Chinese Medical Journal 2007; 120(24):2341-2343
Pituitary apoplexy complicated with subarachnoid hemorrhage
caused by incidentaloma following a head injury: case report
BAO Yi-jun, LI Xin-guo, JING Zhi-tao, OU Shao-wu, WU An-hua and WANG Yun-jie
Keywords: incidentaloma; pituitary apoplexy; subarachnoid hemorrhage
ituitary apoplexy is a rare clinical syndrome caused
by acute enlargement of pituitary adenomas, which
may be secreting or nonfunctioning, and symptomatic or
asymptomatic, resulted from hemorrhage or infarction.1
Subarachnoid hemorrhage (SAH) is an unusual presentation
in patients with pituitary apoplexy, 2 and that following a
head injury is more infrequently reported.3-6 Here, we
report a case of pituitary apoplexy complicated with
subarachnoid hemorrhage caused by an incidentaloma
after head trauma in an aged man, who experienced a
spontaneous regression of the tumor.
A 79-year-old man, who had no history of pituitary
adenoma, was admitted to our hospital because of head
injury. One hour before admission, the patient fell down
accidentally and the occipital region of his head was hurt,
then he was sent to hospital with consciousness, severe
headache, nausea and vomiting. Physical examination
indicated a laceration over the occipital scalp, Glasgow
Coma Scale of 15, neck stiffness, weak movement of
extremities, and negative Barbinski sign; no obvious
changes of visual acuity and field was found. The patient
had histories of primary hypertension, glaucoma,
coronary heart disease, and diabetic mellitus, but never
had evidence of pituitary adenoma, and hypopituitarism
or hypersecretion of the pituitary gland.
One and a half hour after the injury, axial plain CT
showed a high-density lesion at the right frontal lobe, a
heterogeneous mass at the sellar turcica and suprasellar
cistern and SAH around the suprasellar cistern, especially
on the left (Fig. 1A). The cranial CT repeated six hours
after the injury discovered that the SAH was almost
absorbed, and a heterogeneous iso- or hyper-density mass
was found (Fig. 1B). Two weeks later, cranial CT
revealed a right frontal subdural hydroma (not shown);
and non-enhanced MRI demonstrated right frontal
contusion with focal edema (Fig. 2A), a right frontal
subdural hydroma (Fig. 2B), and a heterogeneous
hyper-intensity mass at the sellar region with an elevation
of the optic chiasm on both T1- and T2-weighted images
(Fig. 3, T2WI not shown). A sellar and suprasellar mass
with heterogeneous hyperintense signals was indicated on
non-enhanced coronal and sagittal MRIs (Fig. 3A and C)
and rim enhancement on post-gadolinium-DTPA MRIs
(Fig. 3B and D). In addition, hemorrhage in the sphenoid
sinus (Fig. 3C and D). No aneurysm was found by
cerebral MR angiography (MRA, Figs. not shown).
The patient experienced a long-standing headache.
Hypopituitarism was confirmed by hormonal evaluation
the day after the admission, and then hormone
replacement therapy was applied. Because the patient
rejected surgery, conservative therapy was adopted. He
recovered well and was discharged from hospital after
being suffered from electrolyte disturbance, persistent
fever, pneumonia, and right iliac venous thrombosis for
two months. During an 18-month follow-up, the patient
was in good condition. MRI performed at four months
after the injury suggested the shrinkage of the tumor and
the decompression of the optic chiasm (Fig. 4).
Pituitary apoplexy is a relatively uncommon, yet
potentially life-threatening clinical entity caused by
hemorrhage or massive infarction of pituitary adenomas
that leads to sudden and fulminant expansion.1,7 The
apoplexy incidence of pituitary adenoma varies from 15%
to 27.7%.7 Although most of such patients develop
pituitary apoplexy spontaneously, there exist some
possible predisposing factors
provocation test, general anesthesia, anticoagulant
therapy,8 and head trauma.3-6 A well-known theory of
spontaneous pituitary apoplexy is that the growth of
pituitary adenomas outstrips their blood supply, resulting
in ischemic necrosis and then hemorrhage.1,9 Although
the mechanism and pathogenesis of posttraumatic
pituitary apoplexy as a vascular event is not clearly
understood, it is reasonable to speculate that the change
of blood flow in pituitary adenomas due to the
fluctuations of intracranial pressure and blood pressure
following sever head injury leads to the bleeding in a
pituitary tumor. In our case, pituitary apoplexy was
induced by head injury, which was confirmed by
coexistence of right frontal contusion and apoplectic
sellar tumor on CT and MRI.
such as pituitary
Department of Neurosurgery, First Hospital of China Medical
University, Shenyang 110001, China (Bao YJ, Li XG, Jing ZT, Ou
SW, Wu AH and Wang YJ)
Correspondence to: Dr. BAO Yi-jun, Department of Neurosurgery,
First Hospital of China Medical University, Shenyang 110001,
China (Email: firstname.lastname@example.org)
Chin Med J 2007;120(24):2341-2343
Rarely, subarachnoid hemorrhage occurs in pituitary
apoplexy. The intrasellar pressure is extremely elevated in
pituitary tumor apoplexy.10 Thus, when the pressure
gradient within the sellar turcica exceeds the resistance of
the adjoining structures, blood from the pituitary
adenomas may be expelled into the basal subarachnoid
space producing a clinical presentation of subarachnoid
hemorrhage,1,2 or spread into the ventricle and cerebral
tissue. Wohaibi et al2 reported that the defect in the tumor
capsule on enhanced MRI represents the site of rupture.
Since subarachnoid hemorrhage is a common clinical
presentation of aneurysm, cerebral angiography is
beneficial to exclude intracranial aneurysm.
In our case, CT scan confirmed an apparent subarachnoid
hemorrhage adjoining the apoplectic pituitary adenoma
without spreading into the third ventricle and cerebrum.
Intracranial aneurysm was not detected by MRA. On CT
images, SAH was observable at 1.5 hour after the injury
but disappeared at 6 hours, which indicates that CT
performed at a proper time can be helpful to find SAH.
However, pituitary apoplexy is difficult to be detected by
CT; therefore reasonably, MRI is the best choice for
demonstration of apoplexy in sella turcica.
Pituitary incidentaloma is defined as a pituitary tumor
that is incidentally found without any neurological signs
or symptoms related to the tumor.11 In the era of CT, the
incidence of pituitary incidentaloma was 4% to 20%.12
Semple et al13 found that 81% of the patients with
pituitary apoplexy had no history of pituitary adenomas
or endocrine dysfunction. Our patient was unaware of the
pituitary adenoma, so apoplectic pituitary adenoma was
incidentally found due to his head injury.
In our patient, after four months, MRI indicated a
noticeable reduction of the tumor volume. A similar
phenomenon was also observed in 12% of 242
non-surgical patients with pituitary incidentaloma in
Japan.14 In another report, Armstrong and colleagues15
detected involution of adenoma and reversal of symptoms
following apoplexy that was due to infarction and steroid
treatment in a patient with pituitary macroadenoma.
Although trans-sphenoid surgery combined with corti-
costeroid replacement is generally regarded as the optimal
management for pituitary apoplexy,13 conservative
management including hormonal replacement therapy
was recommended if the patient was unwilling to accept
the surgery. In our patient, a decreased tumor volume and
good recovery were achieved after the therapy.
In conclusion, imaging evaluation is beneficial and
necessary for pituitary incidentaloma. SAH can be caused
by pituitary apoplexy. Conservative observation, supportive
treatment and close follow-up can lead to satisfactory
Fig. 1. Axial plain CT performed on admission. A: One and a half hour after the head injury, a
heterogeneous mass was detected at the sellar turcica and suprasellar cistern, and SAH was shown
around the suprasellar cistern. B: Six hours after the injury, the SAH was absorbed.
Fig. 2. Two weeks after the head trauma, non-enhanced T1-weighted MRI demonstrated a right
frontal hyper-intensity contusion focus with edema and suprasellar hyper-intensity mass (A).
T2-weighted image showed a right frontal subdural hydroma (B).
Fig. 3. Two weeks after the brain trauma, T1-weighted MRI showed heterogeneous sellar and
suprasellar tumor with the elevation of the optic chiasm, rim enhancement of the tumor, and
hemorrhagic signal in the sphenoid sinus. (A and C: without contrast; B and D: with contrast)
Fig. 4. Four months after the brain injury, sagittal T1-weighted MRI without contrast represented
the shrinkage of the tumor, decompression of the optic chiasm, and disappearance of the sphenoid
Chinese Medical Journal 2007; 120(24):2341-2343
recovery for elderly patient with pituitary apoplexy
without progressively deteriorated visual function. The
tumor volume may be reduced following the apoplexy
and steroid treatment.
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(Received March 25, 2007)
Edited by LUO Dan