Location of the chronic subdural haematoma: role of the gravity and cranial morphology

Chronic subdural haematoma (SDH) frequently originates from subdural hygroma (SDG). The cranial morphology can determine the location of SDG. Since SDG is the precursor of chronic SDH, the shapes of the cranium wall act an important role in location of chronic SDH. The authors tried to test this hypothesis. The computed tomographic scans or magnetic resonance images of 118 consecutive patients with chronic SDH were re-evaluated, and the symmetry of the cranium and location of the lesion were checked. The cranium was symmetrical in 55 patients (47%) and asymmetrical in 63 patients (53%). Chronic SDH was bilateral in 25 patients (21%) and unilateral in 93 patients (79%). It was more commonly bilateral in symmetrical craniums than in asymmetrical craniums (29.1% vs. 14.3%) (p = 0.0496). In 63 patients with asymmetric cranium, the chronic SDH was bilateral in nine patients, located on the opposite side of the flat side in 38 patients, and located on the same side of the flat side in 17 patients. This unequal distribution was statistically significant (p = 0.03). In four patients, the haematoma originated from the acute SDH located on the same side of the flat side. No reason could be found in the remaining 13 patients. Chronic SDH originating from SDG usually locates on the opposite to the flat side of the skull. The shape and posture of the cranium can predict the location of chronic SDH, as in the SDG.     

外份性硬膜下积液演变为血肿机制研究

已有越来越多的临床工作者[1-4]注意到头颅损伤后硬膜下积液(traumatic subdural hygroma,TSH)演变为慢性硬膜下血肿(chronic subdural hematoma,CSDH).但这种转变的确切过程及CSDH的自然演化过程尚处于认识阶段.笔者自2001年1月始对临床发现的130例TSH进行了CT追踪和随访,并对部分患者进行了手术干预和组织学检查.本文通过复习文献并结合临床提出TSH演变为CSDH的机理.     

The pathogenesis and clinical significance of traumatic subdural hygroma

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.     

Influence of cranial morphology on the location of chronic subdural haematoma

Background  

The purpose of the present study was to evaluate the relationship between cranial morphology and location of a chronic subdural haematoma (CSDH) in patients with and without intracranial vault asymmetry.     

Protein analysis of subdural hygroma fluid

Summary The pathogenesis of posttraumatic subdural hygroma still remains largely unknown. One of the suggested pathological mechanisms is the traumatic development of an arachnoid tear and the subsequent efflux of CSF into the subdural space. We performed a multifactorial analysis of the hygroma fluid obtained at operation in comparison to the simultaneously taken plasma and lumbar CSF. The results of the protein analysis support the CSF origin of the subdural hygroma fluid.     

Delayed evolution of posttraumatic subdural hygroma

Five hundred and forty-six patients in a consecutive series of 1,601 patients with craniocerebral trauma had computed tomography. One hundred and ninety-six patients had a follow-up CT scan. Thirteen patients (6.6%) developed apparently "silent" subdural hygromas of delayed evolution noted from six to 46 days after injury (average 22 days). Three of 10 patients (30%) improved after operation. No patient with a severe cerebral deficit (decortication or decerebration) improved. The three unoperated hygromas and the six that persisted after operation tended to resolve spontaneously. The infrequent and modest improvement following surgical treatment and the tendency to spontaneous resolution suggest that operation may be unnecessary in many patients with posttraumatic subdural hygroma of delayed evolution.     

Spontaneous evolution of posttraumatic subdural hygroma into chronic subdural haematoma

Summary Thirteen of 145 patients with post-traumatic subdural hygroma (SDHy) developed chronic subdural haematoma (CSDH) at the involved site over a period of 6 years. CSDHs were found at the site of SDHys with no history of further head injury at a mean interval of 56 days. It appeared that these 13 patients did not have any distinguishing clinical features early on. Old age and brain atrophy on CT scans do not seem to be reasonable causative factors in the evolution of SDHy into CSDH. Initial enlargement of subdural accumulations at an early stage of SDHy and a subsequent increase in density at a later stage may point to the development of CSDH from SDHy in some instances. Ten of these 13 CSDH cases underwent surgical drainage, and the remaining 3 cases received no specific management. All resolved completely. The prognosis was good in all patients. The possible mechanism for the evolution of SDHy into CSDH is discussed.     

Cerebrospinal fluid leakage into the subdural space: possible influence on the pathogenesis and recurrence frequency of chronic subdural hematoma and subdural hygroma

OBJECT: The purpose of this study was to clarify whether cerebrospinal fluid (CSF) leakage into the subdural space is involved in the genesis of chronic subdural hematoma (CSDH) and subdural hygroma (SH) and to clarify whether this leakage of CSF into the subdural space influences the postoperative recurrence rate of CSDH and SH. METHODS: In this prospective observational study, 75 cases involving patients treated surgically for CSDH (67 patients) or SH (8 patients) were evaluated with respect to clinical and radiological findings at presentation, the content of beta -trace protein (beta TP) in the subdural fluid (betaTPSF) and serum (betaTPSER), and the CSDH/SH recurrence rate. The betaTPSF was considered to indicate an admixture of CSF to the subdural fluid if betaTPSF/betaTPSER>2. RESULTS: The median beta TPSF level for the whole patient group was 4.29 mg/L (range 0.33-51 mg/L). Cerebrospinal fluid leakage, as indicated by betaTPSF/betaTPSER>2, was found to be present in 93% of the patients with CSDH and in 100% of the patients with SH (p=0.724). In patients who later had to undergo repeated surgery for recurrence of CSDH/SH, the betaTPSF concentrations (median 6.69 mg/L, range 0.59-51 mg/L) were significantly higher (p=0.04) than in patients not requiring reoperation (median 4.12 mg/L, range 0.33-26.8 mg/L). CONCLUSIONS: As indicated by the presence of betaTP in the subdural fluid, CSF leakage into the subdural space is present in the vast majority of patients with CSDH and SH. This leakage could be involved in the pathogenesis of CSDH and SH. Patients who experience recurrences of CSDH and SH have significantly higher concentrations of betaTPSF at initial presentation than patients not requiring reoperation for recurrence. These findings are presented in the literature for the first time and have to be confirmed and expanded upon by further studies.     

Post-traumatic subdural hygroma: diagnostic conditions and therapeutic attitude in Gabon

An excessive collection of cerebrospinal fluid in the subdural space is known as subdural hygroma, or hydroma. By far, the most common cause is severe cranial trauma. The diagnosis can be made by angiography or computer tomography and, with certainly, only by trephine or burr hole evacuation. 11 cases of post-traumatic subdural hygromas, mainly diagnosed during operative interventions, from April 1981 to September 1988, are reported. Most patients had acute forms of hygroma requiring acute surgical intervention. The acuteness could broken down as: coma (medium Glasgow coma scale: 6), lateralizing neurologic signs (4 cases) and temporal lobe herniation signs (7 cases). There were difficulties in obtaining angiographic studies. 10 patients underwent burr hole evacuation. Craniectomy was performed in one case. Time between cranial trauma and surgical intervention varied from 24 hours (6 cases) to 34 days. It appears that the prognosis is related to the extent of primary brain damage and not to the pressure exerted by the (usually) small mass lesion. The authors propose a clinical management of this lesion and hope for improvement in the diagnostic technics available.     

Prognostic significance of subdural hygroma for post-traumatic hydrocephalus after decompressive craniectomy in the traumatic brain injury setting: a systematic review and meta-analysis

Neurosurgical Review - Post-traumatic hydrocephalus (PTH) is a potentially morbid sequela of decompressive craniectomy for traumatic brain injury (TBI). Subdural hygromas are commonly identified...     

Simultaneous cranial and spinal subdural hematoma

A 59-year-old male presented with spinal subdural hematoma (SDH) with concomitant cranial chronic SDH manifesting as mild paraparesis and numbness in both lower extremities. Magnetic resonance (MR) imaging showed simultaneous occurrence of cranial and spinal SDHs. The patient was treated conservatively because of poor medical condition and mild neurological symptoms, and recovered well within 1 month. Serial follow-up MR imaging revealed spontaneous resolution of both lesions, with signal intensity changes suggesting the degenerative process of subacute hematoma. The spinal hematoma may have migrated from the cranial lesion. Spinal SDH is a potential sequela of chronic SDH in the cranium.     

Review: Origin of chronic subdural haematoma and relation to traumatic subdural lesions

The origin of chronic subdural haematoma CSDH and the pathogenesis of subdural hygroma SDG are still controversial issues. These issues and relationships between these traumatic subdural lesions are discussed. The origin of CSDH is usually a SDG, although a few cases are caused by acute subdural haematomas ASDH . Subdural hygroma is produced by separation of the dura arachnoid interface, when there is sufficient subdural space. When the brain remains shrunken, the SDG remains unre solved. Any pathologic condition inducing cleavage of tissue within the dural border layer at the dura arachnoid interface can induce proliferation of dural border cells with production of neomembrane. In growth of new vessels will follow, especially along the outer membrane, then bleeding from these vessels occurs. These unresolved SDGs become CSDHs by repeated microhaemorrhage from the neomembrane. Although most victims with ASDH underwent surgery or died, some patients could be managed conservatively. Since the ASDH is usually absorbed within a few weeks, only a very few ASDHs become CSDHs, when there is a sufficient potential subdural space. Chronic subdural hae matoma can arise from ASDH, but more commonly from SDG. Such transformation, or development of a new subdural lesion, is a function of the premorbid status and the dynamics of absorption and expansion.     

Traumatic subdural hygroma: pathology and meningeal enhancement on magnetic resonance imaging.

Five patients with traumatic subdural hygroma are reported with reference to its pathology and meningeal enhancement on magnetic resonance imaging. Hygromas showed initially iso- and, later, high intensity on both T1- and T2-weighted images compared with the intensity of the cerebrospinal fluid. In all cases of the thick hygromas, magnetic resonance imaging with gadolinium diethylene-triamine-pentaacetic acid showed meningeal enhancement. Intravenously injected radioisotope immediately flowed into the hygromas, but computed tomographic cisternography and gross inspection during the surgery showed no evidence of an influx of cerebrospinal fluid into the hygromas. Microscopic examination of the enhanced meninges revealed vascularized neomembrane with numerous fenestrations and pinocytosis underneath the dura mater. It is suggested from these data that the subdural neomembrane is associated with the development of the traumatic subdural hygromas. Meningeal enhancement would be useful to clarify the growing mechanism of traumatic subdural hygromas.