Atraumatic orbital hemorrhage is typically associated with clinical signs of painful proptosis, lid edema, periorbital bruising along with visual disturbances. The majority of cases are associated with a venous vascular abnormality.1 While both arterial and venous anomalies can result in predisposing blood vessel wall weakness, orbital veins have unique anatomy that leave them further susceptible to sudden rises in venous pressure as would be expected in events resulting in Valsalva maneuver. Peripheral veins have valves that prevent retrograde blood flow. Orbital veins lack these Valves. Therefore, Valsalva maneuver can pool blood into the orbital veins allowing for the direct transfer of pressure to be focused on the orbital venous walls which can ultimately lead to vessel rupture.2 Patients without evidence of venous abnormalities are often found to have underlying physiological or iatrogenic coagulapathies that predispose them to a spontaneous hemorrhage.1

Both of these risk factors are especially enlightening to a case that we encountered. Prior to our patient’s presentation of proptosis, he experienced episodes of vomiting and seizure, both of which can lead To sudden elevations of venous pressure stressing the venous structural integrity. Our patient was also at risk with his underlying thrombocytopenia. While spontaneous bleeding doesn’t commonly occur until platelet levels drop below 10,000, this patient’s thrombocytopenic state compounded with his episodes of vomiting and seizures left him especially susceptible to an atraumatic orbital hemorrhage.


Our patient, a 31-year old male, has struggled with various ailments since birth. His past is riddled with various doctor visits and numerous hospital stays battling his many afflictions: common variable immunodeficiency; craniosynostosis; seizure disorder; obstructive sleep apnea; and mild mental retardation. This time he was at the hospital for a fever where he also exhibited an altered mental status.

After some investigation and a thorough physical exam, the patient was found to have lower extremity cellulitis with compounded septic shock. Appropriately, his doctors started aggressive fluid resuscitation, pressors, broad spectrum antibiotics and intravenous immunoglobulins and his condition slowly improved.

The fifth day at the hospital brought forth complications. He developed conjunctival injection in his left eye. At first glance, the ocular irritation seemed to have developed secondarily to the oxygen face mask. However, upon further examination, the patient was found to have also developed HSV stomatitis.

The complications continued to erupt. A blood test revealed he had thrombocytopenia, which reached a nadir of 60,000 platelets per microliter. The following day, he presented with a generalized seizure and was subsequently started on intravenous acyclovir for suspected HSV encephalitis. The patient’ condition seemingly stabilized. Yet, on the seventh day, he developed chemosis and 4 mm of axial proptosis of his left eye (See Figure 1). The patient’s condition progressed to 7 mm of axial proptosis over the course of two days and was found to have an orbital mass on CT. A follow-up CT was performed the next day revealing a 1.7 x 1.5 x 1.7cm anterior extraconal superolateral left orbital mass, increased size with adjacent fat stranding having a mild mass effect on the left optic nerve (See Figures 2, 3).

Orbital imaging in these patients may reveal a high density mass on CT. Magnetic resonance imaging typically demonstrates hypointense lesions on T1 and T2 sequences with marginal enhancement with gadolinium acutely due to the presence of deoxy-hemoglobin, hyperintensity with a bright peripheral ring increasing centripetally subacutely due to the presence of methemoglobin, hypointensity chronically due to hemosiderin, and ferritin formation.3 

Transfer of Care 

With his other co-morbidities under control, the patient was transferred to our institution on the ninth day to manage his expanding orbital mass. Our exam revealed restriction of the lateral gaze for the left eye with temporal chemosis. His visual acuity was 20/40 for the right eye and 20/30 for the left eye with no relative afferent pupillary defects noted. His intraocular pressure was within normal limits and a dilated fundoscopic evaluation did not show any significant pathology. 

Differential Diagnosis

Initially, an orbital abscess, orbital lymphoma, or viral myositis was suspected in the context of his immunodeficiency, recent cellulitis, and sepsis. The neuroradiologist was consulted and stated that the CT images Were consistent with an orbital abscess given the interval increase in size, enhancement and patient’s history. A left orbitotomy was performed and, unexpectedly, a hemorrhage and a clot was discovered in the lateral orbit (See Figure 4).

Diagnosis and Treatment 

Interestingly, pathological examination of the clot revealed no evidence of infection or malignancy, including negative fungal, viral and bacterial cultures. Postoperatively, the patient had significant reduction in proptosis and was transferred back to his primary hospital on the sixth postoperative day for the completion of his care. He was diagnosed with a spontaneous atraumatic orbital hemorrhage.

Potential for Vision Loss 

While orbital hemorrhaging may look unsightly, most cases do not require surgical management and can be treated conservatively, with most resolving within four to six weeks. Due to the limited space of the orbit, however, hemorrhage can lead to the compression of the optic nerve or increased intraocular pressure. Both of these complications are serious and can lead to permanent vision loss. Therefore, clinicians should always assess for rapid or progressive vision loss as the first step in management where an emergent surgical decompression procedure may be necessary to save a patient’s vision.

The authors are affiliated with the department of ophthalmology and visual sciences at the University of Illinois at Chicago College of Medicine. Contact Dr. Aakalu at 1855 W. Taylor St., MC 648, Chicago, Ill. 60611. Phone: (312) 996-9120; fax: (312) 996-1934; or

1. Sullivan TJ, Wright JE. Non-traumatic orbital haemorrhage. Clin Experiment Ophthalmol 2000;28:26-31.
2. Corl K, Jeffrey Hofmann R, Sutton E. Non-traumatic orbital hemorrhage. J Emerg Med 2010;38(3):378-80. Epub 2008 Mar 19.
3. Provenzale J. CT and MR imaging of acute cranial trauma. Emerg Radiol 2007;14:1-12