Intracerebral Hemorrhage Following Evacuation of a Chronic Subdural Hematoma

Abstract

Burr hole drainage has been widely used to treat chronic subdural hematomas (SDH), and most of them are easily treated by simple trephination and drainage. However, various complications, such as, hematoma recurrence, infection, seizure, cerebral edema, tension pneumocephalus and failure of the brain to expand due to cerebro-cranial disproportion may develop after chronic SDH drainage. Among them, intracerebral hemorrhage after evacuation of a recurrent chronic SDH is very rare. Here, we report a fatal case of delayed intracerebral hemorrhage caused by coagulopathy following evacuation of a chronic SDH. Possible pathogenic mechanisms of this unfavorable complication are discussed and a review of pertinent literature is included.

Subependymal hemorrhage following drainage of chronic subdural hematoma: Probable causative mechanisms and prevention strategies

“…[6] Possible pathogenic mechanisms, for ICH in the thus compromised brain, include hemorrhage into previously undetected areas of contusion, damage to cerebral vasculature secondary to rapid peri-operative parenchymal shift, and sudden increase in cerebral blood flow (post-decompression) combined with focal disruption of autoregulation. [2,3,7] Compression by extra-axial collection decreases cerebral blood flow on the affected hemisphere and alters its vascular self-adjustment. [6,7] Some authors hypothesize that the rapid increase in cerebral blood flow (after drainage) in areas of the brain with altered vascular self-adjustment may be the most likely precipitating mechanism of intracerebral hemorrhage after surgical evacuation of cSDHs.…”

“…[2,3,7] Compression by extra-axial collection decreases cerebral blood flow on the affected hemisphere and alters its vascular self-adjustment. [6,7] Some authors hypothesize that the rapid increase in cerebral blood flow (after drainage) in areas of the brain with altered vascular self-adjustment may be the most likely precipitating mechanism of intracerebral hemorrhage after surgical evacuation of cSDHs. [2,7] This mechanism could have resulted in the subependymal bleed in our patient.…”

“…[6,7] Some authors hypothesize that the rapid increase in cerebral blood flow (after drainage) in areas of the brain with altered vascular self-adjustment may be the most likely precipitating mechanism of intracerebral hemorrhage after surgical evacuation of cSDHs. [2,7] This mechanism could have resulted in the subependymal bleed in our patient. However, as the compressed brain is more toward the surface, this mechanism is likely to explain superficial or lobar hematomas.…”

“…This process placed the controlateral bridging veins under tension, causing their collapse and ultimately resultant venous insufficiency and hemorrhagic infarction. [7] ICH after evacuation of chronic SDH may be caused by a sudden increase of cerebral blood flow following rapid decompression, combined with defective auto-regulation, fragile cerebral vessels, labile hypertension and hemorrhage into missing areas of contusion. [8] It is known that rapid decompression of chronic SDH can increase the amount of ICH due to rapid dynamic intracranial change.…”

Frontal and occipital horn ratio is associated with multifocal intraparenchymal hemorrhages in neonatal shunted hydrocephalus

“…MIPH is observed apart from neonatal shunted hydrocephalus; a similar phenomenon is described in the adult literature in patients who have undergone decompression of chronic subdural hematomas. 6,11 Several hypotheses have been postulated as to the etiology of the parenchymal hemorrhages: 1) perfusion breakthrough bleeding, 2) the effects of disrupted cerebral vascular autoregulation, 3) vascular damage secondary to the mechanical shift of cranial contents, and 4) the interplay between intracranial and venous pressures. [2][3][4] Choi et al 2 hypothesized that MIPH in infants is likely related to increased cerebral perfusion pressure and a premature brain vasculature with limited tolerance to alterations in perfusion.…”