Case Reports Granulocytic Sarcoma of the Orbit Presenting as a Fulminant Orbitopathy in an Adult With Acute Myeloid Leukemia John P. O’Neill, M.D.*, Andrew R. Harrison, M.D.*†, J. Douglas Cameron, M.D., M.B.A.*, and Ali Mokhtarzadeh, M.D.* Abstract: A 64-year-old woman with relapsed acute myelogenous leukemia (AML) undergoing salvage chemotherapy developed rapid onset of right-sided ophthalmoplegia, proptosis, optic neuropathy, and vision loss from 20/30 to hand motions over a 3-hour period on day 4 of her treatment. CT scan of her orbits revealed a superolateral orbital mass and periocular edema. She underwent immediate canthotomy and cantholysis, and lateral orbitotomy with debulking of the mass later the same day. The histopathology was consistent with aggregates of myeloid blasts. Her vision recovered to 20/20 on postoperative day 1. Orbital granulocytic sarcoma is a rare condition often concurrent with AML, typically in the pediatric population and rarely in adults. Presentation as a fulminant orbitopathy with rapidly progressive optic neuropathy and vision loss over several hours has not been previously reported.
G
ranulocytic sarcoma (GS) is an uncommon, localized tumor composed of malignant cells of myeloid origin occurring at anatomical sites other than the bone marrow.1 Orbital GS typically presents in children, although it infrequently occurs in the adult population.2,3 GS can represent a complication of the myelodysplastic syndromes, in particular acute myelogenous leukemia (AML).1,4 The authors present an unusual manifestation of orbital GS as a fulminant orbital process in a 64-year-old woman, with AML presenting with double vision, rapid proptosis, and ultimately dramatic optic neuropathy and vision loss, all occurring over several hours. This report is in full compliance with the Declaration of Helsinki and current Health Insurance Portability and Accountability Act regulations.
CASE REPORT A 64-year-old woman with relapsed AML undergoing salvage chemotherapy with mitoxantrone and etoposide developed rapid onset of unilateral right-sided eye pain and periorbital edema on day 4 of her treatment. Her history was significant for AML, subtype M2, diagnosed 1 year prior. She had initially been treated with cytarabine and idarubicin. Initially, her visual acuity was 20/30 OD, 20/20 OS, with mildly restricted motility *Departments of Ophthalmology and Visual Neurosciences and †Department of Ophthalmology and Otolaryngology, University of Minnesota, Minneapolis, Minnesota Accepted for publication January 24, 2015. This study was supported by an unrestricted grant from the Research to Prevent Blindness (New York, NY), and the Lions and Lionesses of Minnesota. This case has been previously reported at the Fall 2014 ASOPRS meeting in Chicago, IL, by Ali Mokhtarzadeh, MD, and Andrew R. Harrison, MD. The authors have no financial or conflicts of interest to disclose. Address correspondence and reprint requests to Ali Mokhtarzadeh, M.D., Department of Ophthalmology and Visual Neurosciences, University of Minnesota, MMC 493, 420 Delaware St SE, Minneapolis, MN 55455. E-mail: [email protected] DOI: 10.1097/IOP.0000000000000442
Ophthal Plast Reconstr Surg, Vol. XX, No. XX, 2015
to all fields OD. Pupillary function was normal with no afferent pupillary defect. Her intraocular pressure in the OD was elevated to 46 mm Hg, while the left intraocular pressure was in the average range at 17 mm Hg. The only other physical findings were periorbital edema and erythema, as well as conjunctival injection and chemosis. Given her immunocompromised state, initial concern was for an infectious process. CT scan of her orbits revealed a superolateral extraconal mass and periocular edema (Fig. 1A). She had no sinusitis. Over a 3-hour period that same day she developed progressive ophthalmoplegia, markedly worsening proptosis, significant resistance to retropulsion, and a dense afferent pupillary defect, associated with loss of vision in her OD from 20/30 to hand motions, despite maximal medical intervention for intraocular pressure reduction. An immediate canthotomy and inferior cantholysis were performed (Fig. 1B) by the general ophthalmology service for presumed retrobulbar mass effect. The ophthalmic plastic and reconstructive surgery service was consulted, and later that evening, she underwent a lateral orbitotomy to biopsy the mass. Despite her pancytopenia, with platelets being transfused to 20,000 per cubic millimeter, little bleeding was encountered intraoperatively. A firm, white mass was found in the lateral orbit, which was extensively debulked. Both limbs of the lateral canthal tendon were left disinserted. Bacterial and fungal cultures and stains were negative. Histopathology and flow cytometry revealed lacrimal gland and infiltrates of myeloid blasts (Fig. 2). Immunochemistry studies were positive for CD31, CD34, CD43, CD45, CD117, and partial lysozyme. Immunohistochemistry studies were negative for CD3, CD20, myeloperoxidase, and factor VIII. Her vision recovered to 20/20 on postoperative day 1. Full motility returned, and there was no diplopia by postoperative day3. Following her course of salvage chemotherapy, persistent blasts were present on a repeat bone marrow biopsy. She elected palliative care and expired 1 month following the episode. There was complete resolution of all abnormal orbital findings during this period.
DISCUSSION GS, also known as myeloid sarcoma or chloroma, was first reported in 1811 by Allen Burns who described a green tumor involving the orbit.4,5 The greenish coloration of the lesion is attributable to the myeloperoxidase in the cells of granulocytic lineage.4 Orbital GS is a rare condition typically seen in the pediatric population and less commonly in adults.1,4,6–9 Presentation as a fulminant orbitopathy with rapidly progressive optic neuropathy and vision loss over several hours has not been previously reported. Orbital GS is often concurrent with AML, most notably in certain subtypes of AML, in particular M5a (monoblastic), M5b (monocytic), M4 (myelomonocytic), and M2 (myeloblastic with maturation).10 GS can be seen as a manifestation of established disease, although it may appear at anytime during the natural history. AML, myelodysplastic, or other myeloproliferative disorders may initially present with orbital involvement, making a precise diagnosis difficult.1,4,7 Alexiev et al.7 reported 13 patients (range, 25–72 years) with myeloid sarcoma occurring at various sites and showed that 9 of 13 (69%) had concomitant involvement of the bone marrow by acute leukemia, myeloproliferative, or myelodysplastic disorders. The remainder of cases occurred de novo. Another study by Aggarwal et al.2 of 31 patients (range, 3–59 years) with biopsy-proven orbital GS showed concomitant hematologic malignancy in 13 of 31 (42%) cases. Of the
e1
Copyright © 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. Unauthorized reproduction of this article is prohibited.
Ophthal Plast Reconstr Surg, Vol. XX, No. XX, 2015
Case Reports
FIG. 1. A, Axial cut from CT demonstrating proptosis of OD and mass in the extraconal superolateral orbit. B, External photograph of OD after lateral canthotomy and inferior cantholysis demonstrating proptosis and significant chemosis. The chemosis was not hemorrhagic prior to the procedure.
remaining 18 patients, 72% developed AML within 3 to 21 months (median, 11.3 months). Other studies have reiterated that de novo tumor diagnosis often indicates development of peripheral blood or bone marrow involvement within a year.1 Diagnosis of GS can be difficult in the absence of systemic disease and may be confused with lymphoma, rhabdomyosarcoma, neuroblastoma, or other poorly differentiated tumors.1 Clinical and radiologic features do not aid significantly in differential diagnosis as they are not specific for GS. Histologic
features of myeloid differentiation such as eosinophilic granules within the cytoplasm may be helpful in establishing the diagnosis, although these nonspecific findings are not always present.11 The naphthol AS-D chloroacetate esterase stain (Leder stain) to identify cells containing myeloperoxidase has improved the precision of histologic diagnosis; however, the most accurate diagnosis is established with the use of immunochemical panels of stains.7 Commonly included in these immunochemical panels for myeloid sarcomas are myeloperoxidase, lysozyme, CD3, CD4, CD8, CD15, CD20, CD34, CD43, CD68, CD79a, CD117, CD163, factor VIII (FVIII), and glycophorin A.7 In the study by Aggarwal et al.,2 all 31 patients were positive for MPO, CD34, CD43, and CD117. There are no consensus guidelines on how best to treat GS, and therapy can vary depending on presentation at initial diagnosis or at relapse.6 Treatment approaches commonly involve AML chemotherapy, radiation therapy, tumor debulking, and allogeneic hematopoietic cell transplantation.6 Although overall survival rates for patients with leukemia have improved with modern therapies, mortality in patients with orbital leukemic tumors is high. A study on 27 pediatric patients showed median survival of 4.75 years (range 0.1–18 years) after diagnosis of orbital leukemic disease.12 Prompt diagnosis of GS and early treatment of concomitant systemic disease may improve long-term survival. This case is unusual in its fulminant presentation. There was no histologic evidence of an acute inflammatory process adjacent to the mass. There are reports in the literature of GS mimicking intracranial hematoma.13–15 O’Brien et al.15 describe a case of a 34-year-old presenting with acute altered mental status for 1 day found to have a subdural collection. The collection was biopsied and found to be consistent with GS. The patient succumbed to a subdural hematoma with tentorial herniation only 2 days later. McCabe et al.14 described a child presenting with reaccumulating epidural hematoma, which the authors postulate was due to granulocytic sarcoma in the extradural space. In this case, no significant bleeding was encountered during the orbitotomy. Given the rapid progression, it is plausible that the mass effect of the relatively anterior mass in addition to her thrombocytopenia resulted in deeper orbital bleeding. The authors may have only caught “the tip of the iceberg” on the CT scan as her orbit became much more tense in the ensuing hours. Blood products were not encountered perhaps because after debulking the obviously abnormal mass, no further exploration took place. That would also explain why her orbital process responded so well to surgery as the upper and lower limb of the lateral canthal tendon were left free. Another possibility is an acute orbital inflammatory process perhaps adjacent to the mass, with the biopsy specimen not being representative. With a paucity of histologic evidence of an acute inflammatory process, and no other infectious or vascular etiology identified, the authors can only speculate the pathogenesis of this unusual fulminant presentation.
CONCLUSION Orbital GS in adults occurs rarely and is generally a poor prognostic sign for the underlying disease. Biopsy with special histologic staining and immunohistochemistry plays a key role in diagnosis. In cases where GS presents in nonleukemic patients, there is high suspicion for underlying systemic disease, and patients should undergo prompt evaluation and careful monitoring for hematologic malignancy.
REFERENCES FIG. 2. Small aggregates of myeloid blast cells (medium sized mononuclear cells with dispersed chromatin and visible nucleoli).
e2
1. Stockl FA, Dolmetsch AM, Saornil MA, et al. Orbital granulocytic sarcoma. Br J Ophthalmol 1997;81:1084–8.
© 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
Copyright © 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. Unauthorized reproduction of this article is prohibited.
Ophthal Plast Reconstr Surg, Vol. XX, No. XX, 2015
2. Aggarwal E, Mulay K, Honavar SG. Orbital extra-medullary granulocytic sarcoma: clinicopathologic correlation with immunohistochemical features. Surv Ophthalmol 2014;59:232–5. 3. Mangla D, Dewan M, Meyer DR. Adult orbital myeloid sarcoma (granulocytic sarcoma): two cases and review of the literature. Orbit 2012;31:438–40. 4. Shields JA, Stopyra GA, Marr BP, et al. Bilateral orbital myeloid sarcoma as initial sign of acute myeloid leukemia: case report and review of the literature. Arch Ophthalmol 2003;121:138–42. 5. Burns A. Observation on the Surgical Anatomy of the Head Andmneck. 4th ed. Baltimore, MD: Granville Sharp Pattison, 1823. 6. Bakst RL, Tallman MS, Douer D, et al. How I treat extramedullary acute myeloid leukemia. Blood 2011;118:3785–93. 7. Alexiev BA, Wang W, Ning Y, et al. Myeloid sarcomas: a histologic, immunohistochemical, and cytogenetic study. Diagn Pathol 2007;2:42. 8. Yamauchi K, Yasuda M. Comparison in treatments of nonleukemic granulocytic sarcoma: report of two cases and a review of 72 cases in the literature. Cancer 2002;94:1739–46.
Case Reports
9. Zimmerman LE, Font RL. Ophthalmologic manifestations of granulocytic sarcoma (myeloid sarcoma or chloroma). The third Pan American Association of Ophthalmology and American Journal of Ophthalmology Lecture. Am J Ophthalmol 1975;80:975–90. 10. Byrd JC, Edenfield WJ, Shields DJ, et al. Extramedullary myeloid cell tumors in acute nonlymphocytic leukemia: a clinical review. J Clin Oncol 1995;13:1800–16. 11. Hutchison RE, Kurec AS, Davey FR. Granulocytic sarcoma. Clin Lab Med 1990;10:889–901. 12. Bidar M, Wilson MW, Laquis SJ, et al. Clinical and imaging characteristics of orbital leukemic tumors. Ophthal Plast Reconstr Surg 2007;23:87–93. 13. Smidt MH, de Bruin HG, van’t Veer MB, et al. Intracranial granulocytic sarcoma (chloroma) may mimic a subdural hematoma. J Neurol 2005;252:498–9. 14. McCabe MG, Broadbent V, Williams DM. Unusual cause of extradural haemorrhage. Med Pediatr Oncol 2001;36:654–6. 15. O’Brien CE, Saratsis AM, Voyadzis JM. Granulocytic sarcoma in a patient with blast crisis mimicking a chronic subdural hematoma. J Clin Oncol 2011;29:e569–71.
© 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
e3
Copyright © 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. Unauthorized reproduction of this article is prohibited.
G
ranulocytic sarcoma (GS) is an uncommon, localized tumor composed of malignant cells of myeloid origin occurring at anatomical sites other than the bone marrow.1 Orbital GS typically presents in children, although it infrequently occurs in the adult population.2,3 GS can represent a complication of the myelodysplastic syndromes, in particular acute myelogenous leukemia (AML).1,4 The authors present an unusual manifestation of orbital GS as a fulminant orbital process in a 64-year-old woman, with AML presenting with double vision, rapid proptosis, and ultimately dramatic optic neuropathy and vision loss, all occurring over several hours. This report is in full compliance with the Declaration of Helsinki and current Health Insurance Portability and Accountability Act regulations.
CASE REPORT A 64-year-old woman with relapsed AML undergoing salvage chemotherapy with mitoxantrone and etoposide developed rapid onset of unilateral right-sided eye pain and periorbital edema on day 4 of her treatment. Her history was significant for AML, subtype M2, diagnosed 1 year prior. She had initially been treated with cytarabine and idarubicin. Initially, her visual acuity was 20/30 OD, 20/20 OS, with mildly restricted motility *Departments of Ophthalmology and Visual Neurosciences and †Department of Ophthalmology and Otolaryngology, University of Minnesota, Minneapolis, Minnesota Accepted for publication January 24, 2015. This study was supported by an unrestricted grant from the Research to Prevent Blindness (New York, NY), and the Lions and Lionesses of Minnesota. This case has been previously reported at the Fall 2014 ASOPRS meeting in Chicago, IL, by Ali Mokhtarzadeh, MD, and Andrew R. Harrison, MD. The authors have no financial or conflicts of interest to disclose. Address correspondence and reprint requests to Ali Mokhtarzadeh, M.D., Department of Ophthalmology and Visual Neurosciences, University of Minnesota, MMC 493, 420 Delaware St SE, Minneapolis, MN 55455. E-mail: [email protected] DOI: 10.1097/IOP.0000000000000442
Ophthal Plast Reconstr Surg, Vol. XX, No. XX, 2015
to all fields OD. Pupillary function was normal with no afferent pupillary defect. Her intraocular pressure in the OD was elevated to 46 mm Hg, while the left intraocular pressure was in the average range at 17 mm Hg. The only other physical findings were periorbital edema and erythema, as well as conjunctival injection and chemosis. Given her immunocompromised state, initial concern was for an infectious process. CT scan of her orbits revealed a superolateral extraconal mass and periocular edema (Fig. 1A). She had no sinusitis. Over a 3-hour period that same day she developed progressive ophthalmoplegia, markedly worsening proptosis, significant resistance to retropulsion, and a dense afferent pupillary defect, associated with loss of vision in her OD from 20/30 to hand motions, despite maximal medical intervention for intraocular pressure reduction. An immediate canthotomy and inferior cantholysis were performed (Fig. 1B) by the general ophthalmology service for presumed retrobulbar mass effect. The ophthalmic plastic and reconstructive surgery service was consulted, and later that evening, she underwent a lateral orbitotomy to biopsy the mass. Despite her pancytopenia, with platelets being transfused to 20,000 per cubic millimeter, little bleeding was encountered intraoperatively. A firm, white mass was found in the lateral orbit, which was extensively debulked. Both limbs of the lateral canthal tendon were left disinserted. Bacterial and fungal cultures and stains were negative. Histopathology and flow cytometry revealed lacrimal gland and infiltrates of myeloid blasts (Fig. 2). Immunochemistry studies were positive for CD31, CD34, CD43, CD45, CD117, and partial lysozyme. Immunohistochemistry studies were negative for CD3, CD20, myeloperoxidase, and factor VIII. Her vision recovered to 20/20 on postoperative day 1. Full motility returned, and there was no diplopia by postoperative day3. Following her course of salvage chemotherapy, persistent blasts were present on a repeat bone marrow biopsy. She elected palliative care and expired 1 month following the episode. There was complete resolution of all abnormal orbital findings during this period.
DISCUSSION GS, also known as myeloid sarcoma or chloroma, was first reported in 1811 by Allen Burns who described a green tumor involving the orbit.4,5 The greenish coloration of the lesion is attributable to the myeloperoxidase in the cells of granulocytic lineage.4 Orbital GS is a rare condition typically seen in the pediatric population and less commonly in adults.1,4,6–9 Presentation as a fulminant orbitopathy with rapidly progressive optic neuropathy and vision loss over several hours has not been previously reported. Orbital GS is often concurrent with AML, most notably in certain subtypes of AML, in particular M5a (monoblastic), M5b (monocytic), M4 (myelomonocytic), and M2 (myeloblastic with maturation).10 GS can be seen as a manifestation of established disease, although it may appear at anytime during the natural history. AML, myelodysplastic, or other myeloproliferative disorders may initially present with orbital involvement, making a precise diagnosis difficult.1,4,7 Alexiev et al.7 reported 13 patients (range, 25–72 years) with myeloid sarcoma occurring at various sites and showed that 9 of 13 (69%) had concomitant involvement of the bone marrow by acute leukemia, myeloproliferative, or myelodysplastic disorders. The remainder of cases occurred de novo. Another study by Aggarwal et al.2 of 31 patients (range, 3–59 years) with biopsy-proven orbital GS showed concomitant hematologic malignancy in 13 of 31 (42%) cases. Of the
e1
Copyright © 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. Unauthorized reproduction of this article is prohibited.
Ophthal Plast Reconstr Surg, Vol. XX, No. XX, 2015
Case Reports
FIG. 1. A, Axial cut from CT demonstrating proptosis of OD and mass in the extraconal superolateral orbit. B, External photograph of OD after lateral canthotomy and inferior cantholysis demonstrating proptosis and significant chemosis. The chemosis was not hemorrhagic prior to the procedure.
remaining 18 patients, 72% developed AML within 3 to 21 months (median, 11.3 months). Other studies have reiterated that de novo tumor diagnosis often indicates development of peripheral blood or bone marrow involvement within a year.1 Diagnosis of GS can be difficult in the absence of systemic disease and may be confused with lymphoma, rhabdomyosarcoma, neuroblastoma, or other poorly differentiated tumors.1 Clinical and radiologic features do not aid significantly in differential diagnosis as they are not specific for GS. Histologic
features of myeloid differentiation such as eosinophilic granules within the cytoplasm may be helpful in establishing the diagnosis, although these nonspecific findings are not always present.11 The naphthol AS-D chloroacetate esterase stain (Leder stain) to identify cells containing myeloperoxidase has improved the precision of histologic diagnosis; however, the most accurate diagnosis is established with the use of immunochemical panels of stains.7 Commonly included in these immunochemical panels for myeloid sarcomas are myeloperoxidase, lysozyme, CD3, CD4, CD8, CD15, CD20, CD34, CD43, CD68, CD79a, CD117, CD163, factor VIII (FVIII), and glycophorin A.7 In the study by Aggarwal et al.,2 all 31 patients were positive for MPO, CD34, CD43, and CD117. There are no consensus guidelines on how best to treat GS, and therapy can vary depending on presentation at initial diagnosis or at relapse.6 Treatment approaches commonly involve AML chemotherapy, radiation therapy, tumor debulking, and allogeneic hematopoietic cell transplantation.6 Although overall survival rates for patients with leukemia have improved with modern therapies, mortality in patients with orbital leukemic tumors is high. A study on 27 pediatric patients showed median survival of 4.75 years (range 0.1–18 years) after diagnosis of orbital leukemic disease.12 Prompt diagnosis of GS and early treatment of concomitant systemic disease may improve long-term survival. This case is unusual in its fulminant presentation. There was no histologic evidence of an acute inflammatory process adjacent to the mass. There are reports in the literature of GS mimicking intracranial hematoma.13–15 O’Brien et al.15 describe a case of a 34-year-old presenting with acute altered mental status for 1 day found to have a subdural collection. The collection was biopsied and found to be consistent with GS. The patient succumbed to a subdural hematoma with tentorial herniation only 2 days later. McCabe et al.14 described a child presenting with reaccumulating epidural hematoma, which the authors postulate was due to granulocytic sarcoma in the extradural space. In this case, no significant bleeding was encountered during the orbitotomy. Given the rapid progression, it is plausible that the mass effect of the relatively anterior mass in addition to her thrombocytopenia resulted in deeper orbital bleeding. The authors may have only caught “the tip of the iceberg” on the CT scan as her orbit became much more tense in the ensuing hours. Blood products were not encountered perhaps because after debulking the obviously abnormal mass, no further exploration took place. That would also explain why her orbital process responded so well to surgery as the upper and lower limb of the lateral canthal tendon were left free. Another possibility is an acute orbital inflammatory process perhaps adjacent to the mass, with the biopsy specimen not being representative. With a paucity of histologic evidence of an acute inflammatory process, and no other infectious or vascular etiology identified, the authors can only speculate the pathogenesis of this unusual fulminant presentation.
CONCLUSION Orbital GS in adults occurs rarely and is generally a poor prognostic sign for the underlying disease. Biopsy with special histologic staining and immunohistochemistry plays a key role in diagnosis. In cases where GS presents in nonleukemic patients, there is high suspicion for underlying systemic disease, and patients should undergo prompt evaluation and careful monitoring for hematologic malignancy.
REFERENCES FIG. 2. Small aggregates of myeloid blast cells (medium sized mononuclear cells with dispersed chromatin and visible nucleoli).
e2
1. Stockl FA, Dolmetsch AM, Saornil MA, et al. Orbital granulocytic sarcoma. Br J Ophthalmol 1997;81:1084–8.
© 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
Copyright © 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. Unauthorized reproduction of this article is prohibited.
Ophthal Plast Reconstr Surg, Vol. XX, No. XX, 2015
2. Aggarwal E, Mulay K, Honavar SG. Orbital extra-medullary granulocytic sarcoma: clinicopathologic correlation with immunohistochemical features. Surv Ophthalmol 2014;59:232–5. 3. Mangla D, Dewan M, Meyer DR. Adult orbital myeloid sarcoma (granulocytic sarcoma): two cases and review of the literature. Orbit 2012;31:438–40. 4. Shields JA, Stopyra GA, Marr BP, et al. Bilateral orbital myeloid sarcoma as initial sign of acute myeloid leukemia: case report and review of the literature. Arch Ophthalmol 2003;121:138–42. 5. Burns A. Observation on the Surgical Anatomy of the Head Andmneck. 4th ed. Baltimore, MD: Granville Sharp Pattison, 1823. 6. Bakst RL, Tallman MS, Douer D, et al. How I treat extramedullary acute myeloid leukemia. Blood 2011;118:3785–93. 7. Alexiev BA, Wang W, Ning Y, et al. Myeloid sarcomas: a histologic, immunohistochemical, and cytogenetic study. Diagn Pathol 2007;2:42. 8. Yamauchi K, Yasuda M. Comparison in treatments of nonleukemic granulocytic sarcoma: report of two cases and a review of 72 cases in the literature. Cancer 2002;94:1739–46.
Case Reports
9. Zimmerman LE, Font RL. Ophthalmologic manifestations of granulocytic sarcoma (myeloid sarcoma or chloroma). The third Pan American Association of Ophthalmology and American Journal of Ophthalmology Lecture. Am J Ophthalmol 1975;80:975–90. 10. Byrd JC, Edenfield WJ, Shields DJ, et al. Extramedullary myeloid cell tumors in acute nonlymphocytic leukemia: a clinical review. J Clin Oncol 1995;13:1800–16. 11. Hutchison RE, Kurec AS, Davey FR. Granulocytic sarcoma. Clin Lab Med 1990;10:889–901. 12. Bidar M, Wilson MW, Laquis SJ, et al. Clinical and imaging characteristics of orbital leukemic tumors. Ophthal Plast Reconstr Surg 2007;23:87–93. 13. Smidt MH, de Bruin HG, van’t Veer MB, et al. Intracranial granulocytic sarcoma (chloroma) may mimic a subdural hematoma. J Neurol 2005;252:498–9. 14. McCabe MG, Broadbent V, Williams DM. Unusual cause of extradural haemorrhage. Med Pediatr Oncol 2001;36:654–6. 15. O’Brien CE, Saratsis AM, Voyadzis JM. Granulocytic sarcoma in a patient with blast crisis mimicking a chronic subdural hematoma. J Clin Oncol 2011;29:e569–71.
© 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc.
e3
Copyright © 2015 The American Society of Ophthalmic Plastic and Reconstructive Surgery, Inc. Unauthorized reproduction of this article is prohibited.
