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8 Correspondence anaesthetic, but had then developed a twitching of his left arm which subsequently resolved. A diagnosis of a focal seizure with retained consciousness was made by a consultant physician who di d not consider that a n EE G or CT scan were indicated in the absence of focal signs or unprovoked seizures. To date the patient has suffered no further episodes. We believe this case to be of interest for three reasons. Firstly, this report would seem to be the first describing a purely focal event occurring without loss of consciousness. Seizures in the postoperative period following enflurane anaesthesia are well documented [ 141 However, there has been only one previous report of a seizure without loss of consciousness, and this consisted of generalised myoclonic jerks [5]. Secondly, there is the possibility of an interaction with methocarbamol which is promoted for the treatment of acute musculoskeletal disorders, and has a plasma half-life of 2 h [6]. There have been two cases of convulsions following methocarbamol reported to the Committee on Safety of Medicines (Personal communication Ms S. Faithful, Wyeth Laboratories). It seems unlikely, given the short half-life, that methocarbamol was exerting any pharmacological effect in the patient reported at the time of the anaesthetic. However, since he had suffered a focal seizure, a continuin g electrical susceptibility to a recurrenc e may have remained at the time enflurane was administered. Thirdly, there is evidence that diazepam may potentiate enflurane induced electroencephalographic seizure activity [3], and some have concluded that phenytoin or valproate should be used to treat enflurane induced seizures [5]. I n our case diazepam eventually controlled the seizure, although only after repeated doses totalling 30 mg. Whilst it is possible the patient is harbouring a focal structural lesion, we think this unlikely. He has not developed any focal signs on follow-up, and his seizures only occurred when he was exposed to known epileptogenic drugs. Unusual reactions to drugs may have implications for the anaesthetic technique. Royal Berkshire Hospital. Reading RGI 5AN T.J. PARKE R.H. JAGO References [I] ALLAN MWB. Convulsions after enflurane. Anaesthesia 1984; [2] YAZJI NS, SEED F . Convulsive reaction following enflurane 3 9 05-6. anaesthesia. Anaesthesia 1984; 3 9 1249. seizure activity following enflurane anesthesia. Anesthesiology [4] NICOLL JMV. Status epilepticus following enflurane [5] JENKINS , MILNE C. Convulsive reaction following enflurane [6] GOODMAN S GILMAN , eds. The pharmacological basis of [3] KRUCZEK LBIN MS WOLF S BERTON1 JM. Postoperative 1980; 53: 175-6. anaesthesia. Anaesthesia 1986; 41: 927-30. anaesthesia. Anaesthesia 1984; 3 9 4-5. therapeutics, 4th edn. Macmillan, 1970: 226-9. Methaemoglobinaernia and pulse oximetry We were interested to read the letter ‘Prilocaine associated methaemoglobinaemia and pulse oximeter’ by Marks and Desgrand Anaesthesia 1991; 6 : 703). The authors state that after surgery had begun the patient appeared dusky and ‘the pulse oximeter showed a saturation of 75 ’. They also make the observation that the methaemoglobin level was 6.6%. These statements are misleading because in the presence of severe methaemoglobinaemia, the pulse oximeter reading tends towards 85 . Pulse oximeter readings in the presence of methaemoglobin causes a shift towards 85 and do not usually go below this value. The reason this shift occurs is explained by the fact that methaemoglobin absorbs strongly at both the oxyhaemoglobin wavelength (940 nm) and deoxyhaemoglobin wavelength (660 nm). The pulse oximeter determines the ratio of pulsatile absorbances at these two wavelengths and as the ratio approaches unity, the pulse oximeter saturation becomes 85 . Hence in situations of severe methaemoglobinaemia, the patient may have drastically reduced saturation in the presence of less alarming oximeter saturation readings. Furthermore, studies in dogs indicate th at pulse oximeters begin to show spurious readings at a methaemoglobin level o f about 30-35%, at which values the readings are 82-85% and then become virtually, independent of the methaemoglobin level [ 1, 2 1 . Therefore, the cited patients’ m ethaemoglobin level was not significant enough substantially to alter pulse oximeter readings and hence another explanation must exist for her observed saturation reading of 75 . Southwestern Medical Center, L. ELWOO Dallas, Texas 75235-9068, D. OFLAHERTY USA E.J. PREJEAN M. POPAT A.H. GIESECKE References [I] BARKER SJ, TREMPER KK, HYATT J . Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 1989; 70 1 12-7. [2] DELWOOD , OFLAHERTY D, PREIE N EJ. Methemo- globinemia and its effects on pulse oximetry. Critical Care Medicine 1991; 19 988. Nitrous oxide should not be used during laparoscopy nor during other abdominal operations I write to second Dr G Verheecke’s questioning of the wisdom of the use of nitrous oxide during laparoscopic cholecystectomy Anaesthesia 1991; 6 : 698). For 25 years anaesthetists (and ‘anaesthesiologist s’ ) seem to have ignored, and seem to be continuing to ignore, the important work of Eger and his team at the University of California as quoted by Dr Verheecke. Eger showed that the administration of nitrous oxide makes the intestines increase in size because nitrous oxide, with its high solubility, gets into the bowel faster than the normal bowel gases (nitrogen and methane) can get out. There have been even more recent papers confirming Eger’s ideas, yet anaesthetists all over the world continue to administer nitrous oxide as if it were required by our religion, even in operations when we know that its administration is going to make the bowel size greater and, therefore, make the surgeons’s job harder Dr Verheecke asks ‘Why not avoid nitrous oxide by using total intravenous anaesthesia’? That may be all very well, but I would ask too, ‘Why not use old-fashioned
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8 Correspondence

anaesthetic, but had then developed a twitching of his left

arm which subsequently resolved. A diagnosis of

a

focal

seizure with retained consciousness was made by a

consultant physician who did not consider that a n EE G or

CT scan were indicated in the absence of focal signs or

unprovoked seizures. To date the patient has suffered no

further episodes.

We believe this case to be of interest for three reasons.

Firstly, this report would seem to be the first describing a

purely focal event occurring without

loss

of consciousness.

Seizures in the postoperative period following enflurane

anaesthesia are well documented

[141

However, there has

been only one previous report of a seizure without loss of

consciousness, and this consisted of generalised myoclonic

jerks [5].

Secondly, there is the possibility of an interaction with

methocarbamol which is promoted for the treatment of

acute musculoskeletal disorders, and has a plasma half-life

of 2

h

[6]. There have been two cases of convulsions

following methocarbamol reported to the Committee on

Safety of Medicines (Personal communication Ms S.

Faithful, Wyeth Laboratories). It seems unlikely, given the

short half-life, that methocarbamol was exerting any

pharm acolog ical effect

in

the patient reported a t the time of

the anaesthetic. However, since he had suffered a focal

seizure, a continuin g electrical susceptibility to a recurrenc e

may have remained at the time enflurane was administered.

Thirdly, there is evidence that diazepam may potentiate

enflurane induced electroencephalographic seizure

activity [3], and some have concluded tha t phenytoin

or

valproate should be used to treat enflurane induced

seizures [5]. In our case diazepam eventually controlled the

seizure, although only after repeated doses totalling

30

mg.

Whilst it is possible the patient is harbouring a focal

structural lesion, we think this unlikely. He has not

developed any focal signs on follow-up, and his seizures

only occurred when he was exposed to known epileptogenic

drugs. Unusual reactions to drugs may have implications

for the anaesthetic technique.

Royal Berkshire Hospital.

Reading RGI 5AN

T.J . PARKE

R.H. JAGO

References

[I] ALLANMWB. Convulsions after enflurane. Anaesthesia 1984;

[2]

YAZJI

NS,

SEED

F. Convulsive reaction following enflurane

39 05-6.

anaesthesia. Anaesthesia 1984; 39 1249.

seizure activity following enflurane anesthesia. Anesthesiology

[4]

NICOLL

JMV. Status epilepticus following enflurane

[5]

JENKINS

, MILNE

C.

Convulsive reaction following enflurane

[6]

GOODMAN

S GILMAN, eds. The pharmacological basis

of

[3] KRUCZEK

LBINMS WOLFS BERTON1

JM. Postoperative

1980; 53: 175-6.

anaesthesia.

Anaesthesia

1986;

41:

927-30.

anaesthesia.

Anaesthesia

1984;

39

4-5.

therapeutics, 4th edn. Macmillan, 1970: 226-9.

Methaemoglobinaernia and pulse oximetry

We were interested to read the letter ‘Prilocaine associated

methaemoglobinaemia and pulse oximeter’ by Marks and

Desgrand

Anaesthesia

1991;

6:

703). The authors state

that after surgery had begun the patient appeared dusky

and ‘the pulse oximeter showed a saturation of

75 ’.

They

also make the observation that the methaemoglobin level

was 6.6%. These statements are m isleading because in the

presence of severe methaemoglobinaemia, the pulse

oximeter reading tends towards 85 .

Pulse oximeter readings in the presence of

methaemoglobin causes a shift towards

85

and do not

usually go below this value. The reason this shift occurs is

explained by the fact that methaemoglobin absorbs

strongly at both the oxyhaemoglobin wavelength

(940

nm)

and deoxyhaemoglobin wavelength (660 nm). The pulse

oximeter determines the ratio of pulsatile absorbances at

these two wavelengths and as the ratio approaches unity,

the pulse oximeter saturation becomes

8 5 .

Hence in

situations of severe methaemoglobinaemia, the patient may

have drastically reduced saturation in the presence

of

less

alarming oximeter saturation readings. Furthermore,

studies in dogs indicate th at pulse oximeters begin to show

spurious readings at a methaemoglobin level

of

about

30-35%, at which values the readings are 82-85% and then

become virtually, independent of the methaemoglobin

level

[

1, 21. Therefo re, th e cited patients’ m ethaem oglobin

level was not significant enough substantially to alter pulse

oximeter readings and hence another explanation must

exist for her observed saturation reading of 75 .

Southwestern Medical Center,

L. ELWOO

Dallas, Texas 75235-9068,

D . O F L A H E R T Y

U S A

E.J.

PREJEAN

M. POPAT

A.H. GIESECKE

References

[I]

BARKER

SJ,

TREMPER

KK, HYATT J . Effects of

methemoglobinemia on pulse oximetry and mixed venous

oximetry. Anesthesiology 1989; 7 0

1

12-7.

[2]

DELWOOD

, OFLAHERTY

D,

PREIE N

EJ.

Methemo-

globinemia and its effects

on

pulse oximetry.

Critical Care

Medicine

1991;

19

988.

Nitrous oxide should not be used during laparoscopy nor during other abdominal operations

I write to second Dr

G

Verheecke’s questioning

of

the

wisdom of the use of nitrous oxide during laparoscopic

cholecystectomy

Anaesthesia

1991; 6: 698).

For 25 years anaesthe tists (and ‘anaesthesiologists’ )

seem to have ignored, and seem to

be

continuing to ignore,

the important work of Eger and his team at the University

of California as quoted by Dr V erheecke. Eger showed that

the administration of nitrous oxide makes the intestines

increase in size because nitrous oxide, with its high

solubility, gets into the bowel faster than the normal bowel

gases (nitrogen and methane) can get out. There have been

even more recent papers confirming Eger’s ideas, yet

anaesthetists all over the world continue to administer

nitrous oxide as if it were required by our religion, even in

operations when we know that its administration is going

to make the bowel size greater and, therefore, make the

surgeons’s job harder

Dr Verheecke asks ‘Why not avoid nitrous oxide by

using total intravenous anaesthesia’? That may

be

all very

well, but

I

would ask too, ‘Why not use old-fashioned

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8/16/2019 laparoskopi N2O

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general anaesthesia with 1.0 or 1.5 MAC

in oxygen,

of a

good strong volatile agent?’ In the recent British literature,

a report even show ed tha t during colonic surgery, the use

of nitrous oxide actually

delayed

the recovery of bowel

function and the patients’ discharge from hospital [I].

My appeal to your readers, and my advice is, eschew

nitrous oxide in all abdominal cases. Just increase the

amount of the volatile agent by 50 . Patients may take

120

s

more to awaken but your surgeons will praise you

1393 Oak Avenue

Los Altos

Calijornia 94024

U S A

Correspondence

81

D.V. THOMAS

Reference

[ I ]

S C H E I N I N

, LIDGREN, SCHEININM. Perioperative nitrous

oxide delays bowel function after colonic surgery.

British

Journal o Anaesthesia 1990; 6 : 154-8.

Heel blisters and epidural analgesia for postoperative pain relief

We would like to highlight a hazard inherent in continuous

epidural analgesia techniques for postoperative pain relief.

Con tinuou s epidural analgesia fo r the first 24 to 48 h

postoperatively is routine in

our

hospital for the provision

of postoperative pain control in patients undergoing m ajor

gynaecological or abdomina l surgery returning to the ward.

The technique emplo yed is bupivaca ine 0.1 solution with

added fentanyl (2 pg.ml-’) infused epidurally at a rate of

10-12 m1.h-’. This usually results in an excellent sensory

block with preservation of motor function. Patients are

actively encouraged to move their legs frequently as

prophylaxis against deep venous thrombosis.

Over the past year, there have been 12 patients w ho have

suffered from severe heel blisters after surgery. On

questioning these patients,

all

have actively flexed and

extended their knees while immobilised in bed. This has

obviously resulted in friction burns to the skin over the

heels, but because of senso ry analgesia n o pain is felt while

tissue damage is occurring. We would recommend either

the use of heel pads

or

alternatively static isotonic

contraction exercises of the calf muscles postoperatively in

patients having c ontin uou s epidural analgesia.

University College Hospital,

Galway,

Ireland

D.P. O’TOOLE

E. O’DWYER

Epidurals: a comparison of approaches

The article by Mannion et al. Anaesthesia 1991; 4 6

585-7)

makes no mention as to whether the epidurals were

performed by the midline or paramedian approach. The

paramedian a pproach has been shown by Jaucot [I] to

have a significantly lower incidence of vessel catheterisation

by the catheter (1.5 versus 5.6% for the midline

approach). Blomberg

et al.

[2] did not show any difference

in their study, but they only looked at

50

epidurals.

Jaucot [ I ] suggests the lower incidence of vessel

catheterisation with the paramedian approach is due to the

proximity of the venou s plexi which lie on either side of the

midline. If the point of entry of the needle is paraspina l the

catheter runs up between the two plexi. Certainly, the

course of an epidural catheter introduced by the midline

route is diverse and unpredictable, whereas the catheter

appears to travel in a straight cephalad direction when the

param edian appr oac h is used [3]. If the e pidurals in

Mannion et al.’s study were performed in the midline, then

the incidence of complications from epidural analgesia

could be further reduced by e ncouraging the greater use of

the paramedian technique.

University Hospital o Wales,

Cardif f CF4 4X W

M.R.W STACEY

References

[I] JAUCOT. Paramedian approach of the peridural space in

obstetrics. Acta Anaesthesiologica Belgica 1986; 37: 187-92.

[2] BLOMBERG

G,

JAANIVALD, WALTHER. Advantages of the

paramedian approach for lumbar epidural analgesia with

catheter technique. Anaesthesia 1989; 44:742-6.

[3] GAYNOR

.

The lumbar epidural region: anatomy and

approach. In: REYNOLDS. Epidural and spinal blockade in

ohstetrics. Bailliere Tindall. 1990: 3-

18.

Oversedation with patient controlled analgesia

The evaluation of the Graseby PCAS machine by r

Jackson et al. Anaesthesia

1991; 4 6 482-5) includes a

description of the green light on the machine, used by

patients to maximise the delivery of opioid in anticipation

of painful procedures. We too have found the light to w ork

to the patient’s advantage; however, caution must be

exercised in counselling patients as the following case

illustrates.

A 47-year-old patient with carcinoma of the rectum was

admitted for proctectomy and hysterectomy. She had no

relevant medical or surgical history. General anaesthesia,

supplemented by epidural analgesia via a lumbar catheter

was uneventful and the initial postoperative course was

satisfactory; analgesia was maintained with an infusion of

bupivacaine 0.167% and diamorphine 0.2 mg.ml-’ at

4

m1.h-I. Patient-controlled analgesia (PCA) was

substituted after 16 h as pain resulted fro m the acc idental

removal of the epidural catheter. A full explanation of the

use of PCA including the function of the green light was

given to the patient who apparently understood.

Satisfactory analgesia was resumed using morphine, with a

loading dose of 5 mg, a bolus of mg, and a lockout

interval of 5 rnin. The patient was comfortable when

reviewed 2 h late r.

We saw the patient the following morning when the

nursing staff remarked on unusual drowsiness. On

examination, she was sedated but rousable and sensible;

respiratory r ate was 13 beat.min-l. She denied pain except

on movement . She had used 9 6 mg of m orphine in 20 h

(30 mg in the last 4 h). During o u r examination the patient

noticed the green light had become illuminated and she

immediately pressed the button. On further questioning, it

was clear that she thought that the green light was an

indicator to request more analgesia to stay pain free. After