Peri-operative cardiac arrest secondary to adrenal insufficiency

Published: 08 Sep 2016

http://dx.doi.org/10.21466/ac.PCASTAI.2016

© Anaesthesia C ases / 2016-0177 / ISSN 2396-8397

Authors
Dr Sanjay Bhandari [1]
sanjay.bhandari@wales.nhs.uk
Dr Vincent O'keeffe [2]

[1] C linical Fellow, Anaesthetics and Intensive care, Glan C lwyd hospital, Rhyl, United Kingdom
[2] C onsultant, Anaesthetics and Intensive care, Glan C lwyd hospital, Rhyl, United Kingdom

Summary
We describe a patient who suffered a cardiac arrest preceded by bradyarrhythmia in the
immediate postoperative period and further episodes in the high dependency unit (HDU)
that was secondary to a low cortisol level. The patient was managed with hydrocortisone
replacement following which the condition of the patient improved with no further cardiac
arrests. There are few documented cases of cardiac arrest in the peri-operative period
secondary to undiagnosed cortisol deficiency.

Introduction
We report the case of an anxious 47-year-old ASA 1 physical status male with good
cardiorespiratory function who had repair of a complex abdominal hernia. It was a
prolonged procedure following which he suffered a cardiac arrest preceded by a
bradyarrhythmia. Initially thought to be a severe vasovagal event, he later suffered two
similar episodes. On further investigation, the patient was found to have very low serum
cortisol levels and an equivocal short synacthen test. He was treated with hydrocortisone.
He subsequently had no further episodes of bradyarrhythmias and was discharged home
under the care of the endocrinologists.

Report
A 47-year-old male was scheduled for a complex abdominal hernia repair. His medical
history included a blackout 20 years previously following hernia surgery for which no cause
had been found. He also had a history of a head injury 8 years previously from which he
had recovered quickly with no deficit. He was obese with a BMI of 35.8 and an exercise
tolerance of around 7 MET equivalent.
He was very anxious pre-operatively and, considering his surgery was expected to be
complex and long, he underwent cardiopulmonary exercise testing (C PET) which
demonstrated good cardiorespiratory function with a low predicted mortality; an anaerobic
threshold (AT) of 15.6 ml.kg-1 . min-1 , and maximum oxygen consumption (VO 2 ) of 25.3
ml.kg-1 .min-1 .
On the day of surgery, he was anxious. The anaesthetic plan was discussed and he
consented for a combined spinal and general anaesthetic (GA). All his pre-operative
investigations were within normal limits. He had standard AAGBI monitoring along with
bispectral index (BIS) monitoring. A spinal anaesthestic was performed awake using 2 ml
0.5% heavy bupivicaine and diamorphine 500 mcg following which general anaesthesia
was induced with target controlled infusions of propofol and remifentanil. During the intra-
operative period 6.6 mg dexamethasone, 4 mg ondansetron, 1 g paracetamol and a non-
steroidal anti-inflammatory were administered. The surgery lasted 4 hr during which time
the patient was stable.
At the end of the surgery, the patient had a ultrasound-guided bilateral transverse
abdominis plane (TAP) block using 40 ml 0.25% L-bupivicaine. His trachea was extubated
and he was transferred to the recovery area. Here he became bradycardic (heart rate 30
beats.min-1 ) which was followed by a loss of cardiac output. Atropine 0.6 mg was given
intravenously and cardiopulmonary resuscitation (C PR) commenced. He had a return of
spontaneous circulation in one cycle. The patient regained consciousness and was
transferred to the HDU for overnight monitoring. A 12 lead EC G showed an prolonged QTc
of 467 ms with troponin-T levels not elevated. A trans-thoracic echocardiogram was
normal. Serial EC Gs showed normalisation of QTc.

The following day, the patient had an episode of bradycardia (heart rate 35 beats.min-1 )
which increased following atropine administration. Pain was well controlled with morphine
patient controlled analgesia. The patient stated that he was very dizzy when moving
around in his bed, even though he was adequately hydrated.

A random serum cortisol level was performed which was very low at 11 nmol.l-1 . An
endocrinologist was consulted who advised a short synacthen test and an assay of all
pituitary hormones. The following day, he had another episode of bradycardia (heart rate
30 beats.min-1 ), brief loss of consciousness and a seizure-like episode while moving from
the bed to a chair. This improved immediately on lying supine.
All this happened in the presence of a consultant cardiologist who thought that the episode
was non-cardiac in nature. The short synacthen test was within normal limits (70 - 385
nmol.l-1 ), however the patient had already been commenced on hydrocortisone
replacement when this test was performed. All the other pituitary hormone levels were
within the normal range except for slightly low testosterone levels. Magnetic resonance
imaging (MRI) scan of his pituitary gland was normal.
He was started on hydrocortisone (50 mg four times daily) and started feeling better with
no further episodes of bradycardia.

Discussion
We describe an unusual case in which cardiac arrest was the presenting feature of
corticosteroid deficiency [1-2].
One of the first differential diagnoses was vasovagal syncope augmented by relative
hypovolaemia in the peri-operative setting. This could explain the initial episode in
recovery but similar episodes over the next 48 hr, when the patient was well hydrated and
pain was well controlled, were unlikely to be due to vasovagal syncope. This diagnosis
could have been investigated further with tilt table testing but we found that the patient had
low cortisol levels [3].
The second differential diagnosis was a seizure but there were no seizure-like movements
during the initial episodes. The seizure-like movements during the last episode were
probably secondary to loss of cardiac output.

The third differential diagnosis was local anaesthetic toxicity but the TAP block was
performed under ultrasound guidance by a consultant and a toxic dose had not been
exceeded. Indeed, the incidence of local anaesthetic toxicity following a TAP block is low.
The fourth differential diagnosis was a cardiac cause (ischaemia or arrhythmia) but the
troponin-T rise was not significant and a 24-hr EC G did not show any arrhythmias.
We found that the serum cortisol levels were profoundly low and the patient did not suffer
further episodes after he was commenced on steroid replacement therapy. Glucocorticoids
have a permissive function for catecholamines and therefore are essential. With the
initiation of corticosteroid therapy, catecholamines became effective and led to
haemodynamic stabilisation with no further episodes of bradycardia.
The cause for the cortisol deficiency in our patient might be multifactorial. The patient was
given a dose of dexamethasone intra-operatively and there have been reports of a
depressed cortisol response following a single anti-emetic dose of dexamethasone [4].
The patient had a history of a head injury and may have developed pituitary damage which
could have caused secondary adrenal insufficiency, although the response to the short
synacthen test was normal. In addition, MRI scan of his pituitary gland did not show any
abnormalities.
Laboratory tests to investigate cortisol deficiency include a morning plasma cortisol level.
This is used as a test of exclusion. A level below 83 nmol.l-1 is highly suggestive of adrenal
insufficiency. A cortisol level above 497 nmol.l-1 effectively excludes Addison's disease.
C ortisol levels of 83 to 497 nmol.l-1 require further testing with a high-dose AC TH
(adrenocorticotropic hormone) stimulation test to confirm the diagnosis [2]. If cortisol
levels below 497 nmol.l-1 are found at either 30 or 60 min after AC TH stimulation, the
diagnosis of adrenal insufficiency is highly likely. C ortisol levels exceeding 497 nmol.l-1 at
30 or 60 min after administration of high-dose AC TH (250 mcg) exclude the diagnosis of
primary adrenal insufficiency in most instances; however, some patients with secondary
adrenal insufficiency of recent onset or partial AC TH deficiency may manifest a normal
response. In situations where this is suspected, patients should either have the stimulation
test repeated using a low dose of AC TH (1 mcg) or, preferably, have a test of the entire
hypothalamic-pituitary-adrenal axis (e.g. an insulin tolerance test or the overnight
metyrapone test) [5].

Acknowledgements
C onsent from the patient was sought for publication of this report.

Competing Interests
No external funding and no competing interests declared.

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