CLINICAL REPORT
Pituitary apoplexy during general anesthesia in beach chair
position for shoulder joint arthroplasty
Tokito Koga • Mariko Miyao • Masami Sato •
Kiichi Hirota • Masahiro Kakuyama •
Hiroko Tanabe • Kazuhiko Fukuda
Received: 15 December 2009 / Accepted: 26 February 2010 / Published online: 26 March 2010
 Japanese Society of Anesthesiologists 2010
Abstract Pituitary apoplexy is a rare but potentially life-
threatening clinical syndrome caused by the sudden
enlargement of pituitary adenoma secondary to infarction
and/or hemorrhage. It may be the first presentation of
previously undiagnosed pituitary adenoma. Although var-
ious precipitating factors of pituitary apoplexy are indi-
cated, the pathogenesis remains unknown. In this report,
we describe for the first time a case of pituitary apoplexy
developed explicitly during general anesthesia supple-
mented with interscalene brachial plexus block in beach
chair or barbershop position for shoulder joint arthroplasty.
Keywords Beach chair position  Complication 
Interscalene brachial plexus block  Pituitary apoplexy
Introduction
Pituitary apoplexy (PA) is a clinical syndrome resulting
from acute hemorrhage or necrosis or both of a preexisting
pituitary adenoma. PA was first described in 1898 [1], but
the concept of the disease was only established in 1950 [2].
The precipitating factors have been categorized into four
components [3], namely, those associated with reduced
blood flow, an acute increase in blood flow, stimulation of
the pituitary gland, and the anticoagulated state.
In this report, we describe for the first time a case of PA
in a patient that developed explicitly during general anes-
thesia supplemented with an interscalene brachial plexus
block in the beach chair or position during shoulder joint
arthroplasty.
Case report
A 60-year-old male patient with persistent shoulder pain
and stiffness was admitted to our hospital for shoulder joint
arthroplasty. The patient was 183 cm tall and had a body
weight of 72 kg. He had a 5-year history of diabetes mel-
litus and was being treated with insulin and glimepride.
Four years prior, the patient had undergone anterior
transvertebral herniotomy for cervical disc herniation.
Physical examination at admission revealed that the patient
still had numbness in his left upper limb. He had no history
of headache.
Preoperative blood pressure (BP) was 130/75 mmHg in
the supine position. After the patient had been administered
an interscalene brachial plexus block with 30 ml of 0.5%
ropivacaine, general anesthesia was induced by the admin-
istration of 8% sevoflurane, 50 mg propofol, 0.25 l/kg/min
remifentanil, and 45 mg rocuronium. Anesthesia was main-
tained with 1.5–2% sevoflurane and 0.15–0.05 l/kg/min
remifentanil. Immediately after the patient was placed in the
beach chair position, BP measured in the upper arm
decreased to 60/36 mmHg for\5 min; this was treated with
ephedrine administration. After the episode, the BP
remained in the 90- to 100-mmHg systolic range for the
remainder of the anesthesia. Oxygen saturation was 100%,
T. Koga  M. Miyao  M. Sato  K. Hirota (&) 
M. Kakuyama  H. Tanabe  K. Fukuda
Department of Anesthesia, Kyoto University Hospital,
54 Shogoin-Kawaracho, Sakyo-Ku, Kyoto 606-8507, Japan
e-mail: hif1@mac.com
K. Hirota
Day Surgery Unit, Kyoto University Hospital,
Sakyo-Ku, Kyoto, Japan
Present Address:
T. Koga
Department of Anesthesia, Saku Central Hospital, Saku, Japan
123
J Anesth (2010) 24:476–478
DOI 10.1007/s00540-010-0929-y

and end tidal CO2 values were in the 30 s range throughout
the anesthesia. There was little estimated blood loss, and a
total of 1250 ml of crystalloid fluid was infused during the
6 h and 1 min of anesthesia. Immediately upon emerging
from anesthesia, the patient’s BP was 140/87 mmHg in the
supine position.
Upon arrival in the post-anesthesia care unit (PACU),
the patient complained of a severe headache limited to the
right side. The headache was persistent even after the
administration of the nonsteroidal anti-inflammatory drug
flurbiprofen. Despite the severe headache, the patient was
free of neurological symptoms, such as anisocoria, visual
disturbance, nuchal rigidity, abnormal reflex, ocular palsy,
visual disturbance, nausea, and vomiting. He was able to
walk in a straight line unaided. After a 2.5-h stay in the
PACU without remission of headache, the patient was
moved to the ward. The headache persisted at 3.5 h after
emergence from anesthesia, and the patient complained of
nausea and vomited. At 4 h after anesthesia, the patient
underwent a computed tomographic scan (CT) screening to
rule out intracerebral hemorrhage, subarachnoid hemor-
rhage, or infarction. A supraseller mass was visible on the
CT scan (Fig. 1). On post-operative day (POD) 1, a follow-
up magnetic resonance imaging (MRI) study revealed a
2.5 9 1.5-cm supraseller mass extending into the right
cavernous sinus (Fig. 2), leading to a diagnosis of PA. The
results of laboratory tests indicated mild hyponatremia
(133 mEq/L). The results of endocrine studies performed
on POD 1, including thyroid function tests, luteinizing
hormone, follicle stimulating hormone, cortisol, and pro-
lactin, were all within normal limits, indicating the ade-
noma was non-functional. On POD 2, the patient developed
anisocoria (Rt 2.5 mm; Lt 2.0 mm), right ptosis and oph-
thalmoplegia, and palsy of the third nerve without any
general abnormality, such as hemiparesis. On POD 16, the
patient underwent successful transsphenoidal hypophysec-
tomy. Pathological evaluation of the surgical specimen
revealed an infarcted pituitary adenoma with hemorrhage
surrounding the tumor. The finding led to the final diag-
nosis of PA due to tumor infarction followed by hemor-
rhage of a non-functional pituitary adenoma. The
subsequent clinical course and recovery were uneventful.
The patient was discharged day 34 following the devel-
opment of the PA. At the 2-month follow-up, he showed a
gradual recovery of ophthalmoplegia.
Discussion
Pituitary apoplexy is a clinical syndrome resulting from
acute hemorrhage or necrosis, or both, of a preexisting
pituitary adenoma. The pathological syndrome is charac-
terized by headache, visual activity, visual field defect,
ocular palsy, nausea and vomiting, altered mental status,
and hemiparesis. During an acute episode, the expanding
pituitary mass may compress the surrounding structures,
namely, the cavernous sinus and neurovascular bundle,
resulting in cranial nerve palsies and ophthalmoplegia. A
review of published case reports in the English literature
from 1990 to 2006 revealed 97 reported cases of PA. The
precipitating factors were divided into stimulation of the
pituitary gland/tumor, surgery, anticoagulant therapy, head
injury, radiation therapy, and other miscellaneous causes.
Among the 40 patients in whom surgery was implicated as
a precipitating factor, 22 had undergone cardiac surgery,
six had pituitary surgery for large tumors, 11 had under-
gone other surgical procedures, and one had spinal anes-
thesia [1, 4–7]. Patients undergoing cardiac surgery seem
to be at higher risk than those undergoing other types of
surgery [5], possibly due to the frequent use of anticoag-
ulant therapy, cardiac bypass, and more severe hypotension
among this patient group.
Fig. 1 Sagittal computed tomographic image scanned on the show-
ing a supraseller mass (arrow) in a 60-year-old man who underwent
shoulder joint arthroplasty
Fig. 2 Coronal T2-weighted magnetic resonance imaging scan
showing a 2.5 9 1.5-cm supraseller mass (arrow) extending into
the right cavernous sinus in a 60-year-old man who underwent
shoulder joint arthroplasty
J Anesth (2010) 24:476–478 477
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