Acute subdural hematoma from ruptured cerebral aneurysm

The combination of ruptured aneurysms with acute subdural hematomas (aSDHs) is a rare presentation. Patients with aSDH associated with aneurysmal bleeding represent a subgroup within the spectrum of aneurysmatic hemorrhage. We summarize the clinical characteristics, diagnostic evaluation, and management of a series of cases presenting with aSDH associated with aneurysmal subarachnoid hemorrhage (SAH).

Traumatic subarachnoid hemorrhage, basal ganglia hematoma and ischemic stroke caused by a torn lenticulostriate artery

Subarachnoid hemorrhage (SAH), basal ganglia hematoma (BGH) and ischemic stroke are common diseases with diverging therapies. The simultaneous occurrence of these diseases is rare and complicates the therapy. We report the case of a 30-year-old man with a ruptured lenticulostriate artery after traumatic brain injury that caused the combination of SAH, BGH and ischemic stroke and subsequent cerebral vasospasm. This rupture mimicked the pathophysiology and imaging appearance of aneurysmal SAH. The site of rupture was not secured by any treatment; however, hyperdynamic therapy and percutaneous transluminal angioplasty were feasible in this setting to prevent additional delayed neurological deficit.

Management of Patients Presenting with Acute Subdural Hematoma due to Ruptured Intracranial Aneurysm

Acute subdural hematoma is a rare presentation of ruptured aneurysms. The rarity of the disease makes it difficult to establish reliable clinical guidelines. Many patients present comatose and differential diagnosis is complicated due to aneurysm rupture results in or mimics traumatic brain injury. Fast decision-making is required to treat this life-threatening condition. Determining initial diagnostic studies, as well as making treatment decisions, can be complicated by rapid deterioration of the patient, and the mixture of symptoms due to the subarachnoid hemorrhage or mass effect of the hematoma. This paper reviews initial clinical and radiological findings, diagnostic approaches, treatment modalities, and outcome of patients presenting with aneurysmal subarachnoid hemorrhage complicated by acute subdural hematoma. Clinical strategies used by several authors over the past 20 years are discussed and summarized in a proposed treatment flowchart.

Experimental intracerebral hematoma in the rat

Current models of intracerebral hematoma are difficult to use for neurotransplantation studies because of high mortality and important variations of morphology, size and location of blood deposits. We propose a modification of the autologous blood infusion technique in rats to reduce these limitations.

Nontraumatic intracranial epidural hematoma: a case report

An outwardly mummified and inwardly badly decomposed body was found in a garage. At autopsy, no injuries were detected. Apart from coronary heart disease, with an old myocardial scar and a hepatic steatosis, the most striking finding was a large intracranial epidural hemorrhage situated at the left frontal lobe. As a relevant traumatic genesis could be ruled out, we deemed this a nontraumatic epidural hematoma. This finding is extremely rare. Several underlying disorders have been discussed as causes of spontaneous epidural hematomas. In this presented case, the authors discuss possible etiological factors.

Influence of inspired oxygen on glucose-lactate dynamics after subdural hematoma in the rat

The mechanisms causing brain damage after acute subdural hematoma (SDH) are poorly understood. A decrease in cerebral blood flow develops immediately after the hematoma forms, thus reducing cerebral oxygenation. This in turn may activate mitochondrial failure and tissue damage leading to ionic imbalance and possibly to cellular breakdown. The purpose of this study was to test whether a simple therapeutic measure, namely increased fraction of inspired oxygen (FiO2 100), and hence increased arterial and brain tissue oxygen tension, can influence brain glucose and lactate dynamics acutely after subdural hematoma in the rat. Twenty-five male Sprague-Dawley anesthetized rats were studied before, during and after induction of the SDH in two separate groups. The Oxygen group (n = 10) was ventilated with 100% oxygen immediately after induction of the SDH. The Air group (n = 10) was ventilated during the entire study with 21% oxygen. Brain microdialysate samples were analyzed for glucose and lactate. All rats were monitored with femoral arterial blood pressure catheters, arterial blood gas analysis, arterial glucose, lactate and end tidal CO2 (EtCO2). Five male Sprague-Dawley rats were sham operated to measure the effect of oxygen challenge on glucose-lactate dynamics without injury. Arterial oxygen tension in the Oxygen group was 371 +/- 30 mmHg and was associated with significantly greater increase in dialysate lactate in the first 30 min after induction of SDH. Dialysate glucose initially dropped in both groups, after SDH, but then reverted significantly faster to values above baseline in the Oxygen group. Changes in ventilatory parameters had no significant effect on dialysate glucose and lactate parameters in the sham group. Extracellular dialysate lactate and glucose are influenced by administration of 100% O2 after SDH. Dialysate glucose normalizes significantly quicker upon 100% oxygen ventilation. We hypothesize that increased neural tissue oxygen tension, in presence of reduced regional CBF, and possibly compromised mitochondrial function, after acute SDH results in upregulation of rate-limiting enzyme systems responsible for both glycolytic and aerobic metabolism. Similar changes have been seen in severe human head injury, and suggest that a simple therapeutic measure, such as early ventilation with 100% O2, may improve cerebral energy metabolism, early after SDH. Further studies to measure the generation of adenosine triphosphate (ATP) are needed to validate the hypothesis.

Late-onset posttraumatic septal hematoma and abscess formation in a six-year-old Tamil girl--case report and literature review

Nasal septal hematoma with abscess (NSHA) is an uncommon complication of trauma and studies on children are especially rare. We discuss the case of a 6-year-old girl, who was initially evaluated independently by three doctors for minor nasal trauma but had to be re-hospitalized 6 days later with NSHA. Although septal hematoma had initially been excluded (5, 7 and 24 hours after trauma), a secondary accumulation of blood seems to have occured. Delayed hematoma formation has been described in the orbit as a result of possible venous injuries after endoscopic sinus surgery. However, such an observation is new for septal hematoma in children. Thus, we recommend re-evaluation for septal hematoma 48h to 72h after paediatric nasal trauma. Such a scheduled re-examination offers a chance to treat delayed subperichondral hematoma on time before almost inevitable superinfection leads to abscess formation and destruction of the nasal infrastructure. We suggest that parents should be vigilant for delayed nasal obstruction as possible herald of hematoma accumulation within the first week.

Subarachnoid hemorrhage and intracerebral hematoma: incidence, prognostic factors, and outcome

OBJECTIVE: To analyze the incidence and impact of an intracerebral hematoma (ICH) on treatment and outcome in patients with aneurysmal subarachnoid hemorrhage. METHODS: Data of 585 consecutive patients with subarachnoid hemorrhage from June 1999 to December 2005 were prospectively entered in a database. ICH was diagnosed and size was measured by computed tomographic scan before aneurysm occlusion. Fifty patients (8.5%) presented with an ICH larger than 50 cm3. The treatment decision (coil, clip, or hematoma evacuation) was based on an interdisciplinary approach. Patients were stratified into good (Hunt and Hess Grades I-III) versus poor (Hunt and Hess Grades IV and V) grade, and outcome was assessed according to the modified Rankin Scale at 6 months. RESULTS: Overall, 358 patients presented in good grade, with 4 of them having ICH (1.1%); and 227 patients presented in poor grade, with 46 of them having ICH (20.3%, P < 0.01). In good-grade patients with an ICH (n = 4), a favorable outcome (modified Rankin Scale score of 0-2) was achieved in 1 patient (25%), and in 246 patients (75%) without an ICH (P = 0.053; odds ratio, 0.11). A favorable outcome was achieved in 5 poor-grade patients (12.8%) with an ICH and in 40 patients (23.7%) without an ICH (P = 0.19; odds ratio, 0.47). Time to treatment was significantly shorter in patients with an ICH than without an ICH (median, 7 versus 26 h; P < 0.001) and shortest in patients with favorable outcome (3.5 hours; P < 0.01). CONCLUSION: The current data confirm that the presence of an ICH is a predictor of unfavorable outcome. However, despite large ICHs, a significant number of patients have a good outcome. To achieve a favorable outcome, ultra-early treatment with hematoma evacuation and aneurysm obliteration seems to be mandatory.

Erythropoietin neuroprotection is enhanced by direct cortical application following subdural blood evacuation in a rat model of acute subdural hematoma

Recombinant human erythropoietin (EPO) has been successfully tested as neuroprotectant in brain injury models. The first large clinical trial with stroke patients, however, revealed negative results. Reasons are manifold and may include side-effects such as thrombotic complications or interactions with other medication, EPO concentration, penetration of the blood-brain-barrier and/or route of application. The latter is restricted to systemic application. Here we hypothesize that EPO is neuroprotective in a rat model of acute subdural hemorrhage (ASDH) and that direct cortical application is a feasible route of application in this injury type. The subdural hematoma was surgically evacuated and EPO was applied directly onto the surface of the brain. We injected NaCl, 200, 2000 or 20,000IU EPO per rat i.v. at 15min post-ASDH (400μl autologous venous blood) or NaCl, 0.02, 0.2 or 2IU per rat onto the cortical surface after removal of the subdurally infused blood t at 70min post-ASDH. Arterial blood pressure (MAP), blood chemistry, intracranial pressure (ICP), cerebral blood flow (CBF) and brain tissue oxygen (ptiO2) were assessed during the first hour and lesion volume at 2days after ASDH. EPO 20,000IU/rat (i.v.) elevated ICP significantly. EPO at 200 and 2000IU reduced lesion volume from 38.2±0.6mm(3) (NaCl-treated group) to 28.5±0.9 and 22.2±1.3mm(3) (all p<0.05 vs. NaCl). Cortical application of 0.02IU EPO after ASDH evacuation reduced injury from 36.0±5.2 to 11.2±2.1mm(3) (p=0.007), whereas 0.2IU had no effect (38.0±9.0mm(3)). The highest dose of both application routes (i.v. 20,000IU; cortical 2IU) enlarged the ASDH-induced damage significantly to 46.5±1.7 and 67.9±10.4mm(3) (all p<0.05 vs. NaCl). In order to test whether Tween-20, a solvent of EPO formulation 'NeoRecomon®' was responsible for adverse effects two groups were treated with NaCl or Tween-20 after the evacuation of ASDH, but no difference in lesion volume was detected. In conclusion, EPO is neuroprotective in a model of ASDH in rats and was most efficacious at a very low dose in combination with subdural blood removal. High systemic and topically applied concentrations caused adverse effects on lesion size which were partially due to increased ICP. Thus, patients with traumatic ASDH could be treated with cortically applied EPO but with caution concerning concentration.

Dynamic changes of intramural hematoma in patients with acute spontaneous internal carotid artery dissection.

BACKGROUND We prospectively investigated temporal and spatial evolution of intramural hematomas in patients with acute spontaneous internal carotid artery dissection using repeated magnetic resonance imaging over six-months. AIM The aim of the present study was to assess dynamic changes of intramural hematoma in patients with acute spontaneous internal carotid artery dissection at multiple follow-up time-points with T1w, PD/T2w, and magnetic resonance angiography. METHODS We performed serial multiparametric magnetic resonance imaging in 10 patients with spontaneous internal carotid artery dissection on admission, at days 1, 3, 7-14 and at months 1·5, 3, and 6. We calculated the volume and extension of the hyperintense intramural hematoma using T1w and PD/T2w fat suppressed sequences and assessed the degree of stenosis due to the hematoma using magnetic resonance angiography. RESULTS Mean interval from symptom onset to first magnetic resonance imaging was two-days (SD 2·7). Two patients presented with ischemic stroke, three with transient ischemic attacks, and five with pain and local symptoms only. Nine patients had a transient increase of the intramural hematoma volume, mainly up to day 10 after symptom onset. Fifty percent had a transient increase in the degree of the internal carotid artery stenosis on MRA, one resulting in a temporary occlusion. Lesions older than one-week were predominantly characterized by a shift from iso- to hyperintese signal on T2w images. At three-month follow-up, intramural hematoma was no longer detectable in 80% of patients and had completely resolved in all patients after six-months. CONCLUSIONS Spatial and temporal dynamics of intramural hematomas after spontaneous internal carotid artery dissection showed an early volume increase with concomitant progression of the internal carotid artery stenosis in 5 of 10 patients. Although spontaneous internal carotid artery dissection overall carries a good prognosis with spontaneous hematoma resorption in all our patients, early follow-up imaging may be considered, especially in case of new clinical symptoms.

[Spontaneous retropharyngeal hematoma with fatal outcome]

Halsschmerz, Dysphagie und Dyspnoe sind die häufigsten Symptomen, aufgrund derer Patienten einen Arzt aufsuchen. Hierbei handelt es sich um unspezifische Symptome mit vielfältigen Ursachen. Mögliche im Retropharyngealraum lokalisierte Pathologien sind in der überwiegenden Anzahl der Fälle selbst limitierend oder durch medikamentöse Therapien beherrschbar (Bsp.: Pharyngitis, Tonsillitis, Seitenstrangangina). Deutlich seltener sind im Spatium retropharyngeum lokalisierte Abszesse, Neoplasien (Bsp.: Lipome, Neurofibrome, Liposarkome) oder Hämatome (Schmäl F et al. HNO 2002; 50: 418 – 423). Letztlich können auch degenerative Veränderungen der Wirbelsäule, eine ektop verlaufende Arteria carotis interna oder seltene Manifestationen von Systemerkrankungen (Bsp.: Sarkoidose) zu einer unterschiedlich stark ausgeprägten Vorwölbung der Pharynxhinterwand und Einengung der Luft- und Speiseröhre führen. Anhand des vorliegenden Falls wird die klinische Präsentation sowie die radiologische Diagnose eines retropharyngealen Hämatoms diskutiert und die anatomische Beziehung der Halskompartimente mit besonderem Fokus auf den Retropharyngealraum dargestellt.

The Nelaton Catheter Guard for Safe and Effective Placement of Subdural Drain for Two-Burr-Hole Trephination in Chronic Subdural Hematoma: A Technical Note

BACKGROUND For chronic subdural hematoma, placement of a Blake drain with a two-burr-hole craniotomy is often preferred. However, the placement of such drains carries the risk of penetrating the brain surface or damaging superficial venous structures. OBJECTIVE To describe the use of a Nelaton catheter for the placement of a subdural drain in two-burr-hole trephination for chronic subdural hematoma. METHOD A Nelaton catheter was used to guide placement of a Blake drain into the subdural hematoma cavity and provide irrigation of the hematoma cavity. With the two-burr-hole method, the Nelaton catheter could be removed easily via the frontal burr hole after the Blake drain was in place. RESULTS We used the Nelaton catheters in many surgical procedures and found it a safe and easy technique. This method allows the surgeon to safely direct the catheter into the correct position in the subdural space. CONCLUSIONS This tool has two advantages. First, the use of a small and flexible Nelaton catheter is a safe method for irrigation of a chronic subdural hematoma cavity. Second, in comparison with insertion of subdural drainage alone through a burr hole, the placement of the Nelaton catheter in subdural space is easier and the risk of damaging relevant structures such as cortical tissue or bridging veins is lower. Thus this technique may help to avoid complications when placing a subdural drain.