A 36-year-old Persian male was first referred to our hospital because of increasing fatigue, pallor, scattered petechiae, and abnormal gum bleeding. The patient had been otherwise healthy and did not report any past medical conditions. Anemia and thrombocytopenia in initial lab results prompted the hematologist–oncologist to obtain peripheral blood smear (PBS). Upon spotting blasts in the PBS, the hematologist–oncologist requested flow cytometry and bone marrow biopsy analysis, which subsequently confirmed the diagnosis of acute monocytic leukemia (AML-M5). The patient was then started on four sessions of induction chemotherapy, using cytosine arabinoside in combination with daunorubicin in the first session and cytosine arabinoside in combination with idarubicin for the following sessions. The last induction chemotherapy session took place 3 months after the initial diagnosis, after which it was concluded that the patient’s disease had entered remission phase.
Ten days following the last chemotherapy session, the patient presented to the emergency room with complaints of fever, headache, and blurred vision. The patient reported that he experienced fever and chills in the previous 2 days and it was poorly controlled by using acetaminophen. His headache in the frontal region was persistent, moderate in intensity, and started with a sharp, stabbing characteristic but became dull over time. His vital signs, apart from a 39.5 °C fever, were stable. The patient appeared pale and scattered petechiae on the upper extremities were observed. No neurological deficit was detected. The patient was admitted to the internal medicine service. Initial lab results revealed pancytopenia including severe neutropenia [total white blood cell (WBC) count 300 × 109/L], anemia [hemoglobin (Hg) 4.1 g/dL], and thrombocytopenia [platelets (Plt) 7000 109/L]. C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were significantly elevated (176 mg/L and 130 mm/hour, respectively). Coagulation parameters prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR) were normal (12 seconds, 25 seconds, and 1 respectively).
Spinal brain computed tomography (CT) scan was carried out, which indicated subarachnoid hemorrhage (SAH) in the left frontal and parietal lobes of the brain as shown in Fig. 1. Midline shift and intraventricular hemorrhage were not detected. Neurosurgery was consulted and they concluded that no intervention would be necessary because of the self-limited nature of patient’s SAH and absence of neurological deficit.
Due to the patient’s blurred vision, ophthalmology consult was requested. We performed a thorough ophthalmic examination. The patient’s visual acuity consisted of light perception in the right eye and 3-m finger count in the left eye. Pupils of both eyes were midsize and briskly reactive, and no relative afferent pupillary defect was detected. Intraocular pressure (IOP) of both eyes were within normal limits. Conjunctiva and sclera were white and quiet. Cornea was clear. Anterior chamber was deep and quiet, the lenses were clear, and no vitreous hemorrhage was detected. Overall, anterior segment examination was unremarkable. Dilated fundus examination was performed. As shown in Fig. 2, in the right eye subhyaloid hemorrhage along with peripapillary intraretinal and flame-shaped hemorrhages were observed. Subhyaloid and intraretinal hemorrhages, along with a yellowish dense exudate in the fovea, is apparent in the fundus image of the left eye, as shown in Fig. 3. These findings, along with the patient’s underlying pancytopenia as a result of leukemia, confirmed leukemic retinopathy.
Given the patient’s complicated condition, treating the underlying hematologic disturbance that caused SAH and retinal hemorrhages was our main treatment approach. The patient’s thrombocytopenia and anemia were improved by multiple transfusions of platelets and packed cells. He was also started on antibacterial, antifungal, and antiviral medications for neutropenic fever. The patient’s vision did not improve during the course of admission; however, he did not develop any neurologic deficit and his retinal hemorrhage appeared to be limited. Therefore, we decided to continue conservative treatment and observe the patient through regular follow-ups. As a result, vitrectomy or hyaloidotomy was not performed. The patient’s SAH was reduced, no neurological deficit was observed, and further neurosurgical intervention was deemed not necessary. He was discharged after a successful treatment of neutropenic fever and correction of thrombocytopenia and anemia.
We followed up with the patient for a duration of 3 months, during which he has shown significant improvement in his vision and retinal hemorrhage; however, complete resolution has not yet been achieved. The last fundus examination along with OCT are shown in Figs. 4 and 5. Shrinkage of retinal hemorrhages are observed in both eyes. Bilateral macular edema is also detected in OCT pictures.