Posters

Presenting Author Academic/Professional Position

Luis Salcedo

Academic Level (Author 1)

Resident

Discipline/Specialty (Author 1)

Internal Medicine

Academic Level (Author 2)

Resident

Discipline/Specialty (Author 2)

Internal Medicine

Academic Level (Author 3)

Resident

Discipline/Specialty (Author 3)

Internal Medicine

Academic Level (Author 5)

Faculty

Discipline/Specialty (Author 5)

Internal Medicine

Discipline Track

Clinical Science

Abstract Type

Research/Clinical

Abstract

Background: Posterior Reversible Encephalopathy Syndrome (PRES) represents a rare and potentially reversible neurotoxic disorder, distinguished by the presence of acute neurological manifestations and vasogenic edema, frequently detected through neuroimaging techniques. Although traditionally linked to hypertensive crises, renal insufficiency, and cytotoxic therapies, a growing body of evidence suggests that hematological malignancies, specifically acute lymphoblastic leukemia (ALL), should be regarded as an independent risk factor.

Case Presentation: A 73-year-old Hispanic female with a medical history significant for hypertension, type 2 diabetes mellitus, end-stage renal disease requiring hemodialysis, and Parkinson’s disease presented with a progressive decline in strength and altered cognitive status. Upon evaluation, she was diagnosed with acute encephalopathy and subsequently admitted for comprehensive diagnostic assessment. Imaging studies revealed the presence of pulmonary edema. Laboratory investigations identified B-lymphoblasts in the peripheral blood, and a subsequent bone marrow biopsy established a diagnosis of B-cell acute lymphoblastic leukemia (B-ALL).

Despite the administered dialysis and supportive therapeutic measures, her neurological condition continued to deteriorate. Electroencephalography demonstrated diffuse slowing of brain activity without any evidence of epileptiform discharges. A lumbar puncture indicated an elevation in protein levels and the presence of lymphoblasts within the cerebrospinal fluid, thereby suggesting central nervous system involvement. Magnetic resonance imaging (MRI) of the brain exhibited bilateral regions of restricted diffusion impacting multiple lobes, which were consistent with either posterior reversible encephalopathy syndrome or ischemic injury.

Her clinical trajectory was further complicated by the onset of respiratory failure necessitating mechanical ventilation, hemodynamic instability that required the administration of vasopressors, and the development of multiorgan failure. Considering the overall clinical context, imaging results, and the underlying hematologic malignancy, a diagnosis of PRES was strongly contemplated. A transition to palliative care was initiated following an interdisciplinary discussion and in alignment with the preferences of the family.

Discussion: This case exemplifies the intricacies involved in diagnosing Posterior Reversible Encephalopathy Syndrome (PRES) among critically ill patients afflicted with oncological conditions. Although frequently associated with the administration of immunosuppressive agents and chemotherapeutic protocols, PRES can emerge prior to the initiation of oncologic therapies, thereby implicating malignancy-induced endothelial dysfunction and cytokine-mediated neuronal injury as potential etiological factors. In the context of B-acute lymphoblastic leukemia (B-ALL), the presence of leukostasis, systemic inflammatory responses, and central nervous system (CNS) involvement may further aggravate disruptions to the blood-brain barrier, thereby heightening susceptibility to PRES. Furthermore, additional risk factors pertinent to this case encompassed end-stage renal disease (ESRD), poorly regulated hypertension, and metabolic abnormalities.

MRI remains the pivotal modality for diagnosis, typically revealing bilateral posterior white matter edema; however, there exists a possibility of overlap with ischemic alterations, particularly in severe manifestations. EEG generally exhibits nonspecific characteristics, such as generalized slowing of brain activity. Although PRES is frequently reversible with timely identification and intervention of its underlying precipitating factors, its clinical trajectory can be precipitous, particularly among patients experiencing hematological malignancies and multi-organ dysfunction.

Presentation Type

Poster

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Posterior Reversible Encephalopathy Syndrome (PRES) Secondary to B-Cell Acute Lymphoblastic Leukemia: A Case Report

Background: Posterior Reversible Encephalopathy Syndrome (PRES) represents a rare and potentially reversible neurotoxic disorder, distinguished by the presence of acute neurological manifestations and vasogenic edema, frequently detected through neuroimaging techniques. Although traditionally linked to hypertensive crises, renal insufficiency, and cytotoxic therapies, a growing body of evidence suggests that hematological malignancies, specifically acute lymphoblastic leukemia (ALL), should be regarded as an independent risk factor.

Case Presentation: A 73-year-old Hispanic female with a medical history significant for hypertension, type 2 diabetes mellitus, end-stage renal disease requiring hemodialysis, and Parkinson’s disease presented with a progressive decline in strength and altered cognitive status. Upon evaluation, she was diagnosed with acute encephalopathy and subsequently admitted for comprehensive diagnostic assessment. Imaging studies revealed the presence of pulmonary edema. Laboratory investigations identified B-lymphoblasts in the peripheral blood, and a subsequent bone marrow biopsy established a diagnosis of B-cell acute lymphoblastic leukemia (B-ALL).

Despite the administered dialysis and supportive therapeutic measures, her neurological condition continued to deteriorate. Electroencephalography demonstrated diffuse slowing of brain activity without any evidence of epileptiform discharges. A lumbar puncture indicated an elevation in protein levels and the presence of lymphoblasts within the cerebrospinal fluid, thereby suggesting central nervous system involvement. Magnetic resonance imaging (MRI) of the brain exhibited bilateral regions of restricted diffusion impacting multiple lobes, which were consistent with either posterior reversible encephalopathy syndrome or ischemic injury.

Her clinical trajectory was further complicated by the onset of respiratory failure necessitating mechanical ventilation, hemodynamic instability that required the administration of vasopressors, and the development of multiorgan failure. Considering the overall clinical context, imaging results, and the underlying hematologic malignancy, a diagnosis of PRES was strongly contemplated. A transition to palliative care was initiated following an interdisciplinary discussion and in alignment with the preferences of the family.

Discussion: This case exemplifies the intricacies involved in diagnosing Posterior Reversible Encephalopathy Syndrome (PRES) among critically ill patients afflicted with oncological conditions. Although frequently associated with the administration of immunosuppressive agents and chemotherapeutic protocols, PRES can emerge prior to the initiation of oncologic therapies, thereby implicating malignancy-induced endothelial dysfunction and cytokine-mediated neuronal injury as potential etiological factors. In the context of B-acute lymphoblastic leukemia (B-ALL), the presence of leukostasis, systemic inflammatory responses, and central nervous system (CNS) involvement may further aggravate disruptions to the blood-brain barrier, thereby heightening susceptibility to PRES. Furthermore, additional risk factors pertinent to this case encompassed end-stage renal disease (ESRD), poorly regulated hypertension, and metabolic abnormalities.

MRI remains the pivotal modality for diagnosis, typically revealing bilateral posterior white matter edema; however, there exists a possibility of overlap with ischemic alterations, particularly in severe manifestations. EEG generally exhibits nonspecific characteristics, such as generalized slowing of brain activity. Although PRES is frequently reversible with timely identification and intervention of its underlying precipitating factors, its clinical trajectory can be precipitous, particularly among patients experiencing hematological malignancies and multi-organ dysfunction.

 

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