Syncope as Initial Presentation in an Undifferentiated Type Acute Myeloid Leukemia Patient with Acute Intracranial Hemorrhage

Abstract

Intracranial hemorrhage (ICH) is a catastrophic complication in patients with acute myeloid leukemia (AML). AML cells, especially in the acute promyelocytic leukemia subtype, may release microparticles (MPs), tissue factor (TF), and cancer procoagulant (CP) to promote coagulopathy. Hyperfibrinolysis is also triggered via release of annexin II, t-PA, u-PA, and u-PAR. Various inflammatory cytokines from cancer cells, such as IL-1β and TNF-α, activate endothelial cells and promote leukostasis. This condition may increase the ICH risk and lead to poor clinical outcomes. Here, we present a case under a unique situation with acute ICH detected prior to the diagnosis of AML. The patient initially presented with two episodes of syncope. Rapidly progressive ICH was noted in follow-up computed tomography (CT) scans. Therefore, we highlight that AML should be among the differential diagnoses of the etiologies of ICH. Early diagnosis and timely intervention are very important for AML patients.

Keywords: acute myeloid leukemia; blast crisis; hyperleukocytosis; intracranial hemorrhage; syncope.

Figure 1

On the day 1 brain computed tomography (CT), a 13 mm lesion with hyperdensity was found in the left temporal region, with suspected intracerebral hemorrhage. On the day 2 brain CT, multifocal intracranial hemorrhages in bilateral cerebral hemispheres were noted, the largest being a 30 mm lesion in the left thalamus. The midline structures were shifted to the right side. Extensive swelling was present in the cerebellum and brain stem.

Figure 2

In an APL model, the acute myeloid leukemia (AML) cell produces microparticles (MPs), tissue factor (TF), and cancer procoagulant (CP), which act on the coagulation cascade to promote coagulopathy. The release of annexin II, t-PA, u-PA, and u-PAR from AML cells converts plasminogen into plasmin, causing hyperfibrinolysis. Various inflammatory cytokines from cancer cells, such as IL-1β and TNF-α, also activate endothelial cells and promote leukostasis.