Inner calvarial erosion from traumatic subdural haematoma in infancy

Case report This is a report of a case of a subdural haematoma in infancy of possible non-accidental aetiology with raised pericerebral pressure, which we postulate has eroded the inner table of the cranial bones and resulted in leakage of marrow precursor cells into the extradural space.Result Subdural tapping via the fontanelle has created a channel allowing subsequent ingress of nucleated red cell precursors into the subdural space. This addition to the subdural collection has prolonged its course necessitating subduro-peritoneal shunting.     

Chronic subdural haematoma associated with disturbance of consciousness: significance of acute-on-chronic subdural haematoma

Abstract

Objective:

Detailed features of chronic subdural haematoma (cSDH) associated with disturbance of consciousness and acute-on-chronic subdural haematoma (a/cSDH), in which acute subdural haematoma overlaps cSDH, remain poorly understood. The object of this study was to clarify both characteristics of cSDH associated with disturbance of consciousness and the significance of a/cSDH.

Methods:

Clinical factors and computed tomography (CT) findings were retrospectively investigated in 349 consecutive patients admitted between 2006 and 2013 and diagnosed with cSDH.

Results:

Glasgow Coma Scale (GCS) was ≤?8 in 21 patients (6.0%) and 9–14 in 29 patients excluding aphasia and/or dementia (8.3%). Multiple logistic regression analysis indicated that a/cSDH, female sex and haemodialysis were significantly related to severe disturbance of consciousness (GCS?≤?8). Predictors for a/cSDH observed in 29 patients (8.3%) were trauma history within 7?days before admission, high prothrombin time–international rate, and use of anticoagulants and/or antiplatelets. Unfavourable outcomes were observed in 29 of 299 patients (9.7%) without consciousness disturbance, compared to 27 of 50 patients (54%) with consciousness disturbance. Predictors of unfavourable outcome were consciousness disturbance, increase in age, malignancy, trauma history within 7?days and haemodialysis.

Discussion:

Disturbance of consciousness associated with cSDH, often caused by either a/cSDH or concomitant disease, frequently resulted in unfavourable outcomes. As a result, in cSDH patients associated with disturbance of consciousness, underlying conditions, especially a/cSDH, which is often caused by haemostatic abnormality, should be clarified and managed.     

Prospective randomized placebo-controlled double-blind clinical study of adjuvant dexamethasone with surgery for chronic subdural haematoma with post-operative subdural drainage: Interim analysis

Most chronic subdural haematomas (CSDH) are successfully treated neurosurgically. However, operative recurrences occur with a frequency 3–30%, consume resources and potentially prolong length-of stay (LOS). The only adjuvant factor proven to significantly decrease CSDH recurrence rate (RR) is post-operative subdural drainage. Corticosteroids have been used to conservatively manage CSDH. One non-randomised study also compared dexamethasone (DX) as an adjunct to surgery without post-operative drainage: whilst a null effect was observed, the ‘surgery-alone’ group consisted of only n = 13. We present an interim analysis of the first registered prospective randomised placebo-controlled trial (PRPCT) of adjuvant DX on RR and outcome after CSDH surgery with post-operative drainage. Participants were randomised to either placebo or a reducing DX regime over 2 weeks, with CSDH evacuation and post-operative drainage. Post-operative mortality (POMT) and RR were determined at 30 days and 6 months; modified Rankin Score (mRS) at discharge and 6 months. Post-operative morbidity (POMB) and adverse events (AEs) were determined at 30 days. Interim analysis at approximately 50% estimated sample size was performed (n = 47). Recurrences were not observed with DX: only with placebo (0/23 [0%] v 5/24 [20.83%], P = 0.049). There was no significant between-group differences in POMT, POMB, LOS, mRS or AEs.ConclusionsIn this first registered PRPCT, interim analysis suggested that adjuvant DX with post-operative drainage is both safe and may significantly decrease recurrences. A 12.5% point between-groups difference may be reasonable to power a final sample size of approximately n = 89. Future studies could consider adjuvant DX for longer than the arbitrarily-chosen 2 weeks.     

Acute subdural haematoma in a neonate

A male child of Jordanian parentage who was born in an ambulance was immediately admitted to Al-Adan Hospital, Kuwait, with left parietal cephalhaematoma. Two days later he started to convulse on the right side of the body and was found to have a dilated left pupil and spastic right leg. A computed tomographic brain scan showed a large subdural haematoma which extended from the posterior interhemispheric fissure to cover the left convexity of the brain (type II of Hayashi et al. [6]). The subdural haematoma was removed through a left temporoparietal craniectomy. The child had a smooth postoperative recovery and was in a neurologically satisfactory condition during a 16-month follow-up period.     

Chronic subdural haematoma complicating spinal anaesthesia

Abstract Cranial subdural haematoma formation following spinal anaesthesia is exceptionally rare. A 38-year-old male developed headache two days after testicular surgery under spinal anaesthesia. The headache progressed in spite of analgesics, and three weeks later cranial CT showed a large chronic subdural haematoma in the left fronto-parietal region. The patient improved after surgical decompression. The pathogenesis of subdural haematoma formation after dural puncture is discussed and the literature briefly reviewed. Prolonged and severe post-dural puncture headache should be viewed with suspicion and investigated promptly to rule out any intracranial complication.     

Arachnoid cyst with intracystic haemorrhage and subdural haematoma: case report and literature review

Abstract Arachnoid cysts (AC) are usually asymptomatic. However, very rarely they can become symptomatic due to cyst enlargement or haemorrhage, often after head trauma. In such cases bleeding is often confined to the subdural space, but intracystic haemorrhage has rarely been observed. We report a case of a child who had intracranial hypertension syndrome due to a right middle cranial fossa AC with intracystic bleeding and subdural haematoma.     

Bilingual aphasia due to spontaneous acute subdural haematoma from a ruptured intracranial infectious aneurysm

We report a case of spontaneous subdural haematoma due to ruptured intracranial infectious aneurysm, presenting with bilingual aphasia and illustrating differential language recovery. A 62-year-old right-handed bilingual gentleman, with a diagnosis of infective endocarditis, developed headache and became expressively aphasic in the English language. Three days later he was receptively and expressively aphasic in both English and Arabic. Cranial MRI scans showed a left-sided acute subdural haematoma with mass effect and midline shift. Contrast CT brain scans showed an enhancing speck adjacent to the clot and cerebral angiogram confirmed a distal middle cerebral artery aneurysm. He underwent image-guided craniotomy, evacuation of the subdural haematoma and excision of the aneurysm. Histopathological examination was consistent with an infectious intracranial aneurysm. Postoperatively his aphasia did not improve immediately. He had widened pulse pressure due to severe aortic regurgitation, confirmed on echocardiography. He underwent aortic valve replacement and mitral valve repair, following which his aphasia recovered gradually. Initially the recovery of his language was limited to Arabic. About a week later he recovered his English language as well. At 3-year follow-up he is doing well and has no neurological deficits. His aphasia has recovered completely. The present case is unique because of (a) presence of pure subdural haematoma, and (b) the differential susceptibility and recovery of native (L1) and acquired language (L2) in presence of a common pathology. The neurology of language in a bilingual is analysed and possible mechanisms discussed.     

Mathematical formulae to estimate chronic subdural haematoma volume. Flawed assumption regarding ellipsoid morphology

Mathematical formulae are commonly used to estimate intra-cranial haematoma volume. Such formulae tacitly assume an ellipsoid geometrical morphology. Recently, the ‘XYZ/2’ formula has been validated and recommended for chronic subdural haematoma (CSDH) volumetric estimation. We aimed to assess the precision and accuracy of mathematical formulae specifically in estimating CSDH volume, and to determine typical CSDH 3-D morphology. Three extant formulae (‘XYZ/2’, ‘π/6·XYZ’ and ‘2/3S·h’) were compared against computer-assisted 3D volumetric analysis as Gold standard in CTs where CSDH sufficiently contrasted with brain. Scatter-plots (n = 45) indicated that, in contrast to prior reports, all formulae most commonly over-estimated CSDH volume against 3-D Gold standard (‘2/3S·h’: 44.4%, ‘XYZ/2’: 48.84% and ‘π/6·XYZ’: 55.6%). With all formulae, imprecision increased with increased CSDH volume: in particular, with clinically-relevant CSDH volumes (i.e. >50 ml). Deviations >10% of equivalence were observed in 60% of estimates for 2/3S·h, 77.8% for ‘XYZ/2’ and 84.4% for ‘π/6·XYZ’. The maximum error for ‘XYZ/2’ was 142.3% of a clinically-relevant volume. Three-D simulations revealed that only 4/45 (9%) CSDH remotely conformed to ellipsoid geometrical morphology. Most (41/45, 91%) demonstrated highly irregular morphology neither recognisable as ellipsoid, nor as any other regular/non-regular geometric solid. Conclusions: Mathematical formulae, including ‘XYZ/2’, most commonly proved inaccurate and imprecise when applied to CSDH. In contrast to prior studies, all most commonly over-estimated CSDH volume. Imprecision increased with CSDH volume, and was maximal with clinically-relevant CSDH volumes. Errors most commonly related to a flawed assumption regarding ellipsoid 3-D CSDH morphology. The validity of mean comparisons, or correlation analyses, used in prior studies is questioned.     

Arteriovenous malformation presenting as acute subdural haematoma

Abstract

A case of acute subdural haematoma caused by ruptured arteriovenous malformation is reported. At surgery, there was no association with intracerebral haematoma or definite subarachnoid haemorrhage. The mechanism of acute subdural haematoma in the present case was considered to be rupture of an arteriolized bridging vein drained by arteriovenous malformation. [Neurol Res 1993; 15: 353-355]     

Marked alterations in the cellular localisation and levels of apolipoprotein E following acute subdural haematoma in rat

Apolipoprotein E (apoE) plays a role in the response to acute brain injury, the mechanisms as yet remain unknown. In the present study, alterations in the immunohistochemical localisation of apoE in rat cortex were examined at 30 min. 2 h or 4 h following production of an acute subdural haematoma. Levels of apoE were determined in cortex by immunoblotting at 30 min and 4 h post-haematoma. Extensive areas of ischaemic cell damage were observed in the cortex underlying the haematoma with minimal damage observed in shams. In sham animals, apoE immunoreactivity was confined to astrocytes and their processes. Following the haematoma induction, apoE immunoreactivity was dramatically altered. At 30 min post-haematoma, intense apoE staining was observed in clusters of neuronal perikarya and the neuropil throughout the cortical layers underlying the haematoma and this persisted at 2 h and 4 h post-haematoma. Additionally, at 4 h post-haematoma marked apoE staining of discrete foci within the neuropil closely associated with capillaries was consistently observed in the ipsilateral cortex. Immunoblotting indicated there were no significant alterations in the cortical levels of apoE at 30 min post-haematoma but, at 4 h post-haematoma, there was a significant elevation (27%, P < 0.001) in the levels of apoE in cortex underlying the haematoma compared to control levels. The results indicate that following acute subdural haematoma, a rapid cellular redistribution of apoE occurs and precedes a significant elevation in the levels of apoE. These alterations in apoE may occur, at least initially, as part of the brain's protective response to injury.     

Facial nerve palsy—an unusual complication after evacuation of a subdural haematoma or hygroma in children

Objective This paper reports and discusses on the possible etiology of postoperative contralateral facial nerve palsy after uneventful evacuation of a subdural haematoma or hygroma after mild head trauma in two children with pre-existing middle cranial fossa subarachnoid cysts.Results Two 14- and 15-year-old boys had prolonged headaches after mild head injuries. CT showed a right-sided middle cranial fossa arachnoid cyst in each patient. In one patient, an ipsilateral subdural haematoma was identified, and in the other, bilateral hygromas were identified. Exacerbation of symptoms required emergency evacuation of the subdural haematoma in the first child, and bilateral external drainage of the hygroma in the other child. In both children the late postoperative period was complicated by peripheral facial nerve palsies contralateral to the arachnoid cyst.Conclusion Facial nerve palsy may be a complication of hygroma or haematoma drainage. The etiology is not clear; traction of the facial nerve due to displacement of the brainstem may be the most likely explanation.     

Coagulopathy and outcome in patients with chronic subdural haematoma

OBJECTIVE: The coincidence of coagulatopathy and chronic subdural haematoma (CSH) requires correction of coagulation to facilitate surgery. We investigated the correlation between coagulopathy and outcome in CSH patients. MATERIAL AND METHODS: We analysed past medical history, surgical treatment and coagulation parameters of 114 patients. RESULTS: Coagulation disorders were found in 42%. Preoperative treatment with prothrombin complex concentrate was necessary in 14%. A significant difference (P < 0.05) of the preoperative level of platelets was found between recurrent CSH and non-recurrent group. Totally, we had to perform re-operations in 17.5%. Eighty-one patients presented with Glasgow coma scale (GCS) > or = 13. After surgery GCS was > or = 13 in n = 92. There was an improvement of GCS in 46 cases, 61 patients maintained GCS score levels. Outcome was significantly worse in the alcoholic group (P < 0.001), and in the recurrent group (P < 0.05). In patients with substitution of coagulation factors, outcome was worse in the group with post-operative substitution only (P < 0.05). CONCLUSION: In CSH, the coagulation parameters and a subtle correction of coagulation are of special interest, regarding the worse outcome in patients with recurrent CSH and in those requiring post-operative substitution.     

Contralateral acute epidural haematoma following evacuation of a chronic subdural haematoma with burr-hole craniostomy and continuous closed system drainage: a rare complication

Chronic subdural haematoma (CSDH) is one of the most frequent causes for neurosurgical intervention. Although the prognosis is generally good and treatment modalities are well established, some devastating intracranial haematomas can complicate its evacuation. The authors report here a case of an acute epidural haematoma occurring after evacuation of a contralateral chronic subdural haematoma (CSDH) with burr-hole craniostomy and continuous closed system drainage without irrigation. Since this is a rare, but potentially life-threatening, complication, clinicians should suspect its occurrence when an unexpected postoperative course is demonstrated.     

Long-term survival after chronic subdural haematoma

Outcome after chronic subdural haematoma (CSDH) is invariably assumed favourable: however, little data regarding long term survival (LTS) exists. One study reported excess mortality restricted to year 1, but with expected actuarial rates thereafter. We aimed to determine LTS after CSDH in a retrospective analysis relative to actuarial data from age-matched controls. Data was obtained in n = 155, (M:F 97:58, 69.3 ± 2.3 years). Follow-up maxima was 14.19 years (mean: 4.02 ± 3.07 years, median: 5.2 years). Mortality in-hospital, at 6 months, 1 year, 2 years and 5 years was n = 13 (8.39%), n = 22 (14.19%), n = 31 (20.35%), n = 42 (27.1%) and n = 54 (34.84%). LTS was significantly worse than controls (5.29 ± 0.59 years vs. 17.74 ± 1.8 years, hazard ratio [HR]: 3.52, P < 0.0001). Death most frequently related to pneumonia/sepsis and ischemic heart disease (IHD). Median modified Rankin score (mRS) in those discharged home (n = 94, 60.65%) was 2 [IQR: 1–3]. Discharge mRS in those who died at 6 months, 1 year, 2 years and 5 years was 5 [IQR: 3–6], 5 [IQR: 4–6], 3 [IQR: 1–3], 4 [IQR: 2–5]. Discharge mRS was significantly worse with year 1 mortality (P = 0.014). LTS related to discharge mRS (HR: 37.006, P < 0.001), post-operative motor-score (HR: 0.581, P = 0.0026), IHD (HR: 5.186, P = 0.005), warfarin-use (HR: 5.93, P = 0.036) and dementia (HR: 5.39, P = 0.031). No long term recurrences (LTR) were recorded. Although most were discharged home with mRS = 2, LTS was markedly less than previously reported: peers lived 12.4 years longer. Although greater in year 1, excess mortality was not restricted to year 1, but continued throughout prolonged follow-up. LTS related to discharge disability and dependence, and co-morbid risk factors for cerebral atrophy. No LTR suggests that, once ultimately closed, the ‘subdural space’ remains closed. CSDH patients represent a vulnerable group who require continued long-term medical surveillance.     

外伤性急性硬膜下血肿选择性非手术治疗体会

目的探讨急性硬膜下血肿选择性非手术治疗的适应证。方法回顾性分析近5年来保守治疗74例外伤性急性硬膜下血肿患者的临床资料。所有患者入院后即行持续颅内压监护,并根据颅内压的变化随时调整治疗方案。结果62例保守治疗,6例急诊开颅清除血肿,4例亚急性期血肿钻孔冲洗引流,2例慢性硬膜下血肿钻孔引流。结论除急诊手术外,部分急性硬膜下血肿患者在严密监护下,尤其在持续颅内压监护下,保守治疗或延期手术取得良好的效果。     

Anticoagulants and antiplatelet agents and the risk of development and recurrence of chronic subdural haematomas

Seventy-one patients from northern Sweden were diagnosed with chronic subdural haematomas (CSDH) and treated at the Department of Neurosurgery at Umeå University Hospital over 12 months. Fifty-four patients with CSDH had a history of head trauma (trauma group), while 17 patients had no previous head trauma (non-trauma group). In the non-trauma group 71% of patients were treated with anticoagulants or antiplatelet aggregation agents (AAA) compared to 18% in the trauma group. Considering only AAA, 59% of the non-trauma patients were treated with these drugs versus 17% of patients in the trauma group. The recurrence rate for all patients was 17%. These findings confirm that the use of anticoagulants and AAA is over-represented in patients with non-traumatic CSDH. In our study, recurrence was not associated with previous use of anticoagulants or AAA.     

Blood pressure is not associated with haematoma enlargement in acute intracerebral haemorrhage

Background and purpose: We performed an observational study that compared baseline and subsequent blood pressure (BP) measurements and its association with haematoma enlargement (HE) in patients with intracerebral haemorrhage (ICH). Methods: We prospectively studied consecutive patients with supratentorial spontaneous ICH within the first 6 h after the onset of symptoms. HE was defined as an increase ≥33% in the volume of haematoma on the CT obtained 24–48 h after the onset of symptoms as compared with the CT at admission. We recorded systolic BP (SBP), diastolic BP (DBP) and mean BP (MBP) at admission and at 6, 12, 18 and 24 h after onset; the maximum SBP, DBP and MBP during the study period; the maximum SBP and DBP within intervals; the mean of all BP readings; administration of antihypertensive agents. Results: We studied 60 patients whose mean age was 72.1 ± 11.3 years. HE was observed in 27 (45%) patients. No statistically significant differences were observed in any of the analyses that compared BP parameters between the HE and non‐HE groups (two‐way anova ). Conclusions: In an exploratory analysis, we did not find an association between BP and HE within the first 24 h after an acute ICH.     

Occurrence and recurrence of spontaneous chronic subdural haematoma is associated with a factor XIII deficiency

Objective

In some patients, chronic subdural haematoma (cSDH) appears to occur spontaneously with frequent re-bleeding events. The pathophysiology of this phenomenon is still poorly understood. Because coagulation factor XIII (FXIII) is known to be involved in vascular integrity, endothelial barrier function and wound healing, we evaluated the role of FXIII in spontaneous cSDH.

Methods

We prospectively scrutinised the origin of cSDH in 117 patients and identified a subgroup of patients suffering from spontaneous cSDH who were included in this study. We analysed the plasma activity of FXIII and standard coagulation parameters and compared these data to age- and sex-matched healthy controls. We assessed the occurrence of re-bleeding events using clinical and imaging data and compared FXIII activity in patients with and without re-bleeding events.

Results

Out of 117 cSDH patients, 18 individuals suffered from spontaneous cSDH in this study. The patients with spontaneous cSDH showed significantly lower FXIII activity than the control group (65% [52.75, 80.25] (median [IQR]) vs. 93% [81, 111], P = 0.001), whereas standard coagulation parameters did not differ significantly between the groups. Six patients developed re-bleeding events after haematoma evacuation, and these patients expressed significantly lower FXIII activity compared to the other 12 patients (47.5% [33.5, 64] vs. 78.5% [58, 87], P = 0.005). The patient group with FXIII ≤ 68.5% differed significantly from the group with FXIII > 68.5% when categorised by the occurrence of re-bleeding events (n = 6/9 vs. n = 0/9, P = 0.009). This cut-off value predicted the re-bleeding events with a sensitivity of 100% and a specificity of 75% (positive predictive value: 66%, negative predictive value: 100%).

Conclusion

FXIII deficiency may play a pathophysiological role in spontaneous cSDH, so we suggest investigating FXIII activity because it may predict re-bleeding events after treatment. In individuals with considerably low FXIII activity, FXIII substitution may mitigate the chronic nature of this disease.     

Infantile acute subdural hematoma

A retrospective analysis of the infantile acute subdural hematoma was made with special reference to its pathogenesis. In 11 of 15 cases, the hematomas were bilateral or a contralateral subdural fluid collection was present. In 7 of 11 patients who underwent operation the collection was bloody fluid and/or clotted blood. In 3 patients, a subdural membrane, as seen in adult chronic subdural hematoma, was found. In only 1 patient with unilateral hematoma was clotted blood present without subdural membrane. The thickest collection of clotted blood was in the parasagittal region. It is postulated that in most cases hemorrhage occurs after minor head injury, from the bridging veins near the superior sagittal sinus, into a pre-existing subdural fluid collection such as chronic subdural hematoma or subdural effusion with craniocerebral disproportion, and that infants without intracranial disproportion are unlikely to have acute subdural hematoma caused by minor head injury.