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Retinal Hemorrhages in a Patient With Petechiae

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

A 44-year-old man with a 2-week history of fevers, night sweats, chills, and petechiae presented with painless, blurry vision in the left eye. His ocular symptoms began 2 days prior when he noticed dark scotomas in his central field and decreased visual acuity. There was no recent trauma or strenuous physical activity. He had no relevant medical, ocular, or family history, and he denied use of illicit drugs or anticoagulants.

Uncorrected visual acuity was 20/30 OD and 20/400 OS. Extraocular motility and intraocular pressures were normal. Results of an anterior examination was unremarkable. Dilated funduscopic examination of the left eye revealed a pink optic nerve with sharp margins, diffuse intraretinal hemorrhages and Roth spots extending from the posterior pole to the far periphery, and preretinal hemorrhage overlying the central macula (Figure, A). Spectral-domain optical coherence tomography through the preretinal macular hemorrhage demonstrated layered blood in the sub–internal limiting membrane space (Figure, B). The right fundus exhibited a similar appearance aside from the preretinal hemorrhage.

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Acute myeloid leukemia

D. Draw a complete blood cell count with differential to evaluate for leukemic retinopathy or blood dyscrasia

This patient had leukocytosis (white blood cells, 61 700/μL [to convert to cells × 109/L, multiply by 0.001]; normal limits, 4500-12 000/μL) with anemia (red blood cells, 2.71 × 106/μL [to convert to cell × 1012/L, multiply by 1.0]; normal limits, 3.9-5.5 × 106/μL; hemoglobin, 8.9 g/dL [to convert to g/L, multiply by 10.0]; normal limits, 14-18 g/dL; hematocrit, 26.8% [to convert to a proportion of 1.0, convert to 0.01]; normal limits, 40%-54%) and thrombocytopenia (platelet, 3.1 × 103/μL [to convert to cells × 109/L, multiply by 1.0]; normal limits, 150-400 × 103/μL). There were increases in the absolute number of neutrophils (7400/μL [to convert to cells × 109/L,multiply by 0.001]; normal limits, 17 800-53 600/μL), monocytes (18 040/μL [to convert to cells × 109/L, multiply by 0.001]; normal limits, 300-820/μL), basophils (620/μL [to convert to cells × 109/L, multiply by 0.001]; normal limits, 10-80/μL), and eosinophils (3700/μL [to convert to cells × 109/L, multiply by 0.001]; normal limits, 40-540/μL), with a normal lymphocyte count (2470/μL [to convert to  × 109/L, multiply by 0.001]; normal limits, 1320-3570/μL). Peripheral blood smear showed 35% blasts, while bone marrow flow cytometry revealed 50% abnormal monocytes and 23% myeloblasts. All findings were consistent with a diagnosis of acute myeloid leukemia with monocytic features; cytogenetic analysis revealed an inversion on chromosome 16, which has been associated with favorable prognostic outcomes.1

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Article Information

Published Online: February 14, 2019. doi:10.1001/jamaophthalmol.2018.6220

Corresponding Author: Christina Y. Weng, MD, MBA, Department of Ophthalmology, Baylor College of Medicine-Cullen Eye Institute, 1977 Butler Blvd, Houston, TX 77030 (christina.weng@bcm.edu).
Correction: This article was corrected on December 12, 2019, to fix a normal range of red blood cells, which was misreported as 14 to 18 × 106 per microliter. The correct value is 3.9 to 5.5 × 106 per microliter. The article has been corrected.

Author Contributions: Drs Zhuang and Weng had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Zhuang.

Study concept and design: Weng.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Zhuang, Weng.

Critical revision of the manuscript for important intellectual content: All authors.

Administrative, technical, or material support: Gupta, Weng.

Study supervision: Weng.

Conflict of Interest Disclosures: Dr Weng reports personal fees from Allergan Inc and Allimera Sciences Inc outside the submitted work. No other disclosures were reported.

Additional Contributions: We thank the patient for granting permission to publish this information.

References
1.
Estey  EH.  Acute myeloid leukemia: 2014 update on risk-stratification and management.  Am J Hematol. 2014;89(11):1063-1081. doi:10.1002/ajh.23834PubMedGoogle ScholarCrossref
2.
Kincaid  MC, Green  WR.  Ocular and orbital involvement in leukemia.  Surv Ophthalmol. 1983;27(4):211-232. doi:10.1016/0039-6257(83)90123-6PubMedGoogle ScholarCrossref
3.
Reddy  SC, Jackson  N.  Retinopathy in acute leukaemia at initial diagnosis: correlation of fundus lesions and haematological parameters.  Acta Ophthalmol Scand. 2004;82(1):81-85. doi:10.1046/j.1600-0420.2003.00197.xPubMedGoogle ScholarCrossref
4.
Awuah  A, Asiedu  K, Adanusa  M, Ntodie  M, Acquah  E, Kyei  S.  A case of leukemic retinopathy mimicking common ischemic retinopathies.  Clin Case Rep. 2015;4(2):133-137. doi:10.1002/ccr3.457PubMedGoogle ScholarCrossref
5.
Dombret  H, Gardin  C.  An update of current treatments for adult acute myeloid leukemia.  Blood. 2016;127(1):53-61. doi:10.1182/blood-2015-08-604520PubMedGoogle ScholarCrossref
6.
Karesh  JW, Goldman  EJ, Reck  K, Kelman  SE, Lee  EJ, Schiffer  CA.  A prospective ophthalmic evaluation of patients with acute myeloid leukemia: correlation of ocular and hematologic findings.  J Clin Oncol. 1989;7(10):1528-1532. doi:10.1200/JCO.1989.7.10.1528PubMedGoogle ScholarCrossref
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