Purpose Postpartum angiopathy as a cause of hemorrhagic events in young women is well known. It is unknown whether this disorder represents a true inflammatory and eventual autoimmune vasculitis, or represents a transient vasoconstriction related to the hormonal events of pregnancy and the postpartum period. On the other hand, there is debate how these lesions can be prevented or whether vasoconstriction monitoring has any use. Although several previous studies have reported and identified different target factors for events that occur during this specific period, little have been focused on the morphological imaging versatileness. We describe 5 cases with completely different vascular events in the postpartum period.
Materials and Methods From a retrospective cohort of 18 patients with vascular events in the early postpartum period we recruited 5 cases representing unique pathologies. They underwent CT, MRI, MRA, and serial catheter angiographies.
Results Mean age of the patients was 29.2 years. Al of them had history of comorbid pregnancy-related disorder (hypertension #4, preeclampsia #1, thunderclap headache #3). The distribution of morphologic pathology included: Case 1- putaminal hemorrhage due to reversible microaneurysm of lenticulostriate arteries in association with reversible occlusion of basilar and vertebral arteries; Case 2 – ventricular hemorrhage with hemolytic uremic syndrome and kidney failure; Case 3 – spinal, cranial, and abdominal hemorrhage in association with RCVS (reversible cerebral vasoconstriction syndrome); Case 4 – severe RCVS with progressive hemorrhagic ischemia; Case 5 – lacunar ischemia, cerebral hemorrhage due to cortical venous thrombosis. The clinical presentation was encountered from 1 to 4 weeks following an according to medical history uncomplicated pregnancy. All but one (Case 2) had favorable outcome.
Conclusion It is widely acknowledged the postpartum angiopathy may represent a hormonally mediated effect on the brain vessel intima precipitated by acute hypertension, evidently with affection of different territories (Cases 2, 3). Despite of different territorial manifestations the vascular events in this study did demonstrate similar features with an acute self-limited course and clinical symptomatology depending on the location. Various hormonal and biochemical factors have been identified playing a role in the deregulation of cerebral vascular tone of both the postpartum period and the RCVS. Some of them are common for both and may activate or lower the threshold for a progressive alteration of the vascular tone, which in turn drives the performance of different degrees of vascular related abnormalities including vasospasm, ischemia, microaneurysm, or hemorrhage as separated or combined events. Given the significant overlap between the RCVS and the postpartum vascular events, it is possible that they may represent a spectrum of potential morphological and clinical manifestations of a common underlying pathophysiology involving a breakdown in autoregulation with various degrees of altered cerebral vascular tone of mostly cerebral vasculature leading to hyperperfusion with consequent sequels like as reversible vasospasm and hemorrhage. The increasing understanding of possible triggers and overlap of features strongly suggests that the postpartum angiopathy and RCVS may represent a common end point of numerous different disease processes.
Disclosures A. Mironov: None.
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