology,
23, 251.
Barnett, W. O. (1959a). Strangulated intestinal obstruc-
tion: pathophysiology and treatment Arch. Surg.,
79, 864.
(1959b). Lethal factors in intestinal obstruction.
Surg. Gynec. Obstet., 109, 769.
Doyle, R. S. (1958). Effects of neomycin upon
toxicity of peritoneal fluid resulting from strangu-
lated obstruction. Surgery, 44, 442.
Barrow, M. E. H., and Smethurst, J. R. (1963). Suxa-
methonium modified by tetrahydroaminacrine.
Brit. J. Anaesth., 35, 465.
Bergentz, S. E., Gelin, L. E., Rudenstam, C. M., and
Zederfeldt, B. (1961). Indications for the use of
low viscous dextran in surgery. Ada chir. scand.,
122, 343.
Berson, W., and Adriani, J. (1954). "Silent" regurgita-
tion and aspiration during anesthesia. Anesthe-
siology, 16, 644.
Bonica, J. J. (1958). The place of regional anaesthesia
in anaesthetic practice and therapeutics; in
Modern Trends in Anaesthesia (ed. Evans, F. T.,
and Gray, T. C), p. 81. London: Butterworth.
Backup, P. H., Anderson, C. E., Hadfield, D.,
Crepps, W. F., and Monk. B. F. (1957). Peridural
block: analysis of 3.637 cases and a review.
Anesthesiology, 18, 723.
Botha, G. S. M. (1958). Mucosal folds at the cardia as
a component of the gastro-oesophageal closing
mechanism. Brit. J. Surg., 45, 569.
(1959). The closing mechanism between stomach
and oesophagus and its importance in the surgery
of the gastro-oesophageal junction. Ann. roy.
Coll. Surg. Engl., 25, 91.
Braasch, J. W., and Ellis, F. H. (1956). The gastro-
esophageal sphincter mechanism. Surgery, 39, 901.
Brooks, D. K., and Feldman, S. A. (1962). Metabolic
acidosis: a new approach to "neostigmine-
resistant curarisation". Anaesthesia, 17, 161.
BRITISH JOURNAL OF ANAESTHESIA
Brown, H. G. (1963). The applied anatomy of vomit-
ing. Brit. ]. Anaesth., 35, 136.
Burdette, W. J., and Stevens, L. E. (1961). The clinical
management of intestinal obstruction. Arch. Surg.,
83, 120.
Burnett, W. (1960). Value of cholinesterase activity as
a liver function test. Gut, 1, 294.
Bunker, J. P. (1962). Metabolic acidosis during anes-
thesia and surgery. Anesthesiology, 23, 107.
Churchill-Davidson, H. C , and Richardson, A. T.
(1952). Decamethonium iodide: some observations
on its action using electromyography. Proc. roy.
Soc. Med., 45, 179.
Clark, M. M. (1963). Aspiration of stomach contents
in a conscious patient. Brit. ]. Anaesth., 35, 133.
Clark, C. G., and Riddoch, M. E. (1962). Observations
on the human cardia at operation. Brit. J.
Anaesth., 34, 875.
Vane, J. R. (1961). The cardiac sphincter in the
cat. Gut, 2, 252.
Clifton, B. S., and Hotten, W. I. T. (1963). Deaths
associated with anaesthesia Brit. J. Anaesth., 35,
250.
Collins, V. J. (1960). Fatalities in anesthesia and
surgery: fundamental considerations. /. Amer.
med. Ass., 172, 549.
Corrado, A. P. (1963). Respiratory depression due to
antibiotics. Anesth. Analg. Curr. Res., 42, 1.
Crawford, J. J., and Nemir, P. jr. (1960). The clinical
application of recent experimental conclusions in
the treatment of intestinal obstruction. Surg. Clin.
N. Amer., 40, 1513.
Creamer, B. (1955). Oesophageal reflux. Lancet, 1, 279.
Culver, G. A., Makel, H. P., and Beecher, H. K. (1951).
Frequency of aspiration of gastric contents by the
lungs during anesthesia and surgery. Ann. Surg.,
133, 289.
Dines, D. F., Baker, W. G., and Scantland, W. A.
(1961). Aspiration pneumonia: Mendelson's syn-
drome. /. Amer. med. Ass., 176, 229.
Dinnick, O. P. (1961). Hiatus hernia: an anaesthetic
hazard. Lancet, 1, 470.
Dornhorst, A. C , Harrison, K., and Pierce, J. W.
(1954). Observations on the normal oesophagus.
Lancet. 1, 695.
Edwards, G., Morton, H. J. V., Pask. E. A., and Wylie,
W. D. (1956). Deaths associated with anaesthesia.
Anaesthesia, 11, 194.
Egbert, L. D., Tamersoy, K., and Deas, T. C. (1961).
Pulmonary function during spinal anesthesia: the
mechanism of cough depression. Anesthesiology,
22, 882.
Elliott, C. J. R. (1963). A study in rcgurgitation.
Anaesthesia, 18, 324.
Feldman, S. A. (1959). An interesting case of recurari-
zation. Brit. J. Anaesth., 31, 461.
(1963). Effect of changes in electrolytes, hydra-
tion and pH upon the reactions to muscle
relaxants. Brit. J. Anaesth., 35, 546.
Fine, J. (1961). The cause of death in acute intestinal
obstruction. Anesth. Analg. Curr. Res., 40, 150.
ANAESTHETIC PROBLEMS OF INTESTINAL OBSTRUCTION IN ADULTS
Fine, J., Banks, B. M., and Hermanson, L. (1936). Treat-
ment of gaseous distension of the intestine by
inhalation of 95 per cent oxygen. Ann. Surg., 103,
375.
Fisher, C. W. (1953). Prevention of aspiration of
gastric contents. Anesthesiology, 14, 506.
Fleshier, B., Hendrix, T. R., Kramer, P., and Infjel-
finger, F. J. (1958). Resistance and reflex function
of the lower esophageal sphincter. /. appl.
Physiol., 12, 339.
Foldes, F. F. (1957a). The fate of muscle relaxants in
man. Acta anaesth. scand., 1, 63.
(1957b). Muscle Relaxants in Anesthesiology,
pp. 60, 148. Springfield: Thomas.
(1960). The pharmacology of neuromuscular
blocking agents in man. Clin. Pharmacol. Ther.,
1, 345.
Gelin, L. E. (1961). Disturbances of the flow properties
of blood and its counteraction in surgery. Acta
chir. scand., 122, 287.
Zederfeldt, B. (1961). Experimental evidence of
the disturbance in the flow properties of blood.
Acta chir. scand., 122, 336.
Greenan, J. (1961). The cardio-oesophageal junction.
Brit. J. Anaesth., 33, 432.
Greenwood, R. K., Schlegel, J. F., Code, C. F., and
Ellis, F. H. (1962). The effect of sympathectomy,
vagotomy and oesophageal interruption on the
canine gastro-oesophageal junction. Thorax, 17,
310.
Guiffrida, J. G., and Bizzari, D. (1957). Intubation of
the esophagus. Amer. J. Surg., 93, 329.
Hunter, A. R. (1956). Neostigmine-resistant curarisa-
tion. Brit. med. J.. 2, 919.
Ingram, P. R, Respess, J. C , and Muller, W. H. (1959).
The role of an intrinsic mechanism in the pre-
vention of reflux esophagitis. Surg. Gynec.
Obstet., 109, 659.
Inkster, J. S. (1963). The induction of anaesthesia in
patients likely to vomit, with special reference to
intestinal obstruction. Brit. J. Anaesth., 35, 160.
Jenkins, I. R. (1961). Three cases of apparent recura-
rization. Brit. J. Anaesth., 33, 314.
Jones, W. P. G. (1959). Calcium treatment for ineffec-
tive respiration resulting from administration of
neomycin. /. Amer. med. Ass., 170, 943.
Kausch, W. (1903). Zur Narkose bein Ileus. Berl. Klin.
Woch., 40. 753.
Kenton, B. (1963). Correspondence: Suxamethonium
modified by tetrahydroaminacrine. Brit. J.
Anaesth., 35, 825.
Lancet (1962). Leading article: Vomiting during anaes-
thesia. Lancet, 2, 134.
(1964). Leading article: Dextrans for easing
blood-flow. Lancet. 1, 28.
Lee, J. A. (1959). A Synopsis of Anaesthesia, 4th ed.,
p. 301. Bristol: Wright.
Lund, P. C , Cwik, J. C , and Quinn, J. R. (1961).
Experiences with epidural anesthesia, 7,730 cases.
Anesth. Analg. Curr. Res., 40, 153, 164.
449
Macintosh, R. R. (1951). A cuffed stomach tube. Brit,
med. J., 2, 545.
Mushin, W. W., and Epstein, H. G. (1958).
Physics for the Anaesthetist, 2nd ed., p. 244.
Oxford: Blackwell.
Marchand, P. (1954). The gastro-oesophageal "sphinc-
ter" and the mechanism of regurgitation. Brit. J.
Surg., 42, 504.
Marcus, E. (1962). Fluid and electrolyte imbalance and
their management. Surg. Clin. N. Amer., 42, 47.
Mendelson, C L. (1946). Aspiration of stomach con-
tents into the lungs during obstetric anesthesia.
Amer. J. Obstet. Gynec, 52, 191.
Moir, D. D. (1963). Ventilatory function during epi-
dural analgesia. Brit. J. Anaesth., 35, 3.
Moore, D. C. (1955). Complications of Regional
Anaesthesia, p. 165. Oxford: Blackwell.
Moore, F D. (1963). Tris buffer, mannitol, and low
viscous dextran: three new solutions for old
problems. Surg. Clin. N. Amer., 43, 577.
Morton, H. J. V., and Wylie, W. D. (1951). Anaesthetic
deaths due to regurgitation or vomiting. Anaes-
thesia, 6, 190.
Mostert, J. W. (1960). The risk of epidural block in
old people. Brit. J. Anaesth., 32. 613.
Mushin, W. W. (1942). Heavy percaine spinal anaes-
thesia. Brit. med. J., 1, 139.
Nahas, G. G. (1959). Use of organic carbon dioxide
buffer in vivo. Science, 129, 782.
O'Mullane, E. J. (1954). Vomiting and regurgitation
during anaesthesia. Lancet, 1, 1209.
Pandey, K., Kumar, S. and Badola, R. P. (1964).
Neuromuscular blocking and hypotensive actions
of streptomycin and their reversal. Brit. J. Anaesth.,
36, 19.
Pittinger, C. B., Long, J. P., and Miller, J. R. (1958)..
Neuromuscular blocking action of neomycin:
concern of anesthesiologist Anesth. Analg. Curr.
Res., 37, 276.
Pontoppidan, R , and Beecher, H. K. (1960). Progres-
sive loss of protective reflexes with advance of age.
/. Amer. med. Ass., 174, 2209.
Pridgen, J. E. (1956). Respiratory arrest thought to be
due to intraperitoneal neomycin. Surgery, 40. 571.
Robson, J. G., and Welt, P. (1959). Regurgitation in
anaesthesia: a report on some exploratory work
with animals. Canad. Anaesth. Soc. J., 6, 4.
Roc, R. B. (1962). The effect of suxamethonium on
intragastric pressure. Anaesthesia, 17, 179.
Ruben, A., and Ruben, H. (1962). Artificial respira-
tion : problems of regurgitation. Proceedings of
1st European Congress of Anaesthesiology,
Vienna, Vol. 2, No. 131.
Sabawala, P. B., and Dillon, J. B. (1959). The action
of some antibiotics on the human intercostal nerve-
muscle complex. Anesthesiology, 20, 659.
Savage, P. T. (1960). The management of acute intes-
tinal obstruction. Brit. J. Surg., 47, 643.
Scott, p . L. (1961). Anaesthetic experiences in 1,300
maior geriatric operations. Brit. J. Anaesth., 33.
354.
450
Scurr, C. F., and Feldman, S. A. (1%2). Tracheal tug.
Anaesthesia, 17, 111.
Sellick, B. A. (1961). Cricoid pressure to control re-
gurgitation of stomach contents during induction
of anaesthesia. Lancet, 2, 404.
Simenstad, J. O., Galway, C. F., and MacClean, L. D.
(1962). The treatment of aspiration and atelectasis
by tracheobronchial lavage. Surg. Gynec. Obstet.,
115, 721.
Sinclair, R. N. (1959). The oesophageal cardia and re-
gurgitation. Brit. J. Anaesth., 31, 15.
Snow, R. G., and Nunn, J. F. (1959). Induction of
anaesthesia in the foot-down position for patients
with a full stomach. Brit. J. Anaesth., 31, 493.
Taylor, G. J. (1963). Apnoea due to apparent potas-
sium imbalance. Anaesthesia, 18, 9.
Thrower, W. B., Darby, T. D., and Aldinger, E. G.
(1961). Acid-base derangements and myocardial
contractility. Arch. Surg., 82, 56.
Vorhaus, L. J., and Kark, R. M. (1953). Serum cholin-
esterase in health and disease. Amer. J. Med., 14,
707.
Webber, B. M. (1957). Respiratory arrest following
intraperitoneal administration of neomycin Arch.
Surg., 75, 174.
Weiss, W. A. (1950). Regurgitation and aspiration of
stomach contents during anesthesia. Anesthe-
siology, 11, 102.
Wilkinson, A. W., Billing, B. R , Nagy, G., and
Stewart, C. P. (1950). Nitrogen metabolism after
surgery. Lancet, 1, 533.
Wylie, W. D. (1963). The use of muscle relaxants at
the induction of anaesthesia of patients with a full
stomach. Brit. J. Anaesth., 35, 168.
BOOK REVIEW
Anesthesia for Patients with Endocrine Disease. By
M. T. Jenkins and 41 other contributors. Pub-
lished by Blackwell Scientific Publications, Oxford.
Pp. 234 + xiii; indexed; illustrated; 1963. Price 40s.
The problems which arise when anaesthetizing patients
suffering from various disorders of the endocrine
glands are now well known to expert anaesthetists.
It was, therefore, not with any expectation of great
novelty that this book was approached. Almost
immediately, however, the reader is electrified by the
unusual and stimulating manner in which Dr. Jenkins,
the editor, handles his commission. He gives the reader
the impression of sitting with the contributors as a
panel, expressing its views freely on each and every
problem as it arises. The text deals very comprehen-
sively with the whole field of endocrine disease, includ-
ing obesity and disorders of blood pressure, by a
mixture of case reports, comments, and symposium-
like panel discussions. There is hardly an aspect of
this subject which docs not receive novel treatment
and from which the reader does not derive great
benefit. Thus the obese patient and his cardio-respira-
tory difficulty is fully explored; the problems of the
BRITISH JOURNAL OF ANAESTHESIA
PROBLEMES ANESTHESIOLOGIQUES DANS
L'OCCLUSION INTESTINALE CHEZ L'ADULTE
SOMMA1RE
Les problemes anesthesiologiques qu'on rencontre chez
les malades atteints d'occlusion intestinale surgissent
par la ndcessitd d'aspirer le contenu gastrique et
d'essayer de produire un relachcment abdominal suf-
fisant. On discute les incidents et les me'canismes mis
en jeu par les vomissements et les rtgurgitations. Sur
cette base on decrit les mesures pour prgvenir I'aspira-
tion. Pour produire un relachement abdominal sufnsant
il semble indiqud d'utiliser des relaxants musculaire
qui repre'sentent les metiicamcnts de choix malgre' les
n£ponses anormales qu'on observe parfois chez ces
malades. La nature de ces reactions anormales et les
mesures pour les corriger et les preVenir sont discuses
en detail.
ANASTHESIEPROBLEME BEI DARMVER-
SCHLUSS BEIM ERWACHSENEN
ZUSAMMENFASSUNG
Bei der Narkose von Patienten mit Darmverschlufi in
schlechtem Zustand ergeben sich Probleme wegen der
moglichen Aspiration von Mageninhalt und aus den
Bemtlhungen zur Herstellung einer ausreichenden Er-
schlaffung der Bauchmuskulatur. Die Gefahren und
Mechanismen des Erbrechens und Regurgitierens
werden ausfUhrlich diskutiert Auf dieser Basis wird
die BcgrUndung fur die Aspirationsverhinderung
gegeben. Zur Herstellung einer ausreichenden Bauch-
deckenerschlaffun^ scheinen die Muskelrelaxantien
trotz der gelegenthch bei diesen Patienten beobachteten
abnormen Reaktion die Mittel der Wahl zu sein. Die
Art dieser Reaktionen und die Methoden zur
mdglichen Vermeidung werden ausfUhrlich beschrieben.
diabetic patient are given refreshingly reasonable and
logical treatment; while the account of the physiology
of the adrenergic mechanism, and the sympathetic
nervous system in general, will be an eye-opener to
the beginner. Throughout the book the editor sprinkles
his own pithy and always helpful comments. Although
many of the contributors are from the University of
Texas, South Western Medical School, Dr. Jenkins has
not hesitated to range widely in the United States for
his colleagues and even to draw on five British anaes-
thetists as well. Not the least rewarding aspect of this
book is to see the different ways in which a patient and
his problems can be regarded by various experts. That
they sometimes appear to have little in common is
more likely to indicate that they are all right, rather
than the reverse, for each sees the problem from his
own standpoint. Books like this serve an excellent
purpose in bringing specialists together so that they
can develop respect for each other's opinions, to the
ultimate benefit of the patient. Dr. Jenkins's book is
strongly recommended. It will undoubtedly serve as a
model for other editors who have the task of cover-
ing a localized area of anaesthesia with a group of
experts. W. W. Mushin