Cerebral Haemorrhage, secondary to Acute Myeloid Leukaemia - Erler Zimmer
Clinical History
A 22-year-old male presented with a 2-week history of generalized malaise, weight loss, and bruised skin without any trauma. He recently developed 5 days of productive cough and fevers. Despite admission to the hospital for further investigations, he experienced a sudden loss of consciousness and passed away a few minutes after admission.
Pathology
The specimen, a horizontal brain slice displaying the superior cut surface, reveals two large intraparenchymal hemorrhages each measuring 5 cm in maximum diameter in the right frontal and parietal regions. Several smaller hemorrhages are also present in the white matter of both hemispheres. This is an instance of multiple intraparenchymal cerebral hemorrhages in a patient with acute myeloid leukemia (AML).
Further Information
Intraparenchymal brain hemorrhages result from ruptured small vessels within the brain, typically associated with sudden-onset neurological symptoms. The most common causes for spontaneous (non-traumatic) intraparenchymal hemorrhages are hypertension and cerebral amyloid angiopathy, with a peak incidence in the 6th decade of life.
AML, a cancer of hematopoietic progenitors, induces bone marrow failure due to the accumulation of immature blast cells in the marrow. These immature blasts impact the production of other bone marrow-derived cells, leading to bone marrow failure, resulting in anemia (decreased erythrocytes), thrombocytopenia (decreased platelet production and a hemorrhage tendency), and neutropenia (decreased neutrophil production). These complications contribute to a wide spectrum of disease complications, with infections being the leading cause of death in AML due to neutropenia. Intracranial hemorrhage is the second most common cause of death in AML, attributed to low or dysfunctional platelets caused by thrombocytopenia. A severe form of hemorrhage, disseminated intravascular coagulation (DIC), is common in AML, characterized by small blood clots developing throughout the bloodstream, blocking capillaries. Increased clotting depletes the platelets and clotting factors needed to control bleeding, resulting in excessive bleeding.
Symptoms vary based on the location and severity of the bleed. Interventions include surgical evacuation of the hematoma, reversal of coagulopathy, treatment of any seizures, and regulation of intracranial pressure. The severity of the bleed and clinical context determine the interventions. The 30-day mortality for intracerebral hemorrhage ranges from 35-50%, with most deaths occurring in the first 48 hours.
