This case was originally published in 2017. The information provided in this case was accurate and correct at the time of initial program release. Any changes in terminology since the time of initial publication may not be reflected in this case.
A 64-year-old man presented to the emergency department following a motor vehicle accident (MVA). At the time of admission, he was noted to have a small right-sided extra-axial mass. He was placed on observation with no surgical intervention. Six weeks later, the patient developed persistent headaches. He was seen again at the outside hospital where a CT scan (Image A) was obtained. The patient underwent a craniotomy in which the material shown in Image B, Image C, Image D, and Image E was removed. Postoperatively, the patient did well and was discharged.
Whole Slide Image
The whole slide image provided is an H&E stain from a brain craniotomy.
What is the MOST LIKELY diagnosis?
Acute on chronic subdural hematoma
What is the MOST LIKELY significance of the collection of small hyperchromatic cells in Image E?
Langerhans cell histiocytosis
What is the etiology of the mass seen in Image A?
Discussion and Diagnosis
The CT scan (Image A) demonstrates a lesion with mixed densities, indicative of an acute on chronic subdural hematoma in which a chronic subdural hematoma rebled. The surgical pathology specimen seen in Image B is composed of a thick layer of granulation tissue overlain by acute hemorrhage. Image C reveals granulation tissue with a proliferation and ingrowth of capillaries. Image D is remarkable for the sharp border between the layer of acute hemorrhage along the bottom and the layer of granulation tissue with dilated capillaries. Capillaries seen within the region of hemorrhage are frequently the source of spontaneous rebleeding in chronic subdural hematomas. Image E shows a focus of extramedullary hematopoiesis, a phenomenon often seen in organized chronic subdural hematoma, consistent with the six week clinical history. Also noted are scattered hemosiderin-laden macrophages, so-called siderophages.
Subdural hematomas (SDHs) are collections of blood typically derived from rupture of bridging veins that drain the cerebral cortex veins into the sagittal sinus or from lacerations of cortical veins that have dissected between the arachnoid and dura. The vast majority of SDHs arise as a consequence of trauma; however, they may also be encountered in association with bleeding diatheses such as leukemia or rarely from an arterial hemorrhage. The traumatic origin is occasionally associated with the finding of a contrecoup injury. The severity of trauma required to initiate a subdural hematoma is variable and appears to be proportionate to the length of the space the vein must traverse to its dural attachment. Cerebral atrophy or extraventricular hydrocephalus may increase this length as well as the tension on the vein, predisposing it to rupture, even from relatively minor trauma. The “subdural space,” in contrast to the subarachnoid space, is actually not a space at all, virtual or otherwise, since it is adherent to the underlying arachnoid by junctions that weakly bind the arachnoid to the dura. Venous bleeding within the potential subdural space results in a dissection of the arachnoid away from the dura, which inhibits the free flow of blood about the brain and results in a localized mass that compresses the underlying brain. Hematoma formation, organization, and dissolution follow a fairly consistent pattern that has been relied upon in forensic investigations to determine a post traumatic interval (PTI).
- Within PTI 24 hours, free blood begins to organize and clot, laying down strands of fibrin.
- Within PTI 36 hours, fibroblasts derived from the dura form a single cell layer over the outer, or dural, side and are seen to enter the clot within seven to eight days.
- Within four days PTI, red blood cells have begun to fade and lose their bright red color, macrophages infiltrate into the clot, and siderophages are found within five days.
- Between PTI four to eight days, the layers of fibroblasts increase on both the inner and outer surfaces, and capillaries are found growing into the thickening membrane.
The formation of a chronic subdural hematoma is defined histologically by the presence of membrane on the inner surface, which takes between 15 to 21 days. Eventually, the fibroblasts lay down collagen, the membrane shrinks, and the hematoma is identified by only a slightly thickened layer of collagen that may or may not be discolored by hemosiderin.
The healing process, however, can be impacted by a number of factors including the size of the SDH, variations in the immune response, concomitant diseases, intoxications, and/or medications, making the dating of SDH older than 14 days less reliable. The most common factor interfering with accurate dating of chronic SDH is rebleeding. This rebleeding is typically derived from capillaries in the granulation tissue. Factors controlling the speed of rebleeding are poorly understood. While the bleeding is usually incremental, it may be rapid for unknown reasons; however, evidence of large veins bridging the subdural clot implicates a faster bleeding mechanism in some cases. At one time, rebleeding was believed to be related to membranous stretching associated with increased osmotic pressure in the sac from the degenerating cellular debris within the central clot; however, subsequent studies do not support this.
The differential diagnosis of intracranial hemorrhages includes the epidural hematoma, which also presents as an extra-axial hematoma but most commonly is associated with a tear of the middle meningeal artery related to a fracture. Occasionally, a vascular malformation, such as an aneurysm, may rupture into the cerebral parenchyma and break through the cortex to form a subarachnoid hematoma.
Take Home Points
- Subdural hematomas are most commonly caused by trauma and result from tearing of bridging veins which normally drain blood from the cortex into dural sinuses.
- Clotting and organization of a chronic subdural hematoma follows a fairly consistent pattern which facilitates its use in forensic investigations.
- Rebleeding in chronic subdural hematomas may be multifactorial and is most frequently the result of bleeding from new capillaries or from expansion of the subdural sac secondary to cerebrospinal fluid accumulation.
- Chronic subdural hematomas can acutely rebleed without a history of repeat trauma.
- DiMaio VJ, DiMaio D. Forensic Pathology. 2nd ed. Boca Raton, FL: CRC Press; 2001:147-85.
- Haines DE, Harkey HL, al-Mefty O. The “subdural” space: a new look at an outdated concept. Neurosurgery. 1993;32(1):111-20.
- Leestma JE. Forensic Neuropathology. 2nd ed. Boca Raton, FL: CRC Press; 2009:299-555.
- Li R, Reddy VV, Palmer CA. Extramedullary hematopoiesis: an unusual finding in subdural hematomas. Case Rep Pathol. 2011;2011:718585.
- Munro D, Merritt HH. Surgical pathology of subdural hematoma. Based on a study of one hundred and five cases. Arch Neurol Psychiatr. 1936;35:64-78.
- Van den Bos D, Zomer S, Kubat B. Dare to date: age estimation of subdural hematomas, literature, and case analysis. Int J Legal Med. 2014;128(4):631-40.
- What is the MOST LIKELY diagnosis?
- A. Abscess
- B. Acute on chronic subdural hematoma
- C. Granuloma
- D. Lymphoma
- E. Metastatic sarcoma
- What is the MOST LIKELY significance of the collection of small hyperchromatic cells in Image E?
- A. Extramedullary hematopoiesis
- B. Glioma
- C. Langerhans cell histiocytosis
- D. Lymphoma
- E. Meningothelial hyperplasia
- What is the etiology of the mass seen in Image A?
- A. Arachnoidal proliferation
- B. Infection
- C. Neoplasia
- D. Traumatic hemorrhage
- E. Vascular malformation