Address for
Correspondence: Dr Nisha Rajmohan, Consultant
Anaesthetist, Astermedcity. E- mail:
nishavismaya@gmail.com
Keywords: Dilutional hyponatraemia, glycine fluid
overload, operative hysteroscopy, intravascular absorption
syndrome, venous gas embolism
Abstract
Venous gas embolism is a potentially fatal complication during
operative hysteroscopy. Excessive fluid uptake during
operative hysteroscopy with Glycine 1.5% can cause
hyponatraemia, hypo-osmolality, hyperglycinaemia and volume
overload. We present a rare case of venous gas embolism with
Operative Hysteroscopy Intravascular Absorption syndrome
(OHIA) during hysteroscopic myomectomy.
Introduction
Operative hysteroscopy, a widely used procedure is associated
with life threatening complications such as uterine
perforation, haemorrhage, gas or air embolism, sepsis and
fluid overload with hyponatraemia [1,2]. At times a
combination of these complications occur which makes the
diagnosis confusing and management complicated. We present a
case of cardiac arrest probably due to venous gas embolism,
complicated by the presence of operative hysteroscopy
intravascular absorption (OHIA) syndrome.
Case report
A young lady had complaints of menorrhagia since one year. She
was started on haemostatic agents and Tab. Regestrone and
haematinics. Ultrasound showed a 5.8 × 4.9 cm fibroid in the
uterine wall. Her investigations were within normal limits
with serum sodium levels of 138 meq/l and potassium levels of
4.2 meq/l. Two units blood were given to correct anaemia. She
was posted for hysteroscopic myomectomy.
Monitors included electrocardiogram, non-invasive blood
pressure, pulse oximetry, end tidal CO2 and temperature.
Patient was induced with glycopyrrolate 0.2 mg, midazolam 2
mg, ramoseteron 0.3 mg, fentanyl 100 mcg, propofol 80 mg.
Patient was intubated with 7.0 size endotracheal tube after
100 mg of succinyl choline. Anaesthesia was maintained with
nitrous oxide (50%), oxygen (50%), sevoflurane (1%) and
intermittent boluses of atracurium provided the desired
relaxation. The patient was loaded with 500 ml 0.9% saline.
Uterus was distended with glycine 1.5% and the resection of
fibroid was started. Distension pressure was decided by the
minimum pressure required for adequate surgical vision.
One hour after the start of surgery when approximately 2
litres of glycine 1.5% was used, patient developed severe
bradycardia (86/min to 30/min), desaturation (100% to 70%),
hypotension (130/80 mm Hg to 60 /40 mm Hg), hypocarbia (30 mm
Hg to 14 mm Hg) and had a cardiac arrest.
Cardiopulmonary resuscitation was started immediately. She was
resuscitated, ventilated with 100% oxygen and noradrenaline
infusion was started to correct hypotension. Right internal
jugular vein and right radial artery were cannulated. The
central venous pressures were 10-12 cm of water. On
auscultation, chest was clear. Arterial blood gas analysis
showed pH of 7.1, PaO2 of 70 mm Hg, PCO2 65 mm Hg and HCO3 of
12 meq/l, sodium levels of 117 meq/l and potassium of 3.3
meq/l. Calcium and magnesium levels were normal. An
intravenous bolus of sodium bicarbonate 7.5% (50 ml) was
given. The surgery was abandoned after packing the vagina with
wet gauze and the patient shifted to the ICU.
To find out the cause of cardiac arrest an electrocardiogram,
echocardiogram, chest x-ray were asked for and these were
essentially normal. Sodium correction was started as per
protocol with 3% hypertonic saline at the rate of 42 ml/hr,
which increased the sodium level by 0.5 mmol/l/hr till the
sodium level was 120 meg/l after which correction was
continued with 0.9 % saline. Patient was ventilated till fully
awake and was extubated within a few hours. Sodium levels were
corrected over 2 days and she was discharged home after an
uneventful postoperative period.
A retrospective diagnosis of venous air embolism with
Operative Hysteroscopy Intravascular Absorption (OHIA)
syndrome was made. Two months later, she underwent an
uneventful hysteroscopic myomectomy under general anaesthesia
with strict monitoring of ETCO2, SPO2 and arterial blood
pressure and regular sampling of serum electrolytes.
Discussion
VGE is a common complication during operative hysteroscopy
[1]. This can be complicated by Operative Hysteroscopy
Intravascular Absorption (OHIA) syndrome, caused by
intravascular absorption of irrigation fluid during
hysteroscopic surgery [2].
Embolism can occur due to either air (atmospheric air) or gas
(ingress of insufflating gas such as carbon dioxide or smoke
generated during electrothermal procedure) [1]. Embolism of
smoke bubbles can be increased by absorption of irrigating
fluid in excess of one litre [3].
Normally cardiac arrest during TURP/hysteroscopy is
accompanied by volume overload and pulmonary oedema and
arrhythmias such as ventricular tachycardia or ventricular
fibrillation. In this case, we did not encounter any of these.
Hyperkalemia following TURP syndrome could have caused the
cardiac arrest but potassium levels was 3.3. Our initial
diagnosis was a vasovagal attack, which was unlikely because
there were no triggering factor and patient was under deep
planes of anaesthesia. Venous embolism as a cause of asystole
was retrospectively made by exclusion. The supporting
evidences are a fall in BP, SPO2, ETCO2 and cardiac arrest.
Here the venous air embolism was complicated by the presence
of OHIA syndrome. Severe hyponatremia and metabolic acidosis
point to massive absorption of fluid used for uterine
distension. An increased incidence of OHIA syndrome has been
reported in myomectomies [2]. Menstruant women have a high
risk of death and brain damage when they are exposed to modest
hyponatremia and hypo-osmolemia. This is due to the fact that
sex hormones adversely affect the sodium pump in brain cells
leading to cerebral oedema [2].
Metabolic acidosis could have been due to dilution, renal
bicarbonate wasting secondary to auto-volume expansion and
probably related to post cardiac status [5].
The biochemical composition of the instilled fluids determines
the physiologic alterations. Glycine 1.5% when absorbed in
large amounts have been found to be cardiotoxic with
echocardiogram changes, elevation of troponin,
bradyarrhythmias and cardiovascular collapse [6-8]. The use of
Glycine 1.5% might have aggravated the issues in our patients.
Anaesthestic management of these otherwise healthy women
should emphasize the prevention of VGE and OHIA syndrome and
its attendant morbidity and possible mortality.
To prevent VGE, avoidance of Trendelenberg position, nitrous
oxide, ensuring an irrigation system free of air, maintaining
uterine distension pressures to 50-100 mm Hg have been
advocated [1].
To prevent fluid overload fluid deficit has to be calculated
every 10 mins. Accurate calculation of fluid deficit can be
made by the newer automated fluid management systems [2].
Mannitol 5% is safer than glycine. Although regional
anaesthesia is preferred, GA can be given along with regular
monitoring of serum electrolytes. The parotid area sign and
the ethanol breath test can be used as early signs of fluid
overload [9,10]. Bipolar resectoscopes employing normal saline
as distending medium and vaporization techniques are safer
alternatives.
Conclusion
Early detection and prompt management of VAE and massive
absorption of fluid distention medium is important for patient
recovery without neurologic complications. Although treatment
regimens for VAE, hyponatremia, hypo-osmolemia and circulatory
overload are well established, anesthetic management of these
otherwise healthy women should emphasize the prevention of the
OHIA syndrome and VAE and its attendant morbidity and possible
mortality.
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