J Neurosurg 47:599-604, 1977

Pituitary apoplexy producing internal
carotid artery occlusion
Case report

THOMAS J. ROSENBAUM, M . D . , O. WAYNE HOUSER, M . D . ,
AND EDWARD R. LAWS, M . D .

Departments of Neurologic Surgery and Diagnostic Roentgenology, Mayo Clinic and
Mayo Foundation, Rochester, Minnesota
u,' The authors report a case of pituitary apoplexy occurring several hours after
carotid angiography. The event was associated with stupor, focal headache, and left
hemiparesis. Repeat angiography demonstrated intracranial occlusion of the right internal carotid artery. At surgery, a hemorrhagic pituitary adenoma was found to be
compressing the internal carotid artery, and the removal of the tumor resulted in
restoration of flow. The mechanism, presenting symptoms and signs, and treatment of
pituitary apoplexy causing compression of a major vessel are discussed.
KEY WORDS 9 pituitary apoplexy 9 carotid angiography
cerebrovascular disease 9 vascular occlusion

INCE the initial report of Bleibtreu in
1905, 2 hemorrhage into a pituitary
adenoma has been recorded over 200
times in the literature. Many precipitating
factors have been implicated, including
trauma, 2~ radiotherapy, TM anticoagulant therapy, TM nasal catarrh) estrogen treatment, TM
and pneumoencephalography? Hemorrhage
after cerebral angiography has been
reported twice previously) ,xa The usual
presenting symptoms and signs of pituitary
apoplexy are headache, altered consciousness, nausea, extraocular palsies,
pupillary abnormalities, and visual loss. Signs
of focal cerebral hemispheric dysfunction are
uncommon. The following is a case of pituitary apoplexy that occurred after carotid
angiography and was associated with intracranial occlusion of the right internal carotid
artery and left hemiparesis.

S

J. Neurosurg. / Volume 47 / October, 1977

9

Case Report

This 77-year-old farmer was in good health
until 1972, when he first noted some visual
loss. In February, 1976, when he was no
longer able to drive his tractor because of
gradual progression of his visual symptoms,
he sought medical attention and was admitted
to the hospital in April, 1976, for evaluation
of a suspected pituitary tumor. His past
health had been excellent with the exception
of mild diabetes, for which he was taking oral
medication. He gave no history suggestive of
endocrine deficiency.
Examination. The general medical examination was unremarkable. Neurological
examination was normal with the exception
of the visual system. The right eye had vision
for gross hand movement in the nasal field
only, an afferent pupillary defect, and Grade
599

T. J. Rosenbaum, O. W. Houser and E. R. Laws

FIG. 1. Right and left anteroposterior and lateral common carotid angiograms. Bilateral suprasellar
extension of the mass is evident.

4/4 pallor of the disc. The left eye had a complete temporal field loss, nasal field vision of
14/224, and Grade 3/4 pallor of the disc.
The fasting blood sugar was 93 rag/100 ml.
Morning and afternoon corticosteroid levels
were normal (12.0 and 8.8 ug/dl plasma), and
total (4.4 ~tg/dl) and free thyroxine (0.9
~g/dl) were low normal. Electrolytes,
creatinine, and serology were normal, as were
the remainder of the laboratory studies.
Skull roentgenograms showed a large
destructive lesion causing expansion of the
sella. Spiral polytomograms of the sella confirmed the presence of a lesion that seemed to
extend into the sphenoid sinus and to be
larger on the left than on the right side.
The day after admission, after appropriate
preparation with cortisone, bilateral common
carotid angiograms were performed. An intrasellar mass with a capillary blush showing
suprasellar and bilateral parasellar extension
was confirmed (Fig. 1). The diagnosis of a
chromophobe adenoma was made and the
patient was scheduled for transsphenoidal excision the next morning.
600

Twelve hours after angiography the patient
complained of a right-sided headache, but at
midnight he was alert and oriented, and was
able to go to the bathroom unassisted. At
2:30 A.M. the patient became stuporous and
gave inappropriate responses. His blood
pressure rose to 220/120, pulse 60, and
respiration rate 24. His pupils were equal and
unchanged from their appearance at his
hospital admission examination, but his eyes
were tonically deviated to the right. He had a
left central facial weakness, left hemiparesis,
left hypotonia, and a left Babinski sign.
Emergency bilateral common carotid
angiograms were performed. These studies
demonstrated occlusion of the right internal
carotid artery; no contrast medium passed
above the level of C-1. There was focal
narrowing of the supraclinoid portion of the
left internal carotid artery, which was not
present on the previous angiogram and was
believed to represent spasm. The previously
noted elevation of the A-1 segment of the left
anterior cerebral artery was unchanged. The
right anterior cerebral artery now filled from
J. Neurosurg. / Volume 47 / October, 1977

Pituitary apoplexy and carotid obstruction

FIG. 2. Repeat right lateral and left anteroposterior common carotid angiograms following the
apoplectic event. There is total obstruction to the flow of dye past C-1 on the right. The left supraclinoid
internal carotid shows focal narrowing with filling of the right anterior cerebral artery.

the left carotid injection (Fig. 2). These findings were believed to be compatible with
pituitary apoplexy causing obstruction of the
right internal carotid artery in the cavernous
or supraclinoid portion.
Operation. An emergency right frontotemporal craniotomy was done. The right frontal
and temporal lobes appeared slightly pale. A
large pituitary adenoma projected between
the optic nerves anteriorly with a very firm
nodule extending between the right optic
nerve and the right internal carotid artery
posterolaterally. The nodule contained fresh
hemorrhage and was directly compressing the
carotid artery. After the removal of this
nodule, the right carotid artery began to
pulsate normally. A radical subtotal removal
of the tumor was accomplished and
hemostasis was achieved. The intraoperative
pathology report was pituitary adenoma with
recent intraglandular hemorrhage throughout
the majority of specimen removedl
Postoperatively, the patient remained
stuporous and hemiplegic. Over the ensuing 2
days he gradually became more obtunded and
died of respiratory arrest.
Pathological Findings. Autopsy revealed
intrasellar and suprasellar residual pituitary
adenoma, hematoma, and surgical packing.
Atrophy of the right optic nerve and early
partial necrosis of the optic chiasm were present. There was no evidence of an intravascular lesion suggestive of an angiographic
complication such as intimal dissection or
J. Neurosurg. / Volume 47 / October, 1977

hematoma at the puncture site. The carotid
bifurcation had minimal atherosclerosis.
There was atherosclerosis, Grade 2 (50%
narrowing) of the right internal carotid artery
in the cavernous sinus and Grade 3 (90%
narrowing) at the origin of the middle
cerebral artery. Transtentorial herniation
with secondary brain-stem hemorrhages was
present (Fig. 3).
Discussion

Hemiplegia as one of the presenting signs
of pituitary apoplexy is unusual, but it has
been recorded at least eight times. Schnitker
and Lehnert, 17 Rovit and Fein/5 Jolley and
M a b o n / Brougham, et a l . / List, et al., 1~
Wright, et al., 2~ and Epstein, et a l . / each
recorded a confirmed case and Roberts, et
al./4 a single presumptive case. Lopez x:
reported one patient with pituitary apoplexy
and hemiparesis, but the onset of hemiparesis
followed angiography, which was performed
several hours after the initial ictus; therefore
the hemiparesis but not the pituitary apoplexy
could be considered a complication of
angiography? 1
When focal cerebral signs are associated
with pituitary apoplexy, cerebral ischemia
has been postulated to be the mechanism,
resulting from spasm, hypotension, or the
mechanical obstruction pressure effects of an
enlarging mass upon a large artery. After
angiography, hemiplegia may also result
601

T. J. Rosenbaum, O. W. Houser and E. R. Laws

FIG. 3. Pathological specimens: A: Origin of the right middle cerebral artery with 90% atherosclerotic narrowing. B: Gross specimen of the sella demonstrating residual tumor and its relationship to
the carotid arteries. C: Right middle cerebral distribution hemorrhagic infarction. D: Residual
pituitary adenoma removed at postmortem examination.

from emboli formed at the puncture site, dislodged plaque, intimal dissection, toxicity
from contrast substance, or combinations of
these factors. In our case, an embolus from
the carotid puncture site could have produced
the catastrophic event; however, it seems
more likely that the internal carotid artery
was obstructed by an enlarging hemorrhagic
tumor which caused right hemispheric infarction and left hemiparesis. Decompression of
the internal carotid artery resulted in a patent
vessel but may have converted a pale cerebral
infarct into a hemorrhagic infarct.
Schnitker and Lehnert 17 reported on a
patient presenting with the syndrome of middle cerebral artery thrombosis who, at autopsy 16 days later, had a large right hemispheric
infarction and a hemorrhagic pituitary
adenoma that had caused compression of the
right middle cerebral artery. Sakalas, et al.? 6
reported on a 6-year-old boy with visual loss,
lethargy, and a stiff neck. Although
hemiparesis was not a presenting sign,
602

angiography showed that the left carotid
artery was functionally occluded, and
primary filling of the left middle cerebral
artery occurred via the posterior circulation.
At surgery, an eosinophilic adenoma was
found to be compressing the left internal
carotid artery. Thus, including our case, it has
been verified in three cases that large artery
mechanical obstruction can cause decreased
cerebral perfusion.
Vascular spasm has been reported to be
associated with pituitary apoplexy7 but has
not yet been shown to cause cerebral
ischemia. Our patient had spasm of the left
internal carotid artery but the cerebral
ischemia was right-sided secondary to right
internal carotid artery occlusion. Rovit and
Fein 15 detailed a case with left hemiparesis
and narrowing of the right internal carotid
artery, but a prominent mass effect was present and the angiogram may have reflected
direct compression rather than spasm.
Systemic hypotension occurs not uncomJ. Neurosurg. / Volume 4 7 / October, 1977

Pituitary apoplexy and carotid obstruction
monly with pituitary apoplexy, but is
associated with a decreased level of consciousness and not with focal cerebral
hemispheric signs. Unless other factors are
present, hypotension alone should not cause a
focal neurological deficit. Pituitary apoplexy
with hypotension and hemiparesis has been
described twice but in both cases the
hemiparesis occurred several days after the
initial ictus? ,s Angiography after the onset of
hemiparesis was not performed to determine
if other factors were present to account for
this finding.
Pituitary apoplexy with focal cerebral signs
has been reported twice when angiography
revealed a pituitary tumor but did not show
spasm or obstruction of a major vessel. In
these cases, angiography was delayed 1 week
to 1 month; either spasm or obstruction could
have resolved in that period of time, leaving
a residual cerebral infarction and hemiparesis. 6,21
Because of the small number of recorded
cases of hemorrhage into a pituitary adenoma
with associated focal cerebral deficit,
statistical analysis of the efficacy of surgical
intervention for this specific entity is not
possible. Analysis of previously reported
cases and the current case indicates that one
patient did well and two did poorly with conservative therapy, and one did well and four
had significant morbidity or mortality after
surgical decompression. Both patients in
whom improvement followed surgery had
milder preoperative neurological deficits than
did any of the six patients who had an unfavorable outcome. The size of the mass
necessary to produce cerebral ischemia and
the added insult of a cerebral infarction may
be-the cause of the high mortality rate.
Pituitary apoplexy should be suspected if a
catastrophic event occurs in conjunction with
extraocular muscle paresis, visual loss, and an
enlarged sella on x-ray examination.
Angiography is necessary to eliminate the
possibility of aneurysmal rupture and to confirm the presence of a pituitary adenoma.
Preservation of vision is a primary objective
in surgical intervention. P r o m p t transsphenoidal surgical decompressfon has recently been associated with a favorable outcome. 1,4,22 In our case, it is doubtful that
transsphenoidal decompression would have
been sufficient to decompress the right internal carotid artery. If focal cerebral hemiJ. Neurosurg. / Volume 47 / October, 1977

spheric signs are present and angiography
reveals large vessel occlusion, transfrontal
decompression within several hours of the initial ictus may be beneficial.
References

1. Berti G, Heisey WG, Dohn DF: Pituitary
apoplexy treated by stereotactic transphenoidal aspiration. Cleve Clin Q 41:163-175,
1974
2. Bleibtreu L: Ein Fall von Akromeglie
(Zerst6rung der Hypophysis durch Blutung).
Munch Med Wocheoschr 52:2079-2080, 1905
3. Brougham M, Heusner AP, Adams RD:
Acute degenerative changes in adenomas of
the pituitary body - - with special reference to
pituitary apoplexy. J Nenrosurg 7:421-439,
1950
4. Conomy JP, Ferguson JH, Brodkey JS, et al:
Spontaneous infarction in pituitary tumors:
neurologic and therapeutic aspects. Neurology
(Mioneap) 25:580-587, 1975
5. Dawson BH, Kothandaram P: Acute massive
infarction of pituitary adenomas. A study of
five patients. J Neurosurg 37:275-279, 1972
6. Epstein S, Pimstone BL, de Villiers JC, et al:
Pituitary apoplexy in five patients with
pituitary tumours. Br Med J 2:267-270, 1971
7. Goodman JM, Gilson M, Shapiro B: Pituitary
apoplexy - - a cause of sudden blindness. J Indiana State Med Assoc 66:320-321, 1973
8. Jefferson M, Rosenthal FD: Spontaneous
necrosis in pituita~'y tumours (pituitary
apoplexy). Lancet 1:342-344, 1959
9. Jolley FL, Mabon RL: Pituitary apoplexy. J
Med Assoc Ga 47:75-78, 1958
10. List CF, Williams JR, Balyeat GW: Vascular
lesions in pituitary adenomas. J Neurosurg
9:177-187, 1952
11. Lopez IA: Pituitary apoplexy. J Oslo City
Hosp 20:17-27, 1970
12. Nourizadeh AR, Pitts FW: Hemorrhage into
pituitary adenoma during anticoagulant
therapy. JAMA 193:623-625, 1965
13. Pouyanne L, Pouyanne H, Arne L: La forme
h~morragique des ad~nomes ehromophobes
hypophysaires (/t propos de 3 observations),
Hommage h Clovis Vincent, Vol 1. Paris:
Maloine, 1949, pp 81-84
14. Roberts LN, Goldberg WM, Pickard H: Panhypopituitarism in a male following pituitary
apoplexy (treated with ACTH and cortisone).
Can Med Assoc J 66:458-461, 1952
15. Rovit RL, Fein JM: Pituitary apoplexy: a
review and reappraisal. J Neurosurg 37:
280-288, 1972
16. Sakalas R, David RB, Vines FS, et al:
Pituitary apoplexy in a child. Case report. J
Neurosurg 39:519-522, 1973
603

T. J. Rosenbaum, O. W. Houser and E. R. Laws
17. Schnitker MT, Lehnert HB: Apoplexy in a
pituitary chromophobe adenoma producing
the syndrome of middle cerebral artery thrombosis. Case report. J Neurnsurg 9:210-213,
1952
18. Sosman MC: The roentgen therapy of
pituitary adenomas. JAMA 113:1282-1285,
1939
19. Steimle R, Royer J, Oppermann A, et al:
H6matome post-angiographique dans un
ad6nome de l'hypophyse. C~cit6 et troubles
oculo-moteurs r6gressant apr~s intervention
d'urgence. Neurochirurgie 20:599-608, 1974
20. VanWagenen WP: Haemorrhage into a
pituitary tumor following trauma. Ann Snrg
95:625-628, 1932

604

21. Wright RL, Ojemann RG, Drew JH: Hemorrhage into pituitary adenomata. Report of two
cases with spontaneous recovery. Arch Neurol
12:326-331, 1965
22. Zervas NT, Mendelson G: Treatment of acute
haemorrhage of pituitary tumours. Lancet
1:604-605, 1975

Address reprint requests to: Thomas J. Rosenbaum, M.D., Department of Neurologic Surgery,
Mayo Clinic, Rochester, Minnesota 55901.

J. Neurosurg. / Volume 47 / October, 1977