br Introduction Chronic subdural hemorrhage

Introduction Chronic subdural hemorrhage (SDH) is a common disease in clinical neurosurgery. The incidence is 1–2 cases per 100,000 inhabitants and approximately 13.1 cases per 100,000 inhabitants per year on Awaji Island in Japan. A review of surgical treatment of chronic SDH suggests that twist-drill craniostomy or burr-hole craniostomy with closed-system drainage is the most effective treatment. Chronic SDH presents favorable results after surgical drainage. Despite this management, recurrent hemorrhage is a major problem. In addition, there have been case reports describing unexpected postoperative complications after chronic SDH drainage such as acute epidural hemorrhage, acute SDH within the previous hematoma cavity, intracranial hematomas, tension pneumocephalus, subdural empyema, and ischemic cerebral infarction.
Case Report A 55-year-old woman with a history of liver cirrhosis and hepatic encephalopathy (Child classification B) had a motor vehicle accident 3 weeks prior to presentation. Her initial neurological status after the event was clear consciousness with no neurological deficits, except dizziness. However, she complained of having progressive headaches, vomiting, and drowsiness 2 days before she visited our emergency department. Her Glasgow Coma Scale (GCS) score was E2M5V2. Laboratory data revealed a serum ammonia level of 19 mg/dL, platelet count of 85,000/uL, and a mildly prolonged prothrombin time of 13.4/11.9 seconds [international normalized ratio (INR), 1.29]. Head computed tomography (CT) demonstrated bilateral isodense to hyperdense chronic SDH in the frontal, temporal, and parietal regions (Fig. 1). Several hours later, the patient nevertheless suddenly became comatose (her GCS was E1M3V1). The neurological examination revealed a dilated right pupil without pupillary light reflex. The patient was immediately reintubated and reimaged by head CT. The scan image revealed an enclosed residual chronic SDH and additional acute SDH in the right frontotemporal region between the dura and the outer membrane outside the previous chronic SDH (Fig. 2). Postoperative coagulopathy was not assessed until her neurological state suddenly altered. These revealed an INR of 1.65 and a platelet count of 78,400. Her coagulopathy immediately reversed with another 12 units of buy Bleomycin Sulfate and six units of FFP. An emergent right craniotomy was performed. It revealed a fresh clot accumulating between the dura and the outer membrane. This was evacuated with a subsequent outer membranectomy, and the residual chronic SDH was drained. The inner membrane was finally excised as widely as possible to facilitate brain expansion. The procedure was uneventful. Her GCS returned to 15 with full motor power. After the surgical craniotomy, her coagulation data remained within normal limits. Seven days later, she was discharged home with no neurological deficits.
Discussion In 1932, Gardner introduced the osmotic gradient theory as the primary pathophysiology of chronic SDH. This theory suggests that increased protein content in the chronic subdural cavity leads to an influx of fluid as a result of oncotic pressure. The diffusion of fluid across the outer membrane creates a balance between plasma diffusion and/or rebleeding from neomembranes. However, in 1971, Weir disproved this theory on demonstrating that chronic SDH fluid is isosmotic to cerebral spinal fluid (CSF) and blood. Another theory postulates that chronic SDH has a dual origin: one origin is subdural hygroma (SDG) and the other origin is an acute SDH. In an unresolved SDG or acute SDH, the proliferation of dural cells forms an immature neomembrane (i.e., the outer membrane). A repeat microhemorrhage from the fragile new vessels of the neomembrane contributes to the formation of a chronic SDH. When bleeding exceeds absorption beyond the reserve capacity of the cranial cavity, a chronic SDH can enlarge and become symptomatic. Chronic SDH is a common entity in neurosurgery and has favorable treatment results. However, the definitive treatment strategy remains controversial. Various surgical treatments such as burr-hole drainage, enlarged craniotomy with partial membranectomy and drainage, and extended craniotomy with partial membranectomy with drainage have been retrospectively studied. Simple burr-hole drainage exhibits a lower incidence of rebleeding, compared to the latter two, although all three treatments reveal favorable outcomes. The twist-drill craniostomy or burr-hole craniostomy with or without closed-system drainage is the choice treatment because it is a safe and time-saving procedure and relatively decreases the risk of rebleeding. However, postoperative complications such as acute epidural hemorrhage, acute SDH in the previous hematoma cavity, intracranial hematomas, tension pneumocephalus, subdural empyema, and ischemic cerebral infarction remain concerns. The recurrence rate of postoperative chronic SDH is reportedly 2–37%. The most common bleeding site is between the outer and the inner membranes within the original cavity of the chronic SDH.