Anaesthesia, 1975, Volume 30, pages 520-529

Thoughts on immediate care

Anaesthetisfs are being increasingly called upon to give immediate treafmentfor various
I life-threatening conditions in casualty departments and elsewhere. This feature of short
papers by invited experts is designed to describe the proper management of patients who
require immediate care before the opinion of specialists in a particular field can be ob-
tained.

The emergency management of diabetes mellitus

D. S . J . M A W
The improved life expectancy occurring in insulin dependent diabetics over recent
decades and the increased number of mild maturity onset diabetics ensure that the
anaesthetist will regularly come into contact with diabetic patients. Errors in manage-
ment can only be avoided if the anaesthetist is familiar with the basic principles
involved. Many different treatment schedules are available for routine management of
the diabetic patient, for treatment of complications and for control under anaesthesia
and some of these schedules must appear complex to a doctor not actively engaged in
the management of the diabetic The following account is intended to be of
some practical guide to anaesthetists confronted with an emergency situation involving
a diabetic patient. Initially the principles of management of acute diabetic complica-
tions will be discussed followed by an account of control during anaesthesia.

Coma in diabetic patients

Hypoglycaemia
The differential diagnosis of a diabetic patient in coma should not present any undue
difficulty as the clinical pictures of hypoglycaemia (insulin coma) and diabetic ketosis
(diabetic coma) are so dissimilar. The symptoms of hypoglycaemia are caused by a
combination of excess sympathetic activity (e.g. sweating, pallor, palpitations, tremor,
weakness, hunger, apprehension and circumoral numbness), together with a lack of
available glucose for the brain to metabolise (neuroglycopenia) as shown by abnormal
behaviour patterns (irritability, obstinacy, confusion, agitation, ‘drunken behaviour’)
and neurological abnormalities (e.g. diplopia, dysphasia, ataxia, fits and coma).
Hypoglycaemia may also produce severe headaches and it is important to accurately
time the onset of this symptom in relation to the patient’s normal diabetic control and
regime. Clinically the hypoglycaemic patient is not dehydrated, is often sweating with
a normal or slightly raised pulse rate and blood pressure and may exhibit variable
neurological signs (with extensor plantar responses). Urinalysis will usually show that
D. S . J. Maw, MB, BS, MRCP, Consultant Physician, Pembury Hospital &Kent and Sussex Hospital,
Tunbridge Wells, Kent.

520
 Emergency management of diabetes mellitus 521

sugar is absent but occasionally the test may be positive due to the presence of pooled
urine present in the bladder for several hours from a time when the blood sugar was
higher than the renal threshold. Occasionally in patients on oral hypoglycaemic
compounds more chronic hypoglycaemia may be found producing a confusional state
at night (particularly in elderly patients on chlorpropamide).
Treatment. There is usually no problem in the treatment of hypoglycaemic states.
If the patient is sufficiently conscious to take nourishment by mouth, then 10-20
g glucose or equivalent orally will rapidly bring about an improvement in the patient’s
condition. If the patient is unconscious then the intravenous administration of 10-
25 g glucose (20-50 ml of a 50% solution) will be adequate to restore consciousness in
the vast majority of patients. It is, however, always a sensible precaution to take a
blood sugar for estimation before giving the intravenous injection so that the level
can be checked if there is any doubt about the patient’s subsequent condition; rarely
intravenous glucose administration may prove technically difficult in obese, restless
patients and intramuscular glucagon 1 mg may then be prescribed instead followed by
oral glucose when the patient recovers consciousness.
A few patients instead of regaining consciousness immediately remain in a con-
fused, disorientated condition for some minutes or even some hours afterwards. Some
patients who have had severe, prolonged hypoglycaemia may not recover conscious-
ness after glucose either because of the presence of cerebral oedema or irreversible
brain damage; in this small minority of patients who have failed to respond to glucose,
it is worthwhile giving treatment for cerebral oedema such as high dose of glucocorti-
coid therapy (intravenous dexamethasone) or intravenous mannitol (100 ml of 20%
solution). When the patient has regained consciousness, the precipitating factor lead-
ing to hypoglycaemic state should be sought and appropriate adjustments made to the
patient’s regimen.

Diabetic ketosis
The clinical picture of diabetic ketosis takes longer to develop, with a minimum
period of several hours and often several days.
The history is of a progressive illness with increasing malaise, thirst, polyuria and
weight loss. Other symptoms are more variable and may include abdominal pain,
vomiting, confusion leading to coma, etc. but the clinical findings are characteristic.
The patient looks ill, shows signs of dehydration and salt depletion (rapid, weak,
thready pulse, low blood pressure, lack of skin elasticity, dry mouth and sunken eyes).
Respiration is deeper than normal and the rate is usually slightly increased (the air-
hunger of Kussmaul respiration). There is a strong smell of acetone on the breath but
there is a wide variation in sensitivity to this smell in different observers. Urinalysis
shows the presence of heavy glycosuria and ketonuria.
Treatment. Diabetic ketosis is more difficult to treat than hypoglycaemia and,
despite improved biochemical control, there is still a significant morbidity and mor-
tality attached to this complication. Different physicians use various treatment
schedules and medical practitioners, who only occasionally meet the complication,
may find that the therapy is rather confusing in some details. In order to understand
the principles involved, it is necessary to consider the underlying metabolic derange-
ment. If a diabetic is out of control, the lack of insulin leads to hyperglycaemia and
glycosuria-an osmotic diuresis which becomes quantitatively more severe with
 D. S. J. Maw

increasing hyperglycaemia, and also causes some loss of sodium and potassium salts,
The patient feels thirsty and partially corrects the water loss with oral fluids, unless
unable to do so due to vomiting. The lack of insulin means that energy substrates,
other than carbohydrate, have to be mobilised causing breakdown of fat (and protein).
Ketone body production occurs as the process continues. This initially leads to a
compensated metabolic acidosis as ketonuria increases but the ketonuria greatly
increases the osmotic stress and his condition soon deteriorates as a florid metabolic
acidosis develops.
It follows that the following abnormalities require treatment in a patient with
diabetic ketoacidosis, lack of insulin, dehydration, loss of salts (sodium and potas-
sium), metabolic acidosis and any precipitating factor which may be present.
Insulin therapy should begin as soon as the clinical diagnosis is established. It is
important to use only quick-acting soluble insulin, and to administer it by a route
which will make it readily available, i.e. intravenously and/or intramuscularly. It is
illogical to give it subcutaneously when the patient is in a hypotensive and collapsed
condition and the blood supply to subcutaneous tissues is reduced, for insulin so
administered will only be absorbed slowly and in an unpredictable fashion. In a severe
case of diabetic ketoacidosis it may be necessary to give 100 units of insulin initially
(60 units intravenously and 40 units intramuscularly; that is a dose in units approxi-
mately equivalent numerically to l/lOth of the blood sugar level in mg/100 ml or
approximately twice the blood sugar in mmol per litre). Subsequent intramuscular
insulin therapy may be given on a 2-hourly basis, depending on the patient’s clinical
and biochemical response.
Over recent years a great deal of attention has been paid to the action of insulin and
it has been realised that in viuo insulin has a short half life of 5 minutes. This means
that it would clearly be more logical to give small amounts of insulin very frequently
or preferably to give insulin by slow infusion. This last technique is not a practical
proposition for general use as slow infusion pumps are needed and other precautions
have to be taken to avoid absorption of insulin onto glassware and drip tubing. A
satisfactory, simple compromise which has been adopted is the frequent intramuscular
administration of small quantities of insulin (say 10 units hourly)’; this has the ad-
vantage from the practical point of view that it is easy to carry out and the dosage is
easily remembered. When the blood sugar falls below 250 mg/100 ml (13.9 mmol/
litre), or when the glycosuria falls below 2%, the hourly injections of insulin should be
stopped and the patient can then be placed on a sliding scale of insulin on a 6-hourly
basis (Table 1).

Table 1. Sliding scale insulin dose

for emergency use (e.g. 4- or 6-
hourly)

Urine test Dose of soluble

for glucose insulin (units)

2% ++++ 20
1% +++ 16
+% + + 10
I% + 6
0 - 0
 Emergency management of diabetes mellitus 523

Sliding scales of insulin administration have been rightly criticised on the grounds
that either too much or too little insulin is given. They are, however, useful for the
emergency in the first 24 hours while one is assessing the patient's insulin needs. When
an assessment has been made of the approximate overall daily dosage, the sliding scale
principle can still be used but can be tailor-made so as to control diabetes with only a
low amount of glycosuria; as an example a patient normally on 30 units of insulin
would be controlled on the thrice daily sliding scale insulin shown in Table 2, with a
level of 4% glycosurja, but would not show wild swings from 0 to 2% with the same
frequency as the patient treated with the more traditional sliding scale where no insulin
is given if the patient has no glycosuria.

Table 2. Sliding scale insulin dose for patients being restabi-

lised. Example shown for diabetic with estimated insulin
requirements (Y) 30 u. daily

Urine test Approx. dose of soluble insulin (units)

for glucose q.d.s. dose t.d.s. dose
2% + + + + 0.45Y* 14 0.55-0.60Y 18
1% + + + 0.35-0.40 Y 12 0.45 Y 14
YA + + 0.25 Y 8 0.33 Y 10
4% + 0.20 Y 6 0.25 Y 8
0 - 0.12 Y 4 0.20 Y 6

* Y = estimated daily insulin dose from knowledge of

previous insulin therapy or insulin requirements in previous
24 hours.

Intravenous fluids should be given at the same time as insulin therapy is started in
patients with diabetic ketoacidosis. There is often a considerable fluid deficit (possibly
about 7 litres) and it is consequently necessary to give large quantities of intravenous
fluid in the early stages and when the extra-cellular fluid has been replenished to a
significant extent, the pulse rate will begin to decrease and the blood pressure rise and
the renal perfusion will improve.
Physiological saline (0.9% sodium chloride) is the best solution to use in the early
stages; it has the advantage of being readily available on all wards and of being a
solution which does not provide an osmotic distorting stress and hence one which
can be given rapidly intravenously. An average adult will need approximately 1-2
litres of normal saline in the first hour and 1 litre in the second hour. The rate of
infusion should be less in older patients, or in any patients where there may be some
doubt as to myocardial state.
The clinician may need to consider administration of base at the end of the first
2 hours. This is, however, a matter of some controversy, since intravenous fluids
enable the kidneys to excrete more of the ketone load and insulin administration slows
down the rate of production of ketone bodies, both of which lessen the acidosis. The
administration of one-sixth molar sodium lactate has little to recommend it as this is
not active as base until lactate has been metabolised and there is in any case a block
in metabolism of lactate in diabetic ketosis. If on clinical and biochemical criteria the
patient is extremely acidotic (e.g. plasma bicarbonate below 8 mEq/litre or pH below
7.1) the administration of small quantities of sodium bicarbonate may be justified
524 D . S.J. Maw

(perhaps 500-1000 ml of 1.4% sodium bicarbonate over 2-4 hours, or correspond-

ingly less if a stronger solution is used). 8.4% sodium bicarbonate should not be used
in this situation as it is very hypertonic. Sodium bicarbonate should not be prescribed
initially because it is dangerous to give it too quickly in these patients as one may
produce a very rapid change in potassium level, leading to arrhythmias or cardiac
arrest. Similarly if excessive quantities are given one can get the paradoxical state
arising where the extra-cellular acidosis is over corrected but where the patient con-
tinues to hyperventilate because he still has an intracellular acidosis. It is therefore only
in a minority of patients, who have an extremely severe ketoacidosis, that sodium
may need bicarbonate.
The next solution to be given intravenously should be isotonic dextrose-saline
(4.0% dextrose, 0.1 8% sodium chloride), together with potassium supplements,
depending on the results of biochemistry. This has the disadvantage that one is giving
dextrose to a patient whose blood sugar level is already raised and hence tending to
perpetuate the osmotic diuresis but, as the blood sugar will already be coming down at
this stage (4-6 hours after initiating treatment), this objection is more theoretical than
real. It can also be argued that the administration of dextrose-saline has the slight
advantage of minimising the chance of hypoglycaemia developing while at the same
time providing osmotically active water for correcting the dehydration after the dex-
trose has been utilised. If very hypotonic solutions are used there is a real chance of
producing haemolysis in a small proportion of patients if the infusion rate is too quick,
but half normal saline (0.45% sodium chloride) can be used with advantage if the
plasma sodium is greater than 155 mEq/litre. The rate of infusion of potassium supple-
ments does not usually need to exceed 20 mEq per hour (1.5 g potassium chloride) in
hypokalaemic patients and less is usually needed, perhaps 5 mEq of potassium per
hour.
Other general supportive measures are important in management; they include
oxygen administration to hypotensive patients and the aspiration of gastric contents
by naso-gastric tube. Careful records must be kept of fluid balance and other nursing
observations.
Summary of treatment. The above principles for treatment of diabetic ketosis are
covered in the following scheme using a modified low dose regimen :
(1) Take blood for blood sugar, blood urea and electrolyte determination and set
up intravenous infusion of normal saline (0.9% sodium chloride) about 3 litres in 2
hours (less in old patients).
(2) Give 20 units soluble insulin intramuscularly (if the acidosis is severe give 20
units intravenously as well).
(3) Aspirate the stomach contents through a naso-gastric tube, give oxygen and
monitor patient if in coma.
Start treatment of the underlying precipitating cause (e.g. infection), institute
routine nursing observations.
(4) After the first hour start injections of intramuscular soluble insulin 10 units
hourly.
(5) At 2 hours check blood sugar and sodium and potassium. Continue the
intravenous infusion with normal saline for further 2-4 hours but add potassium
supplement (usually 5-10 mEq potassium per hour) e.g. 20 mEq potassium chloride in
1000 mlO*9% saline in 3 hours and consider the addition of a small amount of sodium
bicarbonate if the acidosis is very severe. If the plasma sodium is more than 155
 Emergency management of diabetes mellitus 525

mEq/litre give 0.45% saline if it is available. If the blood sugar level is not falling, give
a double dose of insulin.
(6) Change the intravenous infusion to 4.0% dextrose and 0.18% saline giving
1 litre every 4-6 hours plus additional potassium chloride as indicated by the results of
blood analysis. Measure the blood sugar every 2 hours.
(7) When the blood sugar is below 250 mg/100 ml (13.9 mmolllitre) change to a
sliding scale of insulin administration.

Other causes of coma

If difficulty is encountered in establishing the diagnosis of a disorder in the level of
consciousness in a diabetic patient, it usually means that there is some other factor
involved apart from the blood sugar level. It is important to remember that the
diabetic may lapse into coma for exactly the same reason as a non diabetic (e.g.
cerebrevascular accident, subarachnoid haemorrhage, meningitis, uraemia, drug
overdose, etc.). Less common metabolic disturbances found in diabetics include
hyperosmolar coma, lactic acidosis and cerebral oedema.
Hyperosmolar, non-ketoacidotic diabetic coma has been recognised with increased
frequency over recent years. Dehydration is the predominant clinical feature and
ketonuria is usually slight or absent. The blood sugar is often extremely high. Treat-
ment is similar to that given for diabetic ketoacidosis but sodium bicarbonate is contra-
indicated and hypotonic solutions such as 0.45% saline may be needed to correct
the dehydration.
Severe metabolic acidosis due to lactic acidosis may be found occasionally in
diabetics on biguanide therapy with phenformin. If there is an additional cause for the
lactic acidosis, e.g. hypoxia or hypotension due to vascular disease, the prognosis may
be poor and acidosis difficult to combat, even with liberal quantities of intravenous
sodium bicarbonate.
Cerebral oedema may be found in diabetics with severe, prolonged hypoglycaemia
and also during treatment for diabetic ketosis and hyperosmolar coma, particularly
when intravenous fluids have been given too rapidly. The possibility that this com-
plication may have developed should always be considered in diabetics who are being
restabilised and whose condition suddenly deteriorates.

Anaesthesia
Diabetic patients should be adequately stabilised before undergoing any form of
elective operative treatment. If the procedure is going to be performed under local
anaesthesia there is obviously no particular problem regarding diabetic management.
Traditionally the anaesthetist normally supervises the control of the diabetic patient
over the operation and in the immediate postoperative period, handing control back
to his medical and surgical colleagues on the first postoperative day, although this
may vary in different centres.
The anaesthetist’s most important brief is to ensure that the patient does not suffer
either from hypoglycaemia or diabetic ketosis as a result of the stress of operation or
the illness leading to operation.
526 D.S. J. Maw
Pre-operative routines for all diabetics
A pre-operative blood sugar should be obtained in all diabetic patients to confirm that
diabetic control is adequate and to act as a base line in the event of there being any
problem in the postoperative period. All diabetic patients should be placed on diabetic
urine charts and regular checks carried out for sugar and ketone bodies (e.g. 4-hourly).

Patients treated with diet and oral therapy

Many diabetic patients requiring operative treatment will be mild diabetics controlled
by diet alone or on oral hypoglycaemic compounds. These patients present little
problem in management for the anaesthetist. Diabetics treated by diet alone require
no precautions in the operative periods other than the routine measures described
above. It is, however, important to remember that the stress of any illness may be
sufficient to increase the insulin demands of a patient and that a mild diabetic, nor-
mally controlled on diet or on diet and tablets, may become insulin dependent during
an acute illness. There is consequently no room for complacency in the management
of diabetic patients in the postoperative period and routine urinalysis should be con-
tinued throughout the patient’s stay in hospital, although the frequency can be reduced
if the results are negative.
Oral compounds used for treatment of diabetes are divided into two main groups,
sulphonylureas such as tolbutamide (Rastinon), chlorpropamide (Diabinese) and
glibenclamide (Daonil, Euglucon) and the biguanides, phenformin (Dibotin) and
metformin (Glucophage). Most of these compounds have a short or intermediate
duration of action and it is satisfactory merely to omit the morning dose on the day of
operation and then to restart therapy when the patient is able to take medication by
mouth in the postoperative period. This does not apply to chlorpropamide, however.
This drug has a long half life of 35 hours due to its renal mode of excretion and a high
degree of protein binding in the blood; there is therefore a real risk of producing
hypoglycaemia on the day of operation because of residual activity from the previous
day’s medication and, for this reason, it is often advisable to stop the drug for at least
24 hours before operation and check that the blood sugar is not in the hypoglycaemic
range.
The degree of diabetic control will prove to be inadequate in a few cases and the
dose of tablets will need to be increased or a patient stabilised on insulin. If this latter
course of action is necessary it does not mean that the patient will have to remain on
insulin permanently as it is usually possible to restabilise the patient on his previous
medication when he has recovered from the stress of illness and operation.
It is also important to remember that most anaesthetic agents cause a slight rise in
the blood sugar, although this is not of major importance and there is no particular
reason to favour any one specific anaesthetic agent for use in diabetic patients.

Insulin Dependent Diabetics

Insulin treatment poses certain problems over the operative period and some changes
in the regimen are obviously necessary. Adequate carbohydrate intake must be ensured
on the day of operation but oral glucose must not be given for 6 hours pre-operatively
under any circumstances as gastric emptying will tend to be delayed and there is a
 Emergency management of diabetes mellitus 527

significant risk that vomiting may be produced. Many different schedules for insulin
administration have been described but their suitability depends on the severity of the
diabetes and nature of the operative procedure. The following procedures may be
used :
Soluble insulin in divided doses and intravenous dextrose. This scheme is the most
flexible and generally applicable of the schedules as it can be used on all insulin
dependent diabetics (whether mild or brittle) irrespective of the severity of the surgical
procedure and length of anaesthesia. It combines the advantage of flexibility with the
knowledge that the diabetes will be adequately controlled during the operative period.
It does require pre-operative stabilisation of the patient on twice daily soluble insulin,
however.
The timing of operation is important and it is preferable that the diabetic patient
should be operated on early in the morning list unless there is some cogent reason why
this should not be so.
Two-thirds of the predetermined morning dose of soluble insulin should be ad-
ministered at the usual time and an intravenous drip should be set up with 5%
dextrose to run in at the approximate rate of 500 ml every 6 hours during the period
that the patient is unable to take fluid by mouth. Additional intravenous injections of
glucose should also be given in order to ensure that the patient’s normal carbohydrate
intake is covered. This can be done by giving intravenous injections of 10 g glucose
(20 ml of 50% dextrose solution followed by 20 ml of 0.9% saline to prevent thrombo-
phlebitis).
The pre-operative blood sugar should be checked on the morning of operation and
it is useful to carry out a Dextrostix estimation at the same time as this method may be
used to keep a check on the blood sugar level during anaesthesia and in the immediate
postoperative period. It is, however, sensible to carry out a formal blood sugar
estimation in the Laboratory as well, as very occasionally discrepancies may occur,
usually due to incorrect technique.
The blood sugar should again be checked when the patient has returned to the
ward after operation, and the remaining third of the morning dose of insulin should be
then administered at lunchtime, unless the blood sugar level is on the low side of
normal, say below 110 mg/100 ml(6.1 mmol/litre) in which case it should be withheld.
The predetermined dose of insulin can then be given at the normal time in the
evening, together with oral fluids if the patient is able to take them, depending on the
nature of the surgical procedure. If this is not possible then the patient should con-
tinue with intravenous dextrose (or 4.0% dextrose in 0.18% saline). If the patient is
known to be a very brittle diabetic and very prone to ketosis it is advisable to divide
the insulin into four doFes, with a slightly reduced amount at midnight.

The administration of the normal insulin requirement pre-operatively with intravenous

dextrose
This method involves making no basic alteration to the patient’s normal insulin
dosage but merely covering the normal carbohydrate requirement by giving intra-
venous dextrose.
This regimen can be used in an emergency situation or when there is inadequate
time to restabilise the patient pre-operatively, Its main disadvantage is the lack of
flexibility in patients on long acting insulin as there is a significant risk of producing
528 D . S. J. Maw

nocturnal hypoglycaemia if the patient is unable to take a normal diet. Intravenous

dextrose should be given as already described but stronger solutions will be needed to
replace the carbohydrate load at mealtimes. An intravenous infusion rate of 500 ml
5% dextrose every 6 hours will provide 100 g dextrose per day (less if dextrose-saline
is used) and extra bolus injections of between 30 and 50 g dextrose will be necessary to
cover the main mealtimes, depending on the patient’s normal diet. These injections
should be spread over about a 2-hour period in an attempt to simulate the normal
smooth absorption of carbohydrate administered orally.

Delayed insulin administration until after operation with no intravenous dextrose

This technique is useful for patients who are known not to be prone to ketosis and
who are undergoing relatively minor surgical procedures (e.g. herniorrhaphy).
A pre-operative blood sugar should be obtained to check that the patient is not
hypoglycaemic. The operation can then take place without prior administration of
insulin.
Postoperatively when the patient is able to take oral fluids, the normal dose of
insulin is administered unless one of the main meals has been missed in which case
two-thirds of the usual dose should be prescribed. In cases where mixtures of insulin
are being used the reduction should be made more from the long acting than the short
acting preparation.

Postoperative parenteral nutrition

If the patient has had a major operation or has a severe illness, more prolonged periods
of parenteral nutrition may be necessary. Under these circumstances an intravenous
cannula should be placed into one of the large veins and adequate parenteral nutrition
should be prescribed ; commercially available preparations should be used to ensure
that adequate protein and fat are available as a source of calories, in addition to
approximately 150-200 g dextrose per 24 hours. This will require the administration of
soluble insulin at regular intervals twice or three times daily and possibly small
amounts of isophane insulin to ensure the smooth control.
Surgery should not be undertaken in the presence of diabetic ketosis unless there
is an immediate life threatening condition. The patient should wherever possible be
stabilised over a period of some hours and then reassessed as it may well turn out that
the condition thought to be a surgical emergency was, in fact, part of the picture of
diabetic ketosis the signs of which may include abdominal pain, vomiting, and re-
duced bowel sounds.

Pregnancy
Special precautions need to be taken in pregnant diabetics who are having a caesarean
section. The insulin demand drops within a couple of hours of delivery to the pre-
pregnancy level; if a caesarean section is being undertaken in the morning, the normal
pre-pregnancy dose of insulin should be administered rather than the dose that the
patient has been requiring over the previous few days. If operation is being deferred
until lunchtime or early afternoon, the current dose of soluble insulin may be ad-
ministered (but not isophane) and a close watch should be kept for postoperative
hypoglycaemia.
 Emergency management of diabetes mellitus 529

Summary
Some of the acute metabolic derangements of unstable diabetes have been discussed.
The management of patients undergoing surgical operations has also been considered.
No problems are usually encountered in diabetic patients treated with diet alone or
with oral hypoglycaemic compounds, although chlorpropamide may need to be
stopped sometime before operation. Patients receiving insulin therapy should be
stabilised pre-operatively on a regimen which will allow more flexible management
during operation and in the postoperative period; this can be readily performed by
placing the patient on soluble insulin and giving spaced dosages. Other routines may
be used for minor procedures.
Adequate supplies of carbohydrate should be given in the form of intravenous
dextrose and under no circumstances should oral glucose be given in the 6 hours
before operation.

Acknowledgments
The author wishes to thank Dr R. C. King and Dr M. S. Everest for their helpful
criticism and Mrs L. J. Gosling for secretarial assistance.

References
1. FLETCHER, J., LANGMAN, M.J.S. & KELLOCK, T.D. (1965) Effects of surgery on blood sugar levels
in diabetes mellitus. Lancet, 2, 52.
2. OAKLEY, W.G., PYKE,D.A. & TAYLOR, K.W. (1968) Clinical diabetes and its biochemical basis.
Blackwell Scientific Publications, Oxford.
3 . MARRLE, A., WHITE,P., BRADLEY, R.F. & KRALL, L.P. (1971) Joslin’s diabetes mellitus, 11th edn.
Lea and Febiger, Philadelphia.
4. BLACK,K.O. & KING,R.C. (1971) Anaesthesia in diabetes mellitus. In: General Anaesthesia,
(Ed. by T. C. Gray and J. F. Nunn), 3rd edn, Vol. 2, p. 54. Butterworths, London.
5. ALBERTI, K.G.M., HOCKADAY, T.D.R. & TURNER,R.C. (1973) Small doses of intramuscular
insulin in the treatment of diabetic ‘coma’. Lancet, 2, 515.