Subdural hygroma (SDG) is a common post-traumatic lesion. Despite its common occurrence, the pathogenesis and clinical significance are uncertain. The author reviewed the literature to clarify the present knowledge on the pathogenic, diagnostic and therapeutic aspects of this controversial lesion. A trivial trauma can cause a separation of the dura-arachnoid interface, which is the basic requirement for the development of a SDG. If the brain shrinks due to brain atrophy, excessive dehydration or decreased intracranial pressure, fluid collection may develop by a passive effusion. Most SDGs resolve when the brain is well expanded. However, a few SDGs become chronic subdural haematomas, when the necessary conditions persist over several weeks. Since the majority of patients with a SDG do not show a mass effect, surgery is rarely required. Outcome is closely related to the primary head injury not to the SDG itself. The complexity of SDG depends on various factors including the dynamics of absorption and expansion, duration of observation, and indication and rate of surgery, besides variety of the primary head injury in types and severity. SDG is a common epiphenomenon of head injury.
We present a series of 61 traumatic subdural hygromas, and discuss the pathogenic mechanisms and natural history of this condition. It commonly occurred in patients over 50 years of age and before 5 years of age. Fifty-two cases (85.2%) were diagnosed 3 days after head injury. Glasgow Coma Score (GCS) on admission was 3-8 in 24 (39.3%), 9-12 in 15 (24.6%) and 13-15 in 22 patients (36.1%). Although three patients (4.9%) showed slow deterioration, most hygromas were clinically 'silent'. Thirty-eight patients (62.3%) were managed conservatively and 23 patients (37.7%) underwent surgery. Only five patients (21.7%) showed gross improvement after surgery, even though surgery was performed only for enlarged hygromas shown by serial computed tomography. In five patients (8.2%), a chronic subdural haematoma subsequently developed from a hygroma. A favourable outcome (good recovery or moderate disability) occurred in 59%, an unfavourable outcome (severe disability and vegetative state) in 28%, and death resulted in 13%. Outcome was closely related to the severity of primary head injury.
We compared the ultrasound (US) findings of gallbladder (GB) perforation with computed tomography (CT) in 13 patients with GB perforation confirmed at surgery. The common findings of GB perforation were pericholecystic fluid collection and layering of GB wall on US, pericholecystic fluid collection, streaky omentum or mesentery, and GB wall defect on CT. Pericholecystic fluid collection, layering of GB wall, and cholelithiasis were similarly detected on US or CT. GB wall defect and/or bulging of the GB wall suggested a site of perforation was revealed in five patients (38.5%) on US and nine (69.2%) on CT. CT further disclosed the findings of streaky omentum or mesentery (84.6%). CT was superior to US for diagnosis of GB perforation.
We report three cases of intraperitoneal seeding from hepatoma. Manifestation of intraperitoneal seeding from hepatoma were intraperitoneal masses (N = 2) and peritoneal thickening (N = 1). Main vascular feeder to intraperitoneal masses was omental branches of the gastroduodenal artery and/or the superior mesenteric artery.
Lymphomatoid granulomatosis usually presents as a primary lung affliction with secondary metastatic spread to the central nervous system(CNS), and its initial manifestation purely as a CNS disease is rare. A 57-year-old man with histologically proven lymphomatoid granulomatosis of the brain as the sole manifestation of the disease is presented.
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