Full text of DOI:10.1007/BF03017899

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GENERAL ANESTHESIA
Probable gas embolism during operative hys-
teroscopy caused by products of combustion
[Probabilité d’embolie gazeuse causée par des produits de combustion pendant
l’hystéroscopie peropératoire]
Ngozi Imasogie FRCA, Ron Crago FRCPC, Nicholas A. Leyland FRCSC, Frances Chung FRCPC
Purpose: Gas embolism is a rare but well documented entity dur-
ing operative hysteroscopy, with an incidence of 10–50%.
Catastrophic outcomes occur at a rate of three in 17,000 proce-
dures. The purpose of this report is to present a non-fatal case of
gas embolism probably caused by the gaseous products of com-
bustion.
Clinical features: A 50-yr-old woman with a history of menor-
rhagia was scheduled for hysteroscopy and endometrial ablation
and polypectomy. Fifteen minutes into the procedure, with the
patient in lithotomy position, 20° head down tilt, and breathing
spontaneously, a sudden oxygen desaturation occurred from 97%
to 87%. The patient’s end-tidal carbon dioxide dropped from 46
mmHg to 27 mmHg. The patient’s breathing pattern remained
normal, respiratory rate remained 11–12 breaths·min–1 but ampli-
tude of the reservoir bag movement was increased. Cardiovascular
variables remained stable. She responded rapidly to 100% oxygen
and made an uneventful recovery. Having ruled out other possible
causes, we concluded gas embolism was responsible for the fall in
oxygen saturation and end-tidal CO2.
Conclusion: With all the precautions in place to minimize the like-
lihood of fluid overload and ambient air embolism occurring, we
surmised that products of combustion were the cause of the gas
embolism. During endometrial ablation, gaseous products of com-
bustion, mainly carbon dioxide, accumulate. The gases may then
contribute to the rise in uterine pressure that occurs as irrigation
fluid enters the uterus and this rise in pressure in turn encourages
passage of gas into the open venous sinuses.
présenter un cas d’embolie gazeuse non mortelle causée probable-
ment par des produits de combustion gazeux.
Éléments cliniques : Une femme de 50 ans présentant des antécé-
dents de ménorragie devait subir une hystéroscopie et l’ablation de
l’endomètre ainsi qu’une polypectomie. Quinze minutes après le début
de l’opération, la patiente en position de lithotomie, avec inclinaison de
20° et tête vers le bas, respirait spontanément quand est survenue une
soudaine désaturation en oxygène qui est passé de 97 % à 87 %. Le
gaz carbonique télé-expiratoire du patient a chuté de 46 mmHg à 27
mmHg. Le type de respiration est demeuré normal, le rythme respira-
toire était de 11–12 respirations·min–1, mais l’amplitude du mouve-
ment du sac-réservoir a augmenté. Les variables cardiovasculaires
étaient stables. La patiente a réagi rapidement à l’administration de
100 % d’oxygène et s’est bien rétablie. Après avoir exclu d’autres
causes possibles, nous avons conclu qu’une embolie gazeuse avait
causé la chute de saturation en oxygène et le CO2 télé-expiratoire.
Conclusion : Considérant toutes les précautions mises en place pour
minimiser la probabilité d’une surcharge liquide et d’une embolie à l’air
ambiant, nous avons supposé que les produits de combustion étaient
la cause de l’embolie gazeuse. Pendant l’ablation de l’endomètre, des
produits de combustion gazeux, surtout du gaz carbonique, s’accu-
mulent. Les gaz peuvent ainsi contribuer à l’élévation de la pression
utérine qui survient au moment où le liquide d’irrigation pénètre dans
l’utérus. Cette hausse de pression favorise le passage de gaz dans les
sinus veineux.
AS embolism during operative hys-
teroscopy is a rare but well described enti-
ty1–12 with an incidence ranging from
Objectif : L’embolie gazeuse est un état pathologique rare, mais bien
documentée, survenant pendant l’hystéroscopie peropératoire selon
une incidence de 10–50 %. Des conséquences catastrophiques sur-
viennent dans trois interventions sur 17 000. Nous avons voulu
2,3
G
10–50%.
The true incidence is not
known but catastrophic outcomes occur at a rate of
three in 17,000 procedures.13 The source of the gas
From the Department of Anesthesia, Toronto Western Hospital, University Health Network, University of Toronto, Toronto, Ontario,
Canada.
Address correspondence to:Dr. Ron Crago, Department of Anesthesia, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario
M5T 2S8, Canada. Phone: 416-603-5118; Fax: 416-603-6494; E-mail: ron.crago@uhn.on.ca
Accepted for publication April 25, 2002.
Revision accepted August 14, 2002.
CAN J ANESTH 2002 / 49: 10 / pp 1044–1047

Imasogie et al.: GAS EMBOLISM DURING HYSTEROSCOPY
1045
breaths·min–1 and the breathing pattern showed no
signs of obstruction. The heart rate rose from 66 to
77 beats·min–1 and blood pressure increased to 94/63
from 88/53 mmHg.
may be ambient air which enters the uterine cavity
during the procedure,13–15 or air bubbles within the
distension fluid.13,15 Alternatively, the embolic gas may
be carbon dioxide and carbon monoxide, evaporative
products of combustion as surgery proceeds.2,13 In
this case report we describe a non-fatal case of gas
embolism which we think was due to gaseous prod-
ucts of combustion.
The surgeon was immediately informed, the proce-
dure was rapidly completed and the patient returned
to the supine position. Manually assisted ventilation
was commenced with 100% oxygen. Auscultation of
the chest was clear and no heart murmurs were heard.
In less than five minutes, oxygen saturation rose to
96% and the patient resumed spontaneous ventilation
while emerging from anesthesia. In the postanesthesia
care unit, the patient was awake and alert with blood
pressure 122/73 mmHg, pulse 63 beats·min–1, respi-
ratory rate 18 breaths·min–1, and SpO2 99%. The
patient was observed for four hours in the ambulatory
surgical unit and then discharged home.
Case report
A 50-yr-old, 76.5 kg woman, with a history of men-
orrhagia, was scheduled for hysteroscopy, endometrial
ablation and polypectomy in our ambulatory surgical
unit. She had a past medical history of hypertension
being treated with guinapril hydrochloride 10 mg
daily. The patient was allergic to sulphonamides. Her
past surgical history included uneventful hemor-
rhoidectomy and a dilatation and curettage. Her phys-
ical
examination
was
unremarkable.
The
Discussion
electrocardiogram and complete blood count were
within normal limits (Hb 137 g·L–1). A preoperative
medication of oral naproxen 500 mg and iv cefazolin
1 g was given following insertion of an iv cannula.
Monitoring was established with the electrocardio-
gram, non-invasive blood pressure, oxygen saturation
(SpO2) and end-tidal carbon dioxide (ETCO2).
Anesthesia was induced with fentanyl 100 µg, propofol
350 mg (aliquots of 200, 50 and 100), followed by
insertion of a size 4 laryngeal mask. Anesthesia was
maintained with spontaneous breathing of nitrous
oxide, oxygen and desflurane. The patient was placed in
a lithotomy position with 20° head down tilt prior to
the start of surgery. The patient’s vital signs were stable
with oxygen saturation being 97–98% and ETCO2
44–48 mmHg. The cervix was dilated to 10 mm with-
out difficulty and the last dilator was left in place until
the Storz 10 mm fibreoptic resectoscope was ready for
insertion into the uterus. The instrument, once insert-
ed, delivers fluid distension medium and removes waste
products simultaneously. The distension fluid Cystosol
(sorbitol 3%, mannitol 0.5% in water, Baxter) was sup-
plied in 3 L bags and infused through Y connectors to
allow change over without risk of air bubbles entering
the system. The bags were placed not more than 1 m
above the patient. Air bubbles were flushed out of the
hysteroscope prior to insertion into the uterus.
Pulmonary embolism occurs from a variety of causes:
venous thrombus, amniotic fluid, fat, tumour, foreign
body, and gases. Gases are particularly relevant during
anesthesia, for example air embolus during neuro-
surgery and carbon dioxide embolus during laparo-
scopic surgical procedures. In the case reported here we
believe gas, in the form of gaseous products of com-
bustion, was the cause of the pulmonary embolism.
Gas embolism is a complication of hysteroscopy
and was first reported in 1985.1 It is a potentially fatal
complication in an otherwise healthy woman.2 In this
patient, the sudden fall in both ETCO2 and SpO2,
hallmarks of pulmonary embolism, suggested the
diagnosis. As there was no measurable deficit in the
input/output of the fluid used for distension, nor any
signs suggestive of fluid overload, “female TURP syn-
drome” was ruled out as a differential diagnosis. We
also eliminated obstructed ventilation since the event
occurred acutely and the patient had been breathing
normally for 15 min via a laryngeal mask airway. Gas
embolism was thus thought to be the cause.
For gas embolism to occur, certain conditions have
to be present:2 open venous channels in contact with
gaseous medium, and an operating site above the level
of the heart creating a pressure gradient. In the case of
gas embolism, an added danger exists in that gas bub-
bles may cross to the systemic circulation either
through the pulmonary vasculature or through a
patent foramen ovale. If these paradoxical emboli are
relatively insoluble (for example, air which is 80%
nitrogen), they may cause ischemia and infarction in
organs such as the heart and the brain.13,14
Fifteen minutes after the start of surgery, there was
a sudden and precipitous drop in SpO2 from 97 to
87% and ETCO2 dropped from 46 mmHg to 27
mmHg. The patient appeared to be developing
cyanosis in spite of larger tidal volumes (the reservoir
bag emptying more than at the start of the proce-
dure). The respiratory rate remained 11–12
Whatever the cause of a pulmonary embolus, the
pathophysiologic consequences are well known. When

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CANADIAN JOURNAL OF ANESTHESIA
the embolus reaches the pulmonary circulation, it
immediately creates lung regions with high ventila-
tion/perfusion (V/Q) ratios (alveolar dead space)
resulting in reduced end-tidal carbon dioxide.
Pulmonary artery blood flow is diverted from
embolized regions to unaffected lung regions which
are then overperfused (lung regions with low V/Q
ratio); this shunt will result in hypoxemia and a
decrease in oxygen saturation. Also, the opening of
latent pulmonary arterial-venous shunts may con-
tribute to the hypoxemia. The mechanical obstruction
from the embolus causes a preload reduction to the
left heart leading to possible hypotension.13
In the case presented, the source of the gas embo-
lus may have been 1) ambient air, if the cervix and the
uterus were left open to air after dilatation;14–16 2) air
bubbles in the fluid distension medium; or 3) carbon
dioxide, carbon monoxide and other particulate prod-
ucts of combustion.14,16 Open venous channels may be
created during dilatation of the cervix for insertion of
the hysteroscope; occult false passages may be created
at the level of the internal os; or partial penetration
into the myometrial wall may occur following forceful
dilatation, leaving blood vessels open.2 Ambient air,
pressurized gas such as CO2 distension gas, or gaseous
products of combustion, may then enter the circula-
tion. Dilatation to 10 mm did occur, however, the last
dilator was left in place until the hysteroscope was
ready for insertion, allowing minimal exposure of the
cervix and uterus to room air. Dilatation was per-
formed without difficulty, so false passage creation in
the lower segment of the uterus was unlikely. The hys-
teroscope, once inserted, had bubble-free fluid medi-
um flowing. Therefore, the chance of room air
embolism was minimal in this case.
Gaseous products of combustion are known to col-
lect during endometrial ablation, and CO2 is a major
component of this gas.12 CO2 even though highly sol-
uble, with a high safety profile17 has been reported by
several authors to be the cause of gas embolism.18,19
Brandner et al. prospectively used Doppler sonogra-
phy to detect both clinical and subclinical gas emboli
during CO2 hysteroscopy.3 They concluded that air
was the cause since flushing the tubing with CO2 prior
to the procedure eliminated gas emboli detected by
the Doppler. Following this report, Penny Gorton20
suggested that liquid distension medium would be
associated with no risk of CO2 embolism since both
CO2 and air would be eliminated. But given that the
products of combustion (CO2) can accumulate and
embolize, use of a fluid medium cannot totally prevent
this complication. The pressure within the uterus rises
as fluid medium flows in, aiding the entry of gaseous
products of combustion into the venous system. CO2
embolism has been reported to be short-lived because
CO2 is highly soluble in blood (54 mL·dL–1).2,14
The time frame of adverse events in our patient is
in keeping with our hypothesis that the products of
combustion, particularly CO2, were responsible for
the gas embolism. As surgery proceeded, and gaseous
products collected, endometrial vessels were simulta-
neously disrupted and venous channels opened. The
slight head down tilt and intra-uterine pressure pro-
vided the pressure gradient allowing the accumulated
gas to rapidly enter the venous system. However,
because CO2 is highly soluble, manual ventilation of
the lungs with 100% oxygen was sufficient to support
the patient until the CO2 was absorbed from the pul-
monary circulation and normal V/Q matching
restored in the lungs.
In summary, we have presented a 50-yr-old woman
who suffered a probable gas embolism during fluid
medium operative hysteroscopy. Having taken precau-
tions to prevent air embolism by gentle dilatation of
the cervix, protection of the cervix and uterus from
ambient air, and flushing air bubbles from the fluid
medium, we believe gaseous products of combustion
from the surgery, alongside venous channels opened
by the surgery, and slight head down tilt, provided the
circumstances which led to gas embolism. The prompt
recovery of the vital signs points to a highly soluble
gas such as CO2 as the cause.
References
1 Cooper JM, Brady RM. Intraoperative and early postop-
erative complications of operative steroscopy. Obstet
Gynecol Clin North Am 2000; 27: 347–66.
2
Stoloff DR, Isenberg RA, Brill AI. Venous air and gas
emboli in operative hysteroscopy. J Am Assoc Gynecol
Laparosc 2001; 8: 181–92.
3 Brandner P, Neis KJ, Ehmer C. The etiology, frequen-
cy, and prevention of gas embolism during CO2 hys-
teroscopy. J Am Assoc Gynecol Laparosc 1999; 6:
421–8.
4 Nachum Z, Kol S, Adir Y, Melamed Y. Massive air
embolism–a possible cause of death after operative hys-
teroscopy using a 32% dextran-70 pump. Fertil Steril
1992; 58: 836–8.
5 Micheal A. Endometrial ablation and air embolism
(Letter). Anaesth Intensive Care 1993; 21: 475.
6 Eugster D. Cardiac arrest during endometrial ablation
(Letter). Anaesth Intensive Care 1993; 21: 891–2.
7 Wood SM, Roberts FL. Air embolism during transcervi-
cal resection of endometrium (Letter). BMJ 1990;
300: 945.
8 Loffer FD. Laser ablation of the endometrium. Obstet

Imasogie et al.: GAS EMBOLISM DURING HYSTEROSCOPY
1047
Gynecol Clin North Am 1988; 15: 77–89.
9 Perry PM, Baughman VL. A complication of hys-
teroscopy: air embolism. Anesthesiology 1990; 73:
546–7.
10 Baggish MS, Daniell JF. Death caused by air embolism
associated with neodynium:yttrium-aluminum- garnet
laser surgery and artificial sapphire tips. Am J Obstet
Gynecol 1989; 161: 877–8.
11 Behnia R, Holley HS, Milad M. Successful early inter-
vention in air embolism during hysteroscopy. J Clin
Anesth 1997; 9: 248–50.
12 Gomar C, Fernandez C, Villalonga A, Nalda MA.
Carbon dioxide embolism during laparoscopy and hys-
teroscopy. Ann Fr Anesth Reanim 1985; 4: 380–2.
13 Isaacson KB. Complications of hysteroscopy. Obstet
Gynecol Clin North Am 1999; 26: 39–51.
14 Spencer MP, Oyama Y. Pulmonary capacity for dissipa-
tion of venous gas emboli. Aerospace Med 1971; 42:
822–7.
15 Brooks PG. Venous air embolism during operative hys-
teroscopy. J Am Assoc Gynecol Laparosc 1997; 4:
399–402.
16 Corson SL, Brooks PG, Soderstrom RM. Gynecologic
endoscopic gas embolism. Fertil Steril 1996; 65:
529–33.
17 Corson SL, Hoffman JJ, Jackowski J, Chapman GA.
Cardiopulmonary effects of direct venous CO2 insuffla-
tion in ewes. A model for CO2 hysteroscopy. J Reprod
Med 1988; 33: 440–4.
18 Ditton JN. Presumed carbon dioxide embolism associ-
ated with hysteroscopy (Letter). Anaesth Intensive
Care 1992; 20: 123–4.
19 Sherlock S, Shearer WA, Buist M, Rasiah R, Edwards A.
Carbon dioxide embolism following diagnostic hys-
teroscopy. Anaesth Intensive Care 1998; 26: 674–6.
20 Gorton P. Hysteroscopy and gas embolism (Letter).
Anaesth Intensive Care 1999; 27: 319.