□ CASE REPORT □

Venous Infarction Secondary to Septic Cavernous Sinus
Thrombosis
Masahiro Kamouchi 1,4, Yoko Wakugawa 1, Yasushi Okada 1, Kazuhiro Kishikawa 1,
Ryu Matsuo 1, Kazunori Toyoda 1, Kotaro Yasumori 2, Tooru Inoue 3, Setsuro Ibayashi 4 and
Mitsuo Iida 4

Abstract
A 65-year-old woman with poorly controlled diabetes presented bilateral miosis, bilateral abducens nerve
palsy, and left hemiparesis. On MRI, cavernous sinus thrombosis, subdural empyema and hemorrhagic infarction in the frontotemporal lobe were detected. Cerebral angiogram revealed filling defect in the cavernous sinus with venous congestion but no involvement of internal carotid artery. Postmortem examination demonstrated hemorrhagic infarction in the right frontotemporal lobe as well as hemorrhagic necrosis of the pituitary gland. It should be noted that venous congestion due to cavernous sinus thrombosis may cause these
complications.
Key words: cavernous sinus thrombosis, cerebral veins, brain infarction
(DOI: 10.2169/internalmedicine.45.1430)

of septic cavernous sinus thrombosis, probably due to narrowing or occlusion of the internal carotid artery (ICA) at
the intracavernous portion (5-7).
We herein report a case with septic cavernous sinus
thrombosis complicating hemorrhagic infarction in the frontotemporal lobe and hemorrhagic necrosis of the pituitary
gland.

Introduction
Cavernous sinus thrombosis is a rare but often critical disease which may not only be caused by infectious but also
by noninfectious processes, including vascular, traumatic,
and neoplastic etiologies (1, 2). Septic cavernous sinus
thrombosis was uniformly fatal in the preantibiotic era. Although it is less common in the postantibiotic era, a delay in
the diagnosis results in catastrophe (1, 2). In recent years,
CT and MR imaging enables us to accurately diagnose cavernous sinus thrombosis by direct and indirect signs (3, 4).
Progress in neuroimaging techniques has contributed to an
increased recognition of cavernous sinus thrombosis.
Septic cavernous sinus thrombosis has been reported to be
accompanied by intracranial complications such as meningitis, brain abscess, and subdural empyema possibly as a result of spread from the same primary focus infection (1).
Cerebral infarction has also been reported as a complication

Case Report
A 65-year-old woman was referred to a local medical
doctor with slowly progressive headache for three weeks.
She had a history of hypertension, diabetes, and hyperlipidemia. She received an analgesic, but the symptom became
worse. Moreover, she developed a fever and was treated
with an antibiotic. Two days later, she developed stupor with
left hemiparesis and was transferred to our hospital.
On physical examination, she had a fever of 40℃ and
nuchal rigidity. Blood pressure was 146/72 mmHg and pulse

１

Department of Cerebrovascular Disease, Cerebrovascular Center and Clinical Research Institute, National Kyushu Medical Center, ２ Department
of Neuroradiology, Cerebrovascular Center and Clinical Research Institute, National Kyushu Medical Center, ３ Department of Neurosurgery,
Cerebrovascular Center and Clinical Research Institute, National Kyushu Medical Center and ４ Department of Medicine and Clinical Science,
Graduate School of Medical Sciences, Kyushu University
Received for publication May 20, 2005; Accepted for publication October 13, 2005
Reprint requests should be addressed to Masahiro Kamouchi, Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582

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DOI: 10.2169/internalmedicine.45.1430

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filled with contrast medium (Fig. 2B).
The respiration rhythm was irregular and her respiration
was controlled by the respirator. She was treated with a prolonged course of high dose intravenous cefpirome sulfate, as
well as drainage of the sphenoid sinus. However, the patient’s situation deteriorated progressively and she eventually
died. Autopsy demonstrated chronic inflammation of the
meninx and cavernous sinus. Sinusitis involving the sphenoid and ethmoid sinuses was observed and considered to
be the primary foci associated with septic thrombosis of the
cavernous sinus. Hemorrhagic necrosis of the right frontotemporal lobe and pituitary gland were also seen.

rate was 70 beats/min. Funduscopic examination revealed
bilateral mild papilledema. Neurological examination
showed disturbance of consciousness (Japan coma scale 30)
and bilateral miosis (bilateral 2 mm) with minimal pupillary
light response. Right corneal reflex was slightly depressed.
She had bilateral lateral rectus muscle palsies indicating bilateral abducens nerve palsies, left facial palsy, and left upper and lower limb weakness. The remainder of the physical
examination showed no abnormalities. Laboratory data
showed leukocytosis of 10400/μL (83% neutrophil) and elevated levels of C-reactive protein (37.8 mg/dl) and glycosylated hemoglobin (HbA1c, 12.3%). Chest X-ray showed
cardiomegaly but no other abnormalities. No microorganism
could be identified in the blood, urine and cerebrospinal
fluid. Cerebrospinal fluid contained 210 white blood cells/
mm3 (58% neutrophil) with a protein concentration of 215
mg/dL and a glucose concentration of 89 mg/dL (27% of a
simultaneous blood glucose concentration). Brain CT
showed a high density area in the frontotemporal lobe
(Fig. 1A). On MRI, T2-weighted image disclosed a heterogeneous hyperintense area in right frontotemporal lobe
(Fig. 1B). Gadolinium-enhanced T1-weighted image revealed enlargement of the right cavernous sinus with a heterogeneous hyperintense mass (Fig. 1C) and a hyperintense
area in the subdural space (Fig. 1D). Cerebral angiogram
did not show any involvement of the internal carotid artery
(Fig. 2A). In the venous phase, the cavernous sinus was not

Discussion
It has been reported that cavernous sinus thrombosis is
complicated by brain infarction (5, 6, 8-11). The cavernous
portion of the internal carotid artery is occasionally narrowed or obstructed which results in a diminished flow in
the peripheral lesion (5). Spasm or inflammation of the arterial wall induced by arterial invasion of infection, or both,
have been implicated for lesions in the intracavernous carotid artery (6). In the present case, the infarction was accompanied by hemorrhagic change and was not identical to
the vascular territory without any significant change in ICA.
Recent reports showed that venosinus thrombosis associated
with septic cavernous sinus thrombosis is not restricted to
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DOI: 10.2169/internalmedicine.45.1430

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tarism is a rare complication of cavernous sinus thrombosis,
possibly related to infectious necrosis or aseptic infarction of
the gland, which can develop more than a year after the initial event (1, 2). In the present case, necrosis of the pituitary
gland was observed in the postmortem examination. A
mechanism might be that hemorrhagic necrosis of the pituitary gland is also caused by venous congestion of the pituitary gland due to cavernous sinus thrombosis. These rare
complications should be taken into consideration in patients
with septic cavernous sinus thrombosis.

the superior ophthalmic vein and is more common than previously assumed (4). The veins and venous sinuses that
communicate with cavernous sinus are valveless, and therefore thrombophlebitis may affect the cavernous sinus in a
retrograde fashion. Cavernous sinuses drain the blood from
the orbits and the anterior part of the base of the brain via
the sphenoparietal sinus and the middle cerebral veins. As a
result, thrombosis can extend from the cavernous sinus to
other dural venous sinuses. Thus, hemorrhagic infarction
may have developed due to tributary cerebral venous thrombophlebitis.
Silver et al reported that pituitary insufficiency and the
syndrome of inappropriate antidiuretic hormone secretion
followed thrombosis of the cavernous sinus (12). Hypopitui-

We are grateful to Dr. Morishige Takeshita for his helpful
comments on histopathology.

References
1. DiNubile MJ. Septic thrombosis of the cavernous sinuses. Arch
Neurol 45: 567-572, 1988.
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3. Kriss TC, Kriss VM, Warf BC. Cavernous sinus thrombophlebitis:
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PF. Otocerebral mucormycosis -a case report. Clin Exp Neurol 23:
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10. Macdonald RL, Findlay JM, Tator CH. Sphenoethmoidal sinusitis
complicated by cavernous sinus thrombosis and pontocerebellar
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Ⓒ 2006 The Japanese Society of Internal Medicine
http://www.naika.or.jp/imindex.html

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