No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Traumatic subarachnoid hemorrhage as a predictable indicator of delayed ischemic symptoms
Abstract
This report provides findings of an investigation of the influence of traumatic subarachnoid hemorrhage on the development of delayed cerebral ischemia caused by vasospasm. The authors prospectively studied 130 patients with closed-head trauma, who exhibited subarachnoid blood on admission computerized tomography (CT) scans. Ten (7.7%) of these patients developed delayed ischemic symptoms between Days 4 and 16 after the head injury. They consisted of three (3.0%) of 101 patients with small amounts of subarachnoid blood and seven (24.1%) of 29 patients with massive quantities of subarachnoid blood on admission CT scans. In each of the 10 patients, severe vasospasm was demonstrated by angiography performed soon after development of ischemic symptoms. There was a close correlation between the main site of the subarachnoid blood and the location of severe vasospasm. In seven of the patients, follow-up CT scans showed development of focal ischemic areas in the cerebral territories corresponding to the vasospastic arteries.
These results demonstrate that traumatic subarachnoid hemorrhage, especially if massive, is a predictable indicator of delayed ischemic symptoms.
... Es la manifestación tardía de los daños progresivos o no ocasionados por la lesión primaria y secundaria con necrosis, apoptosis y/o anoikis (muerte celular programada por desconexión, que produce eventos de neurodegeneración y encefalomalasia, entre otros. 9,[11][12][13][14][15][16][17] Deterioro retardado Corresponde al 15% de los pacientes con TCE que no manifiestan síntomas o signos de lesión cerebral, pero en el transcurso de minutos u horas presentan un deterioro neurológico por lesiones que pueden llegar a ser fatales 9 . Por lo anterior, todo paciente con TCE debe ser vigilado durante 24 horas o hasta la resolución de su síndrome de base, además se debe tomar un TAC de cráneo en las primeras 6 horas, el cual se repite antes de dar egreso o si el paciente presenta síntomas o signos neurológicos 9,16,18 . ...
... Los principales síntomas son cefalea persistente, vértigo y diplopía. Algunos de los signos son: Deterioro de la conciencia, papiledema y VI par, reflejo de Cushing, tríada de Cushing, relacionado con herniación cerebelo-tonsilar y compresión del bulbo [11][12][13][14][15][16][17] . ...
... Los síntomas son iguales a la HTEC difusa. Los signos son: III par craneal, convulsión focal, hemiparesia contralateral a la lesión, herniación cerebral 14,18,19,[20][21][22][23][24][25][26][27] cingular o subfalcinam, herniación uncal, trancraneana, tonsilar o de amigdalas cerebelosas, herniación central transtentorial, transtentorial inversa, hipotensión y el síndrome del segundo impacto [11][12][13][14][15][16][17] . Algunos ejemplos son las lesiones específicas que se hablaran en el siguiente párrafo. ...
El trauma craneoencefálico (TCE) es una patología médico-quirúrgica caracterizada por una alteración cerebral secundaria a una lesión traumática en la cabeza generando un daño estructural del contenido de ésta, incluyendo el tejido cerebral y sus vasos sanguíneos. La incidencia es de 200 personas por cada 100.000 habitantes, la etiología más frecuente son los accidentes de tránsito (70%), seguidos de hechos violentos y/o caídas desde su propia altura dependiendo del área geográfica en el que se encuentre. En esta revisión, se explicarán las lesiones primarias, secundarias, terciarias, el deterioro retardado, los tipos de hipertensión endocraneana y las lesiones específicas como fisiopatología del TCE, así como la evaluación clínica e imagenológica de las lesiones y su adecuado tratamiento.
... 52,63 For other authors, cerebral infarction was found in the territories supplied by the vasospastic arteries but severe PTV did not always induce focal ischemic areas on the late CT scans. 8,73 At least a correlation was found between the main side of subarachnoid blood, the localisation of severe PTV and focal ischemia. 73 Differences in outcome after PTV can be explained by the difficulty to detect neurological deterioration in comatose or sedated patients. ...
... 8,73 At least a correlation was found between the main side of subarachnoid blood, the localisation of severe PTV and focal ischemia. 73 Differences in outcome after PTV can be explained by the difficulty to detect neurological deterioration in comatose or sedated patients. 59 Moreover, the incidence of ischemia seems to be less than after aneurismal SAH. ...
... 74 This finding is in contradiction with ancient studies demonstrating severe PTV in all patients who developed delayed ischemic symptoms. 73 ...
Introduction:
Posttraumatic vasospasm (PTV) remains a poorly understood entity. Using a systematic review approach, we examined the incidence, mechanisms, risk factors, impact on outcome and potential therapies of PTV.
Methods:
A search on Medline database up to 2015 performed with "traumatic brain injury" and "vasospasm" key-words retrieved 429 references. This systematic review was reported and analysed following the PRISMA criteria and according to the relevance in human clinical practice.
Results:
The research retrieved 429 references of which 226 were excluded from analysis because of their irrelevance and 87 finally included in the review.
Conclusions:
Mechanical stretching, inflammation, calcium dysregulation, endotelin, contractile proteins, products of cerebral metabolism and Cortical Spreading Depolarisation have been involved in PTV pathophysiology. PTV occurs in up to 30-40% of the patients after severe traumatic brain injury. Usually, PTV starts within the first 3 days following head trauma and may last 5 to 10 days. Young age, low Glasgow coma score at admission and subarachnoid haemorrhage have been identified as risk factors of PTV. Suspected on transcranial Doppler, PTV diagnosis is best confirmed by angiography, CT angiography or MR angiography, and perfusion and ischaemic consequences by perfusion CT or MRI. Early PTV is associated with poor outcome. No PTV prevention strategy has proved efficient up to now. Regarding PTV treatment, only nimodipine and intra-arterial papaverine have been studied up to now. Treatment with milrinone has been described in a few cases reports and may represent a new therapeutic option.
... The incidence of cerebral vasospasm after tSAH is strongly related to the thickness of the SAH. In fact, the latter was correlated to the Fisher Classification commonly used to predict the risk of vasospasm after aSAH (Chieregato et al. 2005;Taneda et al. 1996). Despite the similarities between these two subtypes of SAH, there has been limited investigation in cerebral vasospasm occurring after tSAH. ...
... The development of delayed ischemia in these last patients has been shown to be almost identical to patients who suffered an aSAH. Taneda et al. showed that patients with highergrade tSAH on the Modified Fisher Scale had an increased risk of vasospasm and delayed ischemia (Taneda et al. 1996). These episodes peaked between post-trauma days 4 to 16, just as described in aSAH. ...
... However, there are subtle differences between the two processes. TCD studies have revealed that patients with TBI develop cerebral vasospasm earlier than patients with aSAH (Taneda et al. 1996;Lee et al. 1997;Oertel et al. 2005;Servadei et al. 2002). This earlier onset, usually within 48 hours, is explained by the fact that TBI patients have traumatic forces applied to their cerebral vessels at the time of injury and a release of vasoactive substance from injured brain that can induce earlier vasospasm (Zurynski and Dorsch 1998). ...
Introduction
Traumatic subarachnoid hemorrhage (SAH) is a common intracranial lesion after traumatic brain injury (TBI). As in aneurysmal SAH, cerebral vasospasm is a common cause of secondary brain injury and is associated with the thickness of traumatic SAH. Unfortunately, there is limited literature on an effective treatment of this entity. The vasodilatory and inotropic agent, Milrinone, has been shown to be effective in treating vasospasm following aneurysmal SAH. The authors hypothesized that this agent could be useful and safe in treating vasospasm following tSAH.
Case descriptions
Case reports of 2 TBI cases from a level 1 trauma centre with tSAH and whom developed delayed ischemic neurological deficits (DINDs) are presented. Intravenous Milrinone treatment was provided to each patient following the “Montreal Neurological Hospital Protocol”.
Discussion and evaluation
Both patients had an improvement in their DINDs following the treatment protocol. There were no complications of treatment and the Glasgow Outcome Scores of the patients ranged from 4 to 5.
Conclusion
This is the first report of the use of intravenous Milrinone to treat cerebral vasospasm following traumatic SAH. This treatment option appeared to be safe and potentially useful at treating post-traumatic vasospasm. Prospective studies are necessary to establish Milrinone’s clinical effectiveness in treating this type of cerebral vasospasm.
... In the pre-CT scan era, tSAH was identified as the most frequent traumatic brain lesion by autopsy [2]. It was also identified as an independant predictor of worse clinical outcome [3][4][5][6][7][8] and has been proposed as a causal factor of delayed PTV [7,[9][10][11]. However this association has not been fully elucidated. ...
... In the pre-CT scan era, tSAH was identified as the most frequent traumatic brain lesion by autopsy [2]. It was also identified as an independant predictor of worse clinical outcome [3][4][5][6][7][8] and has been proposed as a causal factor of delayed PTV [7,[9][10][11]. However this association has not been fully elucidated. ...
... Vasospasm resulting from aneurysmal SAH is a well known complication, which occurs up to 40% of patients but results in ischemic neurological symptoms only in 50% of vasospasm cases [12,13], and usually starts around day 3 after SAH onset. Maximal risk of vasospam is about day 7, but risk can persist up to 2 weeks [7,13,14]. On the contrary, the reported incidence of PTV has varied widely, probably because of differences in patient selection criteria, in definition of vasospasm or in method for detecting spasm, and in sample size of studies [6,8,[13][14][15]. The true incidence of PTV is thus uncertain, but with severe head injury, systematic and repeated transcranial doppler (TCD) measurements and use of Lindegaard ratio [16], it is about 40% [8]. ...
This article describes ischemic symptoms following post-traumatic vasospasm in a patient with mild traumatic brain injury. A 17-year-old female presented with left hemiparesia, confusion and right mydriasis 14 days after a moderate head injury resulting in brain contusion and basal cisternal sub-arachnoid hemorrhage. Bilateral supraclinoidal internal carotid artery vasospasm and a right anterior and middle cerebral arteries stroke were diagnosed. She underwent decompressive craniectomy and balloon angioplasty. Patients with mild traumatic brain injury and serious lesions on initial computed tomography should be evaluated by warrant screening strategy using early computed tomographic angiography and transcranial doppler to diagnose
post-traumatic vasospam.
... Two manuscripts [30,31] reported the results of GOS for PTV patients who were managed with dopamine-induced hypertension. A total of 93 PTV patients were included in these studies with a mean age of 42.9 years (range: 4 -91 years). ...
... These results suggest that patients may have a better outcome when receiving some form of treatment to prevent or treat VSP in the setting of TBI. Within the studies examined, VSP was detected via TCD in eight studies [19][20][21][22]26,[28][29][30], via CT head in three studies [23,25,27], via CTA in two studies [24,31], and via SjvO2 monitoring within the jugular vein in one study [18]. There are currently no standardized guidelines documenting which imaging modality is favored to diagnose PTV, but the studies examined here span decades of treatment with TCD being used in the majority of the studies. ...
Background:
Vasospasm occurrence following traumatic brain injury may impact neurologic and functional recovery of patients, yet treatment of post-traumatic vasospasm (PTV) has not been well documented. This systematic review and meta-analysis aims to assess the current evidence regarding favorable outcome as measured by Glasgow Outcome Scale (GOS) scores following treatment of PTV.
Methods:
A systematic review of PubMed, Ovid MEDLINE, and Ovid EMBASE was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Included manuscripts were methodically scrutinized for quality; occurrence of PTV; rate of favorable outcome following each treatment modality; and follow-up duration. Treatments evaluated were calcium channel blockers (CCBs), endovascular intervention, and dopamine-induced hypertension. Outcomes were compared via the random-effects analysis.
Results:
Fourteen studies with 1885 PTV patients were quantitatively analyzed: 982 patients who received tailored therapeutic intervention and 903 patients who did not receive tailored therapy. For patients undergoing treatment, the rate of favorable outcome was 57.3 % (500/872 patients; 95 % CI 54.1 - 60.6 %) following administration of CCBs, 94.1 % (16/17 patients; 95 % CI 82.9 - 100.0 %) following endovascular intervention, and 54.8 % (51/93 patients; 95 % CI 44.7 - 65.0 %) following dopamine-induced hypertension. Of note, the endovascular group had the highest rate of favorable outcome but was also the smallest sample size (n = 17). Patients who received tailored therapeutic intervention for PTV had a higher rate of favorable outcome than patients who did not receive tailored therapy: 57.7 % (567/982 patients; 95 % CI 54.1 - 60.8 %) versus 52.0 % (470/903 patients; 95 % CI 48.8 - 55.3 %), respectively.
Conclusions:
The available data suggests that tailored therapeutic intervention of PTV results in a favorable outcome. While endovascular intervention of PTV had the highest rate of favorable outcome, both CCB administration and dopamine-induced hypertension had similar lower rates of favorable outcome.
... Risk factors for vasospasm following traumatic brain injury include younger age, a low GCS score on admission, and greater cisternal blood volume [2,6,9,10]. Oertel et al. concluded that younger and severe head trauma (≦8) were indicators to develop to vasospasm in head injury patients [6]. ...
... The authors considered that a focally thick traumatic SAH with poor clearance strongly contributes to vasospasm independent of severity of head trauma. Taneda et al. mentioned that severe vasospasm was identified in relationship with the site of major subarachnoid blood [9]. A low GCS score in head trauma patients might be mainly associated with existence of brain contusion, intracerebral hemorrhage, or epidural or subdural hemorrhages, which are frequently associated with traumatic SAH; however, only SAH was significantly related to the development of vasospasm [6]. ...
It is difficult to predict that vasospasm would occur in traumatic subarachnoid hemorrhage (SAH) patients. Younger age, a lower score of Glasgow coma scale (GCS≦8) on admission, and greater cisternal blood volume are considered to correlate with post-traumatic vasospasm.
We present two cases of traumatic SAH with post-traumatic vasospasm; one was a 74-year-old man and the other was a 72-year-old woman. They were alert without any neurological deficits on admission, although the SAH was focally thick as if caused by an aneurysmal rupture. The thick SAH was still identified on follow-up CT performed in a few days. The patients demonstrated cognitive dysfunction at the 4th and 5th day of admission, respectively, and imaging studies revealed vasospasm at the artery in the thick SAH. After treatments, the vasospasm resolved and both patients recovered from the disorientation completely in three weeks. The authors considered that focally thick traumatic SAH with poor clearance is the most influential factor to post-traumatic vasospasm independent of age or a GCS score. A low GCS score in head trauma patients might be mainly associated with existence of brain contusion, intracerebral hemorrhage, epidural, or subdural hemorrhages, which are frequently associated with traumatic SAH. If the traumatic SAH is focally thick with poor clearance, it might be better to initiate prompt treatments for vasospasm within 3 days after trauma. The delay in treatments for vasospasm contributes to poor outcomes.
... Vasospasm is a well-known complication following TBI with an incidence of 25-40% [14,15]. Similar to aneurysmal subarachnoid hemorrhage, Taneda et al. reported that the vasospasm occurred on day 4 to day 16 and a correlation between the traumatic subarachnoid hemorrhage location and vasospastic artery [15]. ...
... Vasospasm is a well-known complication following TBI with an incidence of 25-40% [14,15]. Similar to aneurysmal subarachnoid hemorrhage, Taneda et al. reported that the vasospasm occurred on day 4 to day 16 and a correlation between the traumatic subarachnoid hemorrhage location and vasospastic artery [15]. Chu et al. reported that vasospasm after mild TBI with minimal focal subarachnoid hemorrhage occurred at day 10, and then resolved by day 21 [16]. ...
Patient: Male, 60
Final Diagnosis: Hyponatremia
Symptoms: Alcohol intoxication
Medication: —
Clinical Procedure: —
Specialty: Neurosurgery
Objective
Unusual clinical course
Background
Development of syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting has been commonly noted in post-traumatic brain injury, and this condition may lead to hyponatremia resulting in cerebral edema and possible cerebral herniation. However, the predominant topographic pattern of edema from hyponatremia has not been well documented. Unlike numerous reports on hyponatremia and vasospasm following aneurysmal subarachnoid hemorrhage, the data for traumatic brain injury patient are still limited. We report on a rare patient with malignant middle cerebral artery infarction as a result of hyponatremia following traumatic brain injury.
Case Report
A 60-year-old Native American male with significant past medical history of alcoholism, hypertension, and hemorrhagic stroke presented to the emergency department by emergency medical service after he was struck by a vehicle in a hit-and-run incident. The patient sustained multiple abrasions, and he had elevated alcohol levels. His initial Glasgow Coma Score (GCS) was 14 with a confused conversation (V4). Computer tomography (CT) of the head showed 5 mm thickness acute subdural and subarachnoid hemorrhage of right frontal, temporal, and parietal areas, with 3 mm midline shift at the level of foramen of Monro. Traumatic brain injury conservative treatment was initiated as well as alcoholic withdrawal protocols in the intensive care unit. Patient initially improved neurologically despite low sodium levels. He recouped to fully conscious, with a GCS score of 15, at 24 hours after admission. On day 9, he was found unresponsive with a head CT showed malignant right middle cerebral artery infarction, resulted in 15 mm subfalcine herniation. The patient passed away 48 hours later, as patient’s family declined further intervention.
Conclusions
The management and prevention of post-traumatic vasospasm may be complicated even in asymptomatic and neurologically intact patients. Close neurological monitoring and prevention protocols are important in activating appropriate management.
... Diversos autores [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] han descrito la asociación de lesiones isquémicas cerebrales con el traumatismo craneoencefálico grave. La etiología y la fisiopatología de estas lesiones todavía están poco establecidas, aunque los insultos sistémicos precoces extracraneales (anemia, hipotensión, hipoxemia), la hipertensión intracraneal y otros factores, como la liberación de aminoácidos excitotóxicos, se han implicado en la fase aguda de la isquemia cerebral [33][34][35]. ...
... La utilización de calcioantagonistas para prevenir y tratar el vasoespasmo cerebral que aparece tras la ruptura de un aneurisma intracraneal está ampliamente difundida y su eficacia se ha demos-trado en diversos estudios clínicos [2,[6][7][8]. En trabajos recientes, se ha comunicado que la hemorragia subaracnoidea postraumática es una de las variables independientes de valor pronóstico en los pacientes con traumatismo craneoencefálico grave [15,23,24,27,28,32,42] y, gracias al desarrollo de las técnicas ultrasonográficas, su diagnóstico puede realizarse más precozmente y permitir su monitorización de forma incruenta [39,[41][42][43]62,67]. En diversos estudios se ha comprobado la existencia de una estrecha correlación entre el incremento de las DFV y el descenso del flujo sanguíneo cerebral [16,37,65,66,69]. ...
... tSAH occurs in as high as 60% of patients with TBI, is associated with a two-fold increase in risk of death [15], and is considered as one of the most important negative prognostic risk factors in head injury [15,23]. Whether tSAH is an independent causative factor for worse clinical outcome following TBI by deleterious processes such as vasospasm [12,16,27,32,49,53], or merely a marker of more severely incurred head injury [9,34,43] still remains highly debated [4]. Furthermore, assuming tSAH is an independent causative factor for worse clinical outcome, whether its deleterious effects are through ischemic mechanisms secondary to vasospasm as thought to occur in aSAH is still open to speculation [4]. ...
... Nonetheless, other studies have found that the amount and location of subarachnoid blood plays a role in TBI prognosis [18,34,35]. Direct stretching or mechanical irritation of cerebral arteries are among the other factors thought to lead to the development of post-traumatic vasospasm [5,48,49]. ...
Given the large societal burden from morbidity and mortality associated with traumatic brain injury (TBI), this disease entity has been the focus of extensive research over the past decades. Since primary injury in TBI is preventable whereas secondary injury is treatable, most of the research effort has been targeted at identifying factors that contribute to secondary injury and ways to minimize their deleterious effects. Whether post-traumatic vasospasm is one such factor is open for debate. Although radiological or anatomical vasospasm following head injury has been repeatedly demonstrated using various diagnostic techniques, its clinical significance is still under investigation. At the present time, no proven treatment regimen aimed specifically at decreasing the potential detrimental effects of post-traumatic vasospasm exists. Although calcium channel blockers have shown some promise in decreasing death or severe disability in those with traumatic subarachnoid haemorrhage, whether their mechanism is by minimizing vasospasm is open to speculation. Therefore, currently, vigilant diagnostic surveillance, including serial head CT's and the prevention of secondary brain damage due to hypotension, hypoxia, and intracranial hypertension, may be more cost effective than attempting to minimize post-traumatic vasospasm.
... tSAH occurs in as high as 60% of patients with TBI, is associated with a two-fold increase in risk of death [15], and is considered as one of the most important negative prognostic risk factors in head injury [15,23]. Whether tSAH is an independent causative factor for worse clinical outcome following TBI by deleterious processes such as vasospasm [12,16,27,32,49,53], or merely a marker of more severely incurred head injury [9,34,43] still remains highly debated [4]. Furthermore, assuming tSAH is an independent causative factor for worse clinical outcome, whether its deleterious effects are through ischemic mechanisms secondary to vasospasm as thought to occur in aSAH is still open to speculation [4]. ...
... Nonetheless, other studies have found that the amount and location of subarachnoid blood plays a role in TBI prognosis [18,34,35]. Direct stretching or mechanical irritation of cerebral arteries are among the other factors thought to lead to the development of post-traumatic vasospasm [5,48,49]. ...
Vasospasm following traumatic brain injury (TBI) may dramatically affect the neurological and functional recovery of a vulnerable patient population. While the reported incidence of traumatic vasospasm ranges from 19%-68%, the true incidence remains unknown due to variability in protocols for its detection. Only 3.9%-16.6% of patients exhibit clinical deficits. Compared to vasospasm resulting from aneurysmal SAH (aSAH), the onset occurs earlier and the duration is shorter. Overall, the clinical course tends to be milder, although extreme cases may occur. Traumatic vasospasm can occur in the absence of subarachnoid hemorrhage. Surveillance transcranial Doppler ultrasonography (TCD) has been utilized to monitor for radiographic vasospasm following TBI. However, effective treatment modalities remain limited. Hypertension and hypervolemia, the mainstays of treatment of vasospasm associated with aSAH, must be used judiciously in TBI patients, and calcium-channel blockers have offered mixed clinical results. Currently, the paucity of large prospective cohort studies and level-one data limits the ability to form evidence-based recommendations regarding the diagnosis and management of vasospasm associated with TBI.
... Trauma is the most common cause of subarachnoid haemorrhage. 10,18 This is thought to be caused by a haemorrhagic contusion bleeding into the subarachnoid space (as contusions are the most common accompanying pathology detected on computerized tomography (CT) of the head 5 ), or secondary to intraventricular bleeding due to tearing of the tela choroidea. 3 Other rarer causes of traumatic subarachnoid haemorrhage (TSAH) include rupture of the posterior inferior cerebellar artery, 1 intracranial 14 or extracranial vertebral artery, 2 internal carotid artery, 16 carotid-cavernous fistula 13 and traumatic aneurysms 4,15 in penetrating head injuries. ...
... 6 It is also more likely to be localized to one area, particularly in the vertebro-basilar territory. 17 It thought to be caused by the subarachnoid blood irritating the blood vessel, and its severity is proportional to the blood load on CT. 18 As subarachnoid blood disappears more rapidly in TSAH than for ASAH, in most cases the vasospasm is usually short-lived and does not require treatment. 6 The other known complication is communicating hydrocephalus. ...
... Mechanical stretching and pulling of arteries, local inflammation, and spasmogenic substances released from the brain parenchyma injured by head trauma are thought to play an important role in the pathogenesis of posttraumatic cerebral vasospasm in the absence of SAH [7,8], although the effect of epidural or subdural hematoma, intracerebral hematoma or contusion on the development of cerebral vasospasm is unknown [6]. Our patient demonstrated severe cerebral vasospasm in the absence of SAH after burr hole evacuation of CSDH. ...
Cerebral vasospasm is a frequent complication of subarachnoid hemorrhage. We report a case of chronic subdural hematoma complicated by cerebral vasospasm after burr hole evacuation. A 74-year-old woman underwent burr hole evacuation of a chronic subdural hematoma. She developed left hemiparesis and disturbance of consciousness on postoperative day 3. Magnetic resonance imaging showed a right parietal infarct and decreased cerebral blood flow signal in the right middle cerebral artery territory. Digital subtraction angiography showed multiple segmental narrowings of the right middle cerebral artery. Her neurological symptoms recovered with conservative treatment. Follow-up angiography showed improvement in the arterial narrowing, which finally led to a diagnosis of cerebral vasospasm. Cerebral vasospasm can occur after burr hole evacuation of chronic subdural hematoma. Magnetic resonance angiography is useful for determining the cause of postoperative neurological worsening in chronic subdural hematoma patients.
... (17) giriş GKÖ düşük olan hastalarda kötü sonuç oranını %62 olarak bildirmişlerdir. Bazı çalışmalarda kötü sonuçlar üzerinde vazospazmın da etkili olduğu öne sürülmüştür (18,19). Fainardi ve ark (20) tSAK'larda BT çekilme zamanını araştırmışlar ve ilk saatlerde çekilen BT'nin post travmatik hasarı tam olarak göstermediğini; 12-24 saat veya 24-48 saat sonra çekilen BT'lerde intrakraniyal lezyonların değerlendirilmesinin daha yararlı olduğunu bildirmişlerdir. ...
Özet:
Subaraknoid kanama, subaraknoid mesafeye kanın yayıldığı patolojik bir durumdur. Travmatik subaraknoid kanama ise, intrakranial arterler ve köprü venlerinin, bir travma sonrası yırtılması veya kortikal kontüzyonlardan diffüzyon yoluyla kanın subaraknoid mesafeye dağıldığı durumlardır. Etyolojide en önemli faktör trafik kazaları olup, kırklı yaşlardaki erkek cinsiyette daha sık görülür. Prognozu genellikle Glaskow koma skalası, Fisher kriterleri ve hijdra derecelendirmeleri belirler. Tedavisi temel olarak kanamanın komplikasyonlarına yöneliktir. En önemli komplikasyonları; vazospazma bağlı iskemi, tekrardan kanama, parankimal hematom, intraventriküler hemoraji, hidrosefali ve intrakranial basınç artışıdır.
Anahtar Sözcükler: Fisher kriterleri, Glaskow koma skalası, kanama, travma
Summary:
Subarachnoid hemorrhage is a pathological condition in which blood spreads into the subarachnoid space. Traumatic subarachnoid hemorrhage, on the other hand, is the situation in which blood is distributed to the subarachnoid space by rupture of the intracranial arteries and bridge veins after a trauma or diffusion from cortical contusions. The most important factor in the etiology is traffic accidents and it is more common in men in their forties. Prognosis is generally determined by Glaskow coma scale, Fisher criteria and hijdra grades. Its treatment is mainly directed towards the complications of bleeding. The most important complications; vasospasm-related ischemia, recurrent bleeding, parenchymal hematoma, intraventricular hemorrhage, hydrocephalus and increased intracranial pressure.
... [1][2][3]7,21] Despite this, only 3.9-16.6% of the patients with radiographic evidence of vasospasm following TBI display clinical evidence of vasospasm. [6,12,23,28,29] In the present case, cerebral vasospasm was found to occur within hours of the trauma and continued for at least 13 days post-trauma. It was difficult initially to distinguish cerebral vasospasm from hypoplastic A1s which are typical variants of the circle of Willis that limit collateral flow. ...
Background
Direct, Type A, cavernous-carotid fistulas (CCFs) are predominantly caused by head trauma, especially when basilar skull fractures are present. Transarterial endovascular treatment of direct CCFs is the preferred method of treatment. Bilateral CCFs are estimated to be present in 1–2% of the cases. The treatment of bilateral CCFs is difficult often requiring a combination of endovascular and open surgical approaches.
Case Description
We present a case of traumatic bilateral CCFs presenting with vasospasm of the anterior circulation seen on the initial angiogram on day 1 and our treatment paradigm.
Conclusion
This case illustrates the challenges in managing bilateral CCFs as well as the changes in collateral circulation because of cerebral vasospasm which affected our treatment paradigm.
... Current interest is driven by recent studies suggesting that Hp phenotypes, primarily associated with different affinities to bind free hemoglobin and affinity of the hemoglobin-Hp complex to its receptors, may be associated with differential outcomes in subarachnoid hemorrhages (Chaichana et al., 2007(Chaichana et al., , 2010Leclerc et al., 2015) and that Hp may play an important role in the development of secondary injuries, particularly delayed arterial vasospasm and brain ischemia (Nonaka et al., 1979;Borsody et al., 2006). Of interest, post-traumatic cerebral vasospasm is a common complication of TBI, with incidences ranging from 2 to 63% mainly depending on the severity of injury and the method of diagnostics (Macpherson and Graham, 1978;Taneda et al., 1996;Mattioli et al., 2003). Although there is a strong association of cerebral vasospasm with traumatic subarachnoid hemorrhage (Macpherson and Graham, 1978;Gomez et al., 1991;Steiger et al., 1994;Kordestani et al., 1997;Aminmansour et al., 2009), it is also common in patients with subdural hematomas, intraventricular hemorrhage, and contusions (Mattioli et al., 2003;Oertel et al., 2005;Kalanuria et al., 2013). ...
Neurodegeneration is characterized by the progressive loss of neural tissue that result in various neurodegeneration-initiated cerebral failures and complex diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease. All these medical conditions are accompanied by the disruption of blood-brain barrier (BBB). The BBB is an interface, separating the brain from the circulatory system and protecting the central nervous system from potentially harmful chemicals while regulating transport of essential molecules and maintaining a stable environment. Owing to the inability of the neurons to regenerate on their own after neurodegeneration or severe damage to the neural tissue, neurodegenerative disorders do not have natural cures on their own. Neuroregeneration is a viable way to curb neurodegeneration. One of the current approaches is stem cell-based therapy that has been shown to be potentially helpful for the application of neuronal cell replacement for neuroregeneration.
... Vasospasm associated with traumatic SAH was thought to be a possible mechanism of PTCI (10,18). However, our study failed to prove that the severity of traumatic SAH was a risk factor for the development of PTCI. ...
Aim:
To investigate the incidence, timing, risk factors of posttraumatic cerebral infarction (PTCI) and its influence on mortality in patients with moderate to severe traumatic brain injury (TBI).
Material and methods:
After reviewing the medical records and radiographs over a 6-year period, 173 patients with moderate to severe TBI were enrolled to determine the risk factors for the development of PTCI following unilateral decompressive craniectomy (DC).
Results:
The incidence of PTCI following DC was 31.2%. Infarction in the posterior cerebral artery territory was the most common site of PTCI. The PTCI group had a significantly increased mortality (p 0.001) and unfavorable outcome (p 0.001). After stepwise logistic regression analysis, preoperative Glasgow Coma Scale (GCS) score (p 0.001, odds ratio [OR] = 0.536, 95% confidence interval [CI] = 0.407-0.706), pupillary dilation (p = 0.016, OR = 3.2, 95% CI = 1.24-8.28), subdural hematoma (SDH) (p = 0.01, OR = 16.87, 95% CI = 1.97-144.30) and craniectomy size (p = 0.017, OR = 1.02, 95% CI = 1.0-1.04) remained independently associated with PTCI development following DC.
Conclusion:
Our study demonstrated PTCI is a severe complication in patients with acute TBI. We recommend repeating computed tomography within 3 days of trauma to detect the occurrence of PTCI in patients with subdural hematoma who have low preoperative GCS score and pupillary dilation, irrespective of neurologic status. More studies are necessary to clarify the role and benefit of DC in patients with a GCS score of 5 or less.
... These 2 main types were believed to have different aetiology. TSAH has higher incidence rate than sSAH but better prognosis when compared to sSAH [9,10]. sSAH or non-traumatic SAH has long recognised to be related with pre-existing intracranial aneurysms [11]. ...
Introduction: In the setting of trauma, the cause of intracranial haemorrhage is frequently attributed to the physical, traumatic event. The actual incidence of underlying aneurysms in patients with SAH after a head trauma is not well clear or studied previously. The role for immediate Computed Tomography Angiography (CTA) still remains controversial to evaluate for non-traumatic causes.
Methods: This study reviewed a total of 797 CT angiograms of the brain conducted in the 2 major hospitals over period 48 months, between February 2013 and February 2017. 170 CTAs were performed on patient with classical thunderclap headache (spontaneous group) while 58 CTAs were performed on patient with head trauma (trauma group).
Results: This study found that 16 plain CT Brains with positive SAH for the Spontaneous group and Traumatic group. Meanwhile, 16 CTAs in Spontaneous group had positive findings intracranial aneurysms compared to 4 from the Traumatic group. Overall incidence of intracranial aneurysms in spontaneous group is 9.4% compared 6.8% in traumatic group (p=0.590) and has no statistically significant difference when comparing the groups.
In regards to primary outcome, 9 patients in Spontaneous group with SAH found to have intracranial aneurysms on CTA compared to 2 patients in Traumatic group (p=0.065). This comparison did not show statistically significant difference.
The study also shown that 7 patients in Spontaneous group with positive SAH on plain CT brain had no aneurysms on CTAs as compared to 12 in Traumatic group. In terms of incidental findings of pre-existing aneurysms, 7 patients from Spontaneous group found to have aneurysms without SAH compared to 2 from Traumatic group.
Conclusion: Prevalence of pre-existing aneurysms in patients with traumatic subarachnoid haemorrhage is comparable with spontaneous type and may had been underestimated and therefore performing CT cerebral angiogram is recommended to evaluate non-traumatic cause of SAH.
... Cerebral vasospasm, ischemia, hypoxia, edema, seizures, and hydrocephalus are all sequelae of SAH [11]. The risk of cerebral vasospasm is increased by SAH, and in adult, sTBI patients are associated with ischemic injury [11,[13][14][15][16]. In contrast, a link between traumatic SAH and cerebral vasospasm in children is lacking [17,18]. ...
BACKGROUND
Subarachnoid hemorrhage (SAH) is an independent prognostic indicator of outcome in adult patients who have suffered a severe traumatic brain injury (sTBI). There is a paucity of investigations on SAH in pediatric sTBI.
OBJECTIVES
The goal of this study was to determine SAH incidence, associated factors and its relationship to outcome in pediatric sTBI patients.
DESIGN/METHODS
Included were 171 sTBI patients (pre-sedation GCS ≤8 and head MAIS ≥4) who underwent CT head imaging within the first 24 h of hospital admission
RESULTS
We found that 42% of sTBI patients had SAH (n=71 of 171), and that SAH was more frequently associated with cerebral edema, diffuse axonal injury, contusion and intraventricular hemorrhage (P<0.05). Patients with SAH had higher injury severity scores (P=0.032) and a greater frequency of fixed pupil(s) on admission (P=0.001). There were no significant differences in etiologies between sTBI patients with and without SAH. Worse disposition occurred in sTBI patients with SAH, including increased mortality (P=0.009), increased episodes of central diabetes insipidus (P=0.002), greater infection rates (P=0.002) and fewer ventilator-free days (P=0.001). In sTBI survivors, SAH was associated with increased lengths of stay (P<0.001) and a higher level of care required on discharge (P=0.004). Despite a strong relationship between SAH and sTBI outcome on univariate analysis, multivariate analysis failed to demonstrate that SAH had an independent association with mortality (P=0.969).
CONCLUSIONS
In conclusion, SAH was a frequent head imaging abnormality in almost half of pediatric sTBI patients and it appeared to be indicative of more severe TBI. As opposed to adult sTBI, SAH in pediatric patients was not independently associated with increased risk of mortality.
... [10][11][12] Vasospasm due to tSAH leads to decreased cerebral blood flow, 11,13,14 ischemia, and infarction in up to 17% of cases. [15][16][17][18][19] While tSAH may lead to delayed cerebral ischemia, there is a paucity of data to guide physicians in managing the mildest cases of TBI with minimal tSAH. Current guidelines suggest monitoring such patients for at least 24 hours. ...
Background:
Recent studies suggest that traumatic brain injury (TBI) is a risk factor for subsequent ischemic stroke, even years after the initial insult. The mechanisms of the association remain unclear. The presence of traumatic subarachnoid hemorrhage (tSAH) may mediate the effect of TBI on long-term stroke risk, as it has previously been linked to short-term vasospasm and delayed cerebral ischemia.
Methods:
Using administrative claims data, we conducted a retrospective cohort study of acute care hospitalizations. Patients discharged with a first-recorded diagnosis of tSAH were followed for a primary diagnosis of stroke. They were matched to patients with TBI but not tSAH. Cox proportional hazards modeling was used to assess the association between tSAH and stroke while adjusting for covariates.
Results:
We identified 40 908 patients with TBI (20 454 patients with tSAH) who were followed for a mean of 4.3 + 1.8 years. A total of 531 had an ischemic stroke after discharge. There was no significant difference in stroke risk between those with tSAH (1.79%; 95% confidence interval [CI] 1.54%-2.08%) versus without tSAH (2.12%; 95% CI 1.83%-2.44%). The same pattern was found in adjusted analyses even when the group was stratified by age-group or by proxies of TBI severity.
Conclusions:
Our findings do not support a role of tSAH in mediating the association between TBI and protracted stroke risk. Further study is required to elucidate the mechanisms of long-term increased stroke risk after TBI.
... Current interest is driven by recent studies suggesting that Hp phenotypes, primarily associated with different affinities to bind free hemoglobin and affinity of the hemoglobin-Hp complex to its receptors, may be associated with differential outcomes in subarachnoid hemorrhages (Chaichana et al., 2007(Chaichana et al., , 2010Leclerc et al., 2015) and that Hp may play an important role in the development of secondary injuries, particularly delayed arterial vasospasm and brain ischemia (Nonaka et al., 1979;Borsody et al., 2006). Of interest, post-traumatic cerebral vasospasm is a common complication of TBI, with incidences ranging from 2 to 63% mainly depending on the severity of injury and the method of diagnostics (Macpherson and Graham, 1978;Taneda et al., 1996;Mattioli et al., 2003). Although there is a strong association of cerebral vasospasm with traumatic subarachnoid hemorrhage (Macpherson and Graham, 1978;Gomez et al., 1991;Steiger et al., 1994;Kordestani et al., 1997;Aminmansour et al., 2009), it is also common in patients with subdural hematomas, intraventricular hemorrhage, and contusions (Mattioli et al., 2003;Oertel et al., 2005;Kalanuria et al., 2013). ...
Cerebral hemorrhages are common features of traumatic brain injury (TBI) and their presence is associated with chronic disabilities. Recent clinical and experimental evidence suggests that haptoglobin (Hp), an endogenous hemoglobin-binding protein most abundant in blood plasma, is involved in the intrinsic molecular defensive mechanism, though its role in TBI is poorly understood. The aim of this study was to investigate the effects of Hp deletion on the anatomical and behavioral outcomes in the controlled cortical impact model using wildtype (WT) C57BL/6 mice and genetically modified mice lacking the Hp gene (Hp−∕−) in two age cohorts [2–4 mo-old (young adult) and 7–8 mo-old (older adult)]. The data obtained suggest age-dependent significant effects on behavioral and anatomical TBI outcomes and recovery from injury. Moreover, in the adult cohort, neurological deficits in Hp−∕− mice at 24 h were significantly improved compared to WT, whereas there were no significant differences in brain pathology between these genotypes. In contrast, in the older adult cohort, Hp−∕− mice had significantly larger lesion volumes compared to WT, but neurological deficits were not significantly different. Immunohistochemistry for ionized calcium-binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) revealed significant differences in microglial and astrocytic reactivity between Hp−∕− and WT in selected brain regions of the adult but not the older adult-aged cohort. In conclusion, the data obtained in the study provide clarification on the age-dependent aspects of the intrinsic defensive mechanisms involving Hp that might be involved in complex pathways differentially affecting acute brain trauma outcomes.
... Whether the relationship of tSAH with poor outcome in TBI is merely an epiphenomenon or the result of some direct cause is unclear. Some investigators believe that tSAH is merely a part of an otherwise severe TBI [12], while others argue that it directly causes additional independent adverse reactions such as vasospasm and ischemia [13]. Chieregato et al. [14] evaluated 141 patients with a CT diagnosis of tSAH to determine whether the amount of subarachnoid blood and the presence of associated parenchymal damage are powerful independent factors associated with poor outcomes. ...
Background: The Marshall computed tomography (CT) system for classification of traumatic brain injury (TBI) includes the most important independent prognostic variables except for traumatic subarachnoid hemorrhage (tSAH).
Objectives: To evaluate the prognostic effect of tSAH on different injury types based on the Marshall CT system.
Methods: We performed a retrospective study. All patients with severe closed head injury admitted from February 2011 to July 2012 were included. Their scans were classified into two groups: localized injury and diffuse injury using the Marshall classification. Outcomes were compared between patients with tSAH and those without tSAH among the two groups.
Results: Ninety-six patients were included in this study. Seventy-two (75%) were found to have tSAH, and outcomes significantly negatively correlated with tSAH in both localized injury and diffused injury groups.
Conclusions: tSAH had an important effect on the patients’ outcome. Although the Marshall classification includes important independent prognostic variables, tSAH should also be added.
... 150,151 In patients with TBI, DSA demonstration of cerebral VSP has been well documented with incidence ranging from 2% to 63%. [152][153][154] Kordestani and coauthors demonstrated that delayed cerebral VSP is strongly associated with tSAH, and is usually distributed across all levels of TBI severity, as defined by the GCS score. 155 Posttraumatic VSP can be seen in patients with tSAH, intraventricular hemorrhage, subdural hematoma, and contusions. ...
The incidence of traumatic brain injury (TBI) in the United States was 3.5 million cases in 2009, according to the Centers for Disease Control and Prevention.1 It is a contributing factor in 30.5% of injury-related deaths among civilians.2 Additionally, since 2000, over 260,000 service members were diagnosed with TBI, with the vast majority classified as mild or concussive (76 percent). The objective assessment of TBI via imaging is a critical research gap, both in the military and civilian communities. In 2011, the Department of Defense (DoD) prepared a congressional report summarizing the effectiveness of seven neuroimaging modalities (computed tomography [CT], magnetic resonance imaging [MRI], transcranial Doppler [TCD], positron emission tomography [PET], single photon emission computed tomography [SPECT], electrophysiologic techniques (magnetoencephalography and electroencephalography), and functional near-infrared spectroscopy [fNIRS]) to assess the spectrum of TBI from concussion to coma. For this report, neuroimaging experts identified the most relevant peer-reviewed publications and assessed the quality of the literature for each imaging technique in the clinical and research settings. Although CT, MRI, and TCD were determined to be the most useful modalities in the clinical setting, no single imaging modality proved sufficient for all patients due to the heterogeneity of TBI. All imaging modalities reviewed demonstrated the potential to emerge as part of future clinical care. This paper describes and updates the results of the DoD report and also expands on the use of angiography in patients with TBI.
... Das Ausmaß der tSAB hängt im Wesentlichen vom Ausmaß des Traumas ab. Ferner wird ihre Bedeutung kontroversiell betrachtet [5,6]. Die Prognose jedoch ist insgesamt von der Schwere des Schädel-Hirn-Traumas selbst abhängig [7]. ...
Eine subarachnoidale Blutung (SAB) wird überwiegend durch eine Ruptur eines intrakraniellen Aneurysmas verursacht. Dabei handelt es sich um ein akutes lebensbedrohliches Krankheitsbild. SAB anderer Genese haben einen ungleichen Krankheitswert. Bei Patienten in gutem klinischem Zustand hat sich der Trend zu einer frühen Behandlung (innerhalb von 72 Stunden) durchgesetzt, um die Gefahr einer frühen Rezidivblutung zu bannen. Um dieses Ziel zu erreichen, ist es von eminenter Bedeutung, rechtzeitig eine exakte Diagnose zu stellen. Bei kritischer Betrachtung zitierbarer Daten ist die Rate von Fehlinterpretationen einer SAB, trotz allen Fortschrittes der medizinischen Möglichkeiten, nicht außer Acht zu lassen. Bei jedem dritten bis vierten Patienten wird eine SAB verkannt bzw. zu spät erkannt. Dabei ist zu berücksichtigen, dass gerade Patienten mit geringen Symptomen das höchste Potential für eine ausgezeichnete Prognose haben.
... Travmatik subaraknoid kanamalı hastalardaki gecikmiş mortalite, iskemik hasarın gelişmesine bağlanmıştır (2,18) . Ayrıca travmatik SAK'lı hastalar arasındaki ölüm oranının, gecikmiş vazospazmın etkileri ve iskemik beyin hasarından daha çok başlangıçtaki mekanik hasarın şiddetine bağlı olduğunu savunanlar da olmuştur (14,17) . Böylece travmatik subaraknoid kanama, kafa travmalarındaki kötü sonuçlar üzerinde önemli bir prognostik faktör olarak değerlendirilmiştir. ...
1 Süleyman Demirel Üniversitesi Tıp Fakültesi Nöroşirurji Anabilim Dalı, Isparta 2 Gülhane Askeri Tıp Fakültesi Hastanesi, Ankara 4 Ca antagonisti olan nimodipinin, anevrizmaya bağlı subaraknoid kanamalı hastalarda damar düz kas hücrelerine kalsiyum girişini engelleyerek, vazospazmı önlediği böylece azalan serebral kan akımı ve iskemiye karşı olan toleransı arttırdığı düşünülmektedir. Travmatik subraknoid kanamalı hastalardaki etkinliği ise hâlâ tartışılmaktadır. Bu derlemede, nimodipinin kafa travma sonrası ortaya çıkan subaraknoid kanamalarda tedavi edici etkisi literatür eşliğinde tartışılmak istenmiş-tir. Anahtar kelimeler: Nimodipin, kafa travması, subaraknoid kanama J Nervous Sys Surgery 2009; 2(4):200-204 The Therapeutic Effects of Nimodipine in Traumatic Subarachnoid Hemorrhage 4 It is thought that nimodipine, a calcium antagonist increases the tolerance of neural tissue to ischemia via antagonizing calcium influx into the smooth muscle cells of arteries and thus preven-ting vasospams in aneurysmatic subarachnoid bleedings However, the efficacy in traumatic suba-rachnoid hemorrhages is still debatable. In this review article, we discussed the potential benefici-al role of nimodipine in traumatic subarachnoid hemorrhages in the light of relevant literature.
... Cerebral vasospasm, ischemia, hypoxia, edema, seizures, and hydrocephalus are all sequelae of SAH [11]. The risk of cerebral vasospasm is increased by SAH, and in adult, sTBI patients are associated with ischemic injury [11,[13][14][15][16]. In contrast, a link between traumatic SAH and cerebral vasospasm in children is lacking [17,18]. ...
Subarachnoid hemorrhage (SAH) is an independent prognostic indicator of outcome in adult severe traumatic brain injury (sTBI). There is a paucity of investigations on SAH in pediatric sTBI. The goal of this study was to determine in pediatric sTBI patients SAH prevalence, associated factors, and its relationship to short-term outcome.
We retrospectively analyzed 171 sTBI patients (pre-sedation GCS ≤8 and head MAIS ≥4) who underwent CT head imaging within the first 24 h of hospital admission. Data were analyzed with both univariate and multivariate techniques.
SAH was found in 42 % of sTBI patients (n = 71/171), and it was more frequently associated with skull fractures, cerebral edema, diffuse axonal injury, contusion, and intraventricular hemorrhage (p < 0.05). Patients with SAH had higher Injury Severity Scores (p = 0.032) and a greater frequency of fixed pupil(s) on admission (p = 0.001). There were no significant differences in etiologies between sTBI patients with and without SAH. Worse disposition occurred in sTBI patients with SAH, including increased mortality (p = 0.009), increased episodes of central diabetes insipidus (p = 0.002), greater infection rates (p = 0.002), and fewer ventilator-free days (p = 0.001). In sTBI survivors, SAH was associated with increased lengths of stay (p < 0.001) and a higher level of care required on discharge (p = 0.004). Despite evidence that SAH is linked to poorer outcomes on univariate analyses, multivariate analysis failed to demonstrate an independent association between SAH and mortality (p = 0.969).
SAH was present in almost half of pediatric sTBI patients, and it was indicative of TBI severity and a higher level of care on discharge. SAH in pediatric patients was not independently associated with increased risk of mortality.
... These findings suggest that besides the mechanisms important in the development of vasospasm after spontaneous SAH, other processes are involved after TBI, such as direct stretching and mechanical irritation [86]. Furthermore the relation between cerebral vasospasm and the development of secondary ischemia is still a point of debate, and there are only few prospective studies on this matter [86,87]. Besides macrovascular changes, the microvasculature is also involved. ...
The endotheliumis key in the pathophysiology of numerous diseases as a result of its precarious function in the regulation of tissue
homeostasis. Therefore, its clinical evaluation providing diagnostic and prognostic markers, as well as its role as a therapeutic target,
is the focus of intense research in patientswith severe illnesses. In the critically ill with sepsis and acute brain injury, the endothelium
has a cardinal function in the development of organ failure and secondary ischemia, respectively. Cellular markers of endothelial
function such as endothelial progenitor cells (EPC) and endothelialmicroparticles (EMP) are gaining interest as biomarkers due to
their accessibility, although the lack of standardization of EPC and EMP detection remains a drawback for their routine clinical use.
In this paper we will review data available on EPC, as a general marker of endothelial repair, and EMP as an equivalent of damage
in critical illnesses, in particular sepsis and acute brain injury. Their determination has resulted in new insights into endothelial
dysfunction in the critically ill. It remains speculative whether their determination might guide therapy in these devastating acute
disorders in the near future.
... TSAH has been reported to occur in 39 %-65 % of all TBI cases [5-7], with 10 %-30 % having TBI-associated radiographic cVSP in the presence of SAH on head computed tomography (hCT) [7][8][9]. Its presence has been independently associated with poor functional outcome [6, 10, 11] albeit SAH may just be a marker of more severe TBI and not causing cVSP. ...
Opinion statement:
Cerebral vasospasm (cVSP) consists of the vasoconstriction of large and small intracranial vessels which can lead to cerebral hypoperfusion, and in extreme cases, delayed ischemic deficits with stroke. While most commonly observed after aneurysmal subarachnoid hemorrhage (aSAH), cVSP can also occur after traumatic brain injury (TBI) as we have described in detail in this review. For the past decades, the research attention has focused on cVSP because of its association with delayed cerebral ischemia, which is the largest contributor of morbidity and mortality after aSAH. New discoveries in the cVSP pathophysiology involving multifactorial complex cascades and pathways pose new targets for therapeutic interventions in the prevention and treatment of cVSP. The goal of this review is to demonstrate the commonalities and differences in epidemiology and pathophysiology of both aSAH and TBI-associated cVSP, and highlight the more recently discovered pathways of cVSP. Finally, the latest cVSP surveillance methods and treatment options are illustrated.
Stroke refers to any new neurological symptoms with sudden onset. This commonly used term can refer to any cerebrovascular disease of the nervous system that interrupts neural tissue function abruptly. When patients present to the emergency room with an abrupt onset of new focal neurologic deficits, the etiology of 95 % will be vascular (i.e., stroke), and 5 % will be other disease processes such as seizures, tumor, or psychogenic. Stroke is most commonly used to describe an ischemic event involving an acute occlusion of an artery supplying neural tissue. However, stroke can also result from loss of neural tissue function secondary to sudden hemorrhage into the neural tissue. Approximately 85 % of all strokes are ischemic in nature, while the remaining 15 % of strokes are hemorrhagic in nature [1].
Background:
Symptomatic cerebral vasospasm has been reported in a low percentage of patients with moderate or severe traumatic brain injury as defined by Glasgow Coma Score (GCS). Here, we present case of mild traumatic brain injury (GCS 14) complicated by early and severe symptomatic cerebral vasospasm.
Case description:
A 63-year-old female was admitted following mild traumatic brain injury with a Glasgow Coma Score of 14. Concurrent with the onset of sonographic vasospasm, the patient developed severe neurological symptoms consistent with ischemia of the left middle cerebral artery territory. Confounding causes of these symptoms were excluded. Each occurrence of these symptoms resolved with intra-arterial calcium channel blocker therapy.
Conclusion:
Early and severe symptomatic vasospasm may occur as a complication of mild traumatic brain injury. GCS score alone may be an inadequate risk predictor of symptomatic cerebral vasospasm. Aggressive interventional management may be justified, such as with intra-arterial calcium channel blockers, to optimize the likelihood of a favorable outcome.
Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease responsible for 5 % of stroke cases and affects approximately 28,000 North Americans annually. Even though its incidence is dwarfed by other subtypes of stroke, the relative youth of the affected patients with a mean age of 50 years [1, 2] and that fewer than 40 % of them so stricken return to functional life despite modern treatment mean that this disease accounts for around 25 % of loss of productive life years, a magnitude comparable to ischemic stroke, the most frequent subtype of stroke [3–5].
Severe head injuries place a tremendous burden upon the society, partly because of the high mortality and morbidity, and partly because the economical resources used during the acute phase in the neurosurgical intensive care unit and during rehabilitation are very high. Even with the best results moderate and severe disability may be expected in 20–30% of the patients.
Understanding the physiology underlying intracranial pressure is critical to developing sound management plans for central nervous system pathology. Principles of treatment are based upon a variety of complex interactions between cerebral blood supply and drainage, tissue oxygenation and ischemia, brain tissue edema, and a variety of other pathophysiological mechanisms. Molecular, cellular, tissue, and organ pathologies vary according to the primary insult, but management of ICP elevation is crucial for the reduction of further injury, debility, and death.
Skull fractures and structural brain injuries encompass a heterogeneous set of pathologies that may confer significant morbidity and mortality in the setting of head trauma. Skull fractures can be classified according to their shape (linear, comminuted, and depressed) and if there is overlying disruption of the galea aponeurotica and skin (open vs. closed). Structural brain injuries of clinical relevance include epidural/extradural hematomas, subdural hematomas, traumatic subarachnoid hemorrhage, and intracerebral/intraparenchymal hemorrhage. Though certainly known to occur in athletic settings, these injuries are more typically associated with motor vehicle-related accidents, significant falls, and violence as significant energy is required to cause disruption of the cranial vault’s natural structural integrity. When suspected, rapid assessment and diagnosis are critical to maximizing patient outcomes. Accurate, thorough, and focused history and physical examination can help guide the physician through selection of further workup, often with some form of neuroimaging. Treatment of many of these lesions is surgical in nature and is typically aimed at reducing mass effect on critical neural structures and repairing any disrupted anatomy.
Several studies have investigated the incidence and risk factors of hydrocephalus after decompressive craniectomy (DC) for malignant hemispheric cerebral infarction. However, the results are controversial. Therefore, the following is a retrospective cohort study to determine the incidence and risk factors of hydrocephalus after DC for malignant hemispheric cerebral infarction.
From January 2004 to June 2014, patients at two medical centres in southwest China who underwent DC for malignant hemispheric cerebral infarction were included. The patients' clinical and radiologic findings were retrospectively reviewed. A chi-square test, Mann-Whitney U-test and logistic regression model were used to identify the risk factors.
A total of 128 patients were included in the study. The incidence of ventriculomegaly and shunt-dependent hydrocephalus were 42.2% (54/128) and 14.8% (19/128), respectively. Lower preoperative GCS score and presence of subarachnoid haemorrhage (SAH) were factors significantly associated with the development of postoperative hydrocephalus after DC. Conclusions Cerebral infarction patients receiving DC have a moderate tendency to suffer from postoperative hydrocephalus. A poor GCS score and the presence of SAH were significantly associated with the development of hydrocephalus after DC.
To gain a description of the prevalence and time course of vasospasm in children suffering moderate-to-severe traumatic brain injury.
A prospective, observational study was performed. Children with a diagnosis of traumatic brain injury, a Glasgow Coma Score less than or equal to 12, and abnormal head imaging were enrolled. Transcranial Doppler ultrasound was performed to identify and follow vasospasm. Diagnostic criteria included flow velocity elevation more than or equal to 2 sd above age and gender normal values for the middle cerebral and basilar arteries. Additional criteria required for vasospasm diagnosis in the middle cerebral artery was a ratio of flow in the middle cerebral artery to extracranial internal carotid artery more than or equal to 3.
None.
Sixty-nine children were included. The prevalence of middle cerebral artery vasospasm in children with moderate traumatic brain injury (Glasgow Coma Score, 9-12) was 8.5% and was 33.5% in those with severe traumatic brain injury (Glasgow Coma Score, ≤ 8). The prevalence of basilar artery vasospasm in children with moderate traumatic brain injury was 3% and with severe traumatic brain injury was 21%. Mean time to onset of vasospasm was 4 days (± 2 d) in the middle cerebral arteries and 5 days (± 2.5 d) in the basilar artery. Mean duration of vasospasm in the middle cerebral artery was 2 days (± 2 d) and 1.5 days (± 1 d) in the basilar artery. Children in whom vasospasm developed were more likely to have been involved in motor vehicle accidents, had higher Injury Severity Scores, had fever at admission, and had lower Glasgow Coma Score scores. Good neurologic outcome (Glasgow Outcome Score Extended Pediatric version of ≥ 4) at 1 month from injury was seen in 76% of those with moderate traumatic brain injury without vasospasm and in 40% of those with vasospasm. In those with severe traumatic brain injury, good neurologic outcome was seen in 29% of those children without vasospasm and in 15% of those with vasospasm.
Vasospasm occurs in a sizeable number of children with moderate and severe traumatic brain injury. Children in whom vasospasm developed were more likely to have been involved in a motor vehicle accident, had higher Injury Severity Scores, had fever at admission, and had lower Glasgow Coma scores than in those whom vasospasm did not develop. Based on these findings, we recommend aggressive screening for posttraumatic vasospasm in these patients. Future studies should establish the relationship between vasospasm and long-term functional outcomes and should also evaluate potential preventative or therapeutic options for vasospasm in these children.
Objective
Traumatic brain injury (TBI) is one of the leading cause of death in many developing countries. The intention of this study was to develop a predictor model – to identify high death risk of severely head-injured patients in an early period in order to plan an effective and efficient treatment strategy.
Method
We conducted a retrospective cross-sectional study with subjects of severe TBI patients (n = 61) from 1st of January to 31st December 2010. Variables included age, gender, blood pressure, mean arterial pressure, pulse rate, respiration rate, temperature, Glasgow Coma Scale (GCS) score, motor response, choice of treatment and head computed tomography (CT) profiles. These models – then analyzed using multiple logistic regression.
Results
The outcome of this study produced five factors that correlated significantly with the survival of these patients: compression in basal cistern, low motor response (<4), presence of intradural lesion, mean arterial pressure, and midline shift. We divided these factors into major and minor factor according to their contribution to survival. Compression of basal cistern compression and low motor response (<4) are the most significant factors in predicting mortality (sensitivity greater than 90%).
Conclusion
Basal cistern compression and motor response were the most valuable factors in determining the risk of death in severe TBI patients.
Recent studies have shown that isolated traumatic subarachnoid hemorrhage (tSAH) in the setting of a high Glasgow Coma Scale (GCS) score (13-15) is a relatively benign finding not likely requiring operative neurosurgical intervention. This study sought to provide a more comprehensive assessment of isolated tSAH among patients with any GCS score, and to expand the analysis to examine the potential need for aggressive medical or endovascular (not just neurosurgical) interventions in these patients. By undertaking a retrospective review of all patients admitted to our trauma center from 2003-2012, we identified 661 patients with isolated tSAH. Only 4 patients (0.61%) underwent any sort of aggressive neurosurgical, medical or endovascular intervention, regardless of GCS score. Most tSAH patients without additional systemic injury were discharged home (68%), including 53% of patients with a GCS score of 3-8. However, older patients were more likely to be discharged to a rehabilitation facility (p < 0.01). There were 6 (1.7%) in-hospital deaths, 5 of whom were > 80 years of age. We conclude that isolated tSAH, regardless of admission GCS score, is typically a benign intracranial injury that is highly unlikely to require aggressive operative, medical or endovascular intervention, and is unlikely to be associated with major neurologic morbidity or mortality, except perhaps in elderly patients. Based upon our findings, we argue impaired consciousness in the setting of isolated tSAH should strongly compel a consideration of non-traumatic factors in the etiology of the altered neurologic status.
Minor craneoencephalic trauma is one of the most common neurologic disorders seen at hospital urgency units. We report the clinical course in a 66 year old male who had suffered a traffic accident, presented a Glasgow Coma Score of 15 and in whom CT revealed a skullll base fracture, diffuse pneumoencephalus, subdural frontotemporal hematoma with right hemispheric swelling, massive subarachnoid hemorrhage and midline shift of the midle line. Conservative treatment was carried out and the patient recovered well.
Subarachnoid hemorrhage (SAH) is defined as bleeding into the subarachnoid space of the brain. The most common etiology of SAH is trauma, and Other etiologies includes aneurysmal SAH, perimesencephalic hemorrhage, vertebral artery dissection, and arteriovenous malformations (AVMs) to name a few. This chapter focuses on aneurysmal SAH that accounts for approximately 85% of all causes of non-traumatic SAH, and reviews perimesencephalic SAH and SAH from vertebral artery dissection and traumatic SAH. Intracranial aneurysms are uncommon vascular lesions that can cause significant morbidity and mortality if they rupture. Intracranial aneurysms can be defined by their morphology. The majority are saccular in nature although fusiform aneurysms occur. Saccular aneurysms are usually acquired and are believed to result from prolonged hemodynamic stress and subsequent arterial degeneration, particularly at branch points. Hypertension, cigarette smoking, oral contraceptives, alcohol consumption, pregnancy, and cocaine use are all risk factors for aneurysm formation and probably increase the risk of rupture. The four main complications following rupture of an intracranial aneurysm are cerebral vasospasm, aneurismal re-hemorrhage, hydrocephalus, and seizures. The chapter discusses the genetics of intracranial aneurysm formation, diagnostic approach to aneurysmal SAH, pathology of SAH, treatment of ruptured cerebral aneurysms, and other causes of SAH.
Post-traumatic vasospasm is a well-recognized complication of head injury. However, symptomatic vasospasm rarely occurs in patients with mild head injuries. A 58-year-old female patient presented with head injury and a traumatic subarachnoid hematoma along the left lateral fi ssure, which subsequently induced symptomatic vasospasm. Magnetic resonance imaging of her brain showed acute infarction of the left middle cerebral artery. Angiography demonstrated multiple segmental narrowing of the left middle cerebral artery near the hematoma spatially in accordance with PTSV. In conclusion, early recognition of PTSV is crucial to improving neurological outcomes.
Vasospasm and consequent cerebral ischaemia in aneurysmal subarachnoid haemorrhage are well-described. The development of cerebral ischaemia following pituitary tumour surgery is under-appreciated, and can be attributed to mainly cerebral vasospasm or internal carotid artery compression. We report on two patients with pituitary tumours who developed delayed cerebral ischaemia after transsphenoidal and transcranial pituitary macroadenoma decompression. The patients had vasospasm of intracranial vessels demonstrable on magnetic resonance angiogram. One recovered neurologically following nimodipine and hypertensive-hypervolaemia therapy while the other developed fulminant cerebral infarction. We discuss the complex multi-factorial mechanisms of cerebral ischaemia in pituitary disorders, as well as the management strategies and their limitations.
EIGHTY-SIX PATIENTS WITH head injuries with an admission Glasgow Coma Scale score between 3 and 12 were studied sequentially by transcranial and cervical Doppler sonography. On a subset of 26 patients, sequential autoregulation and CO2 reactivity testing was also performed. Patient characteristics and hemodynamic data were correlated and analyzed with respect to the final outcome. The internal carotid artery (ICA) and middle cerebral artery flow velocities followed a typical pattern. Both were depressed during the first 3 days after the trauma and then increased to a maximum between Days 5 and 7. The increase of the middle cerebral artery flow velocities was more pronounced than the increase of the ICA flow velocities, thus indicating some degree of vasospasm. The amount of subarachnoid hemorrhage on the initial computed tomography correlated with the average middle cerebral artery/ICA flow velocity ratio (r = 0.5). Subarachnoid hemorrhages on computed tomography and, to a lesser degree, subdural and intracerebral hematomas were correlated with an unfavorable outcome. Vasospasm remained subcritical, and no negative relationship to outcome could be identified. Hyperperfusion, as based on ICA flow velocities, and vasospasm were correlated with diminished vasoreactivity. However, disturbed vasoreactivities, particularly during the first days, were common and did not necessarily predict an unfavorable outcome.
Persisting disability after brain damage usually comprises both mental and physical handicap. The mental component is often the more important in contributing to overall social disability. Lack of an objective scale leads to vague and over-optimistic estimates of outcome, which obscure the ultimate results of early management. A five-point scale is described—death, persistent vegetative state, severe disability, moderate disability, and good recovery. Duration as well as intensity of disability should be included in an index of ill-health; this applies particularly after head injury, because many disabled survivors are young.
Persisting disability after brain damage usually comprises both mental and physical handicap. The mental component is often the more important in contributing to overall social disability. Lack of an objective scale leads to vague and over-optimistic estimates of outcome, which obscure the ultimate results of early management. A five-point scale is described--death, persistent vegetative state, severe disability, moderate disability, and good recovery. Duration as well as intensity of disability should be included in an index of ill-health; this applies particularly after head injury, because many disabled survivors are young.
Measurements were made at eight predetermined positions on 627 sets of angiograms from 293 patients with aneurysms. A ratio between the sum of the vessel diameters in the subarachnoid space to the sum in the base of skull and neck was calculated and plotted against time. Vasospasm has its onset in man about Day 3 after subarachnoid hemorrhage, is maximal at Days 6 to 8, and is gone by Day 12. There is a tendency for patients in poor clinical grades to have more vasospasm. The patients with most vasospasm have a significantly higher mortality than those with the least.
The carotid angiograms of 96 patients who had died from non-missile head injury were reviewed and assessed for evidence of arterial spasm, slowing of the cerebral circulation, and the presence of intracranial haemotoma. As bilateral angiography had been done in 44 cases the results are based on a correlation between the angiographic appearances and the presence or absence of ischaemic brain damage in the cortex of 140 cerebral hemispheres. There was a significant relationship between spasm alone, the presence of intracranial haematoma alone, or their combination, and ischaemic damage in the ipsilateral cortex. Apart from an association between the more severe grades of spasm and slowing of circulation in the group with ischaemia within arterial territories, there was none between slowing of the circulation or the combination of slowing with either spasm or haematoma and ischaemic brain damage.
Thirty patients admitted after suffering closed head injuries, with Glasgow Coma Scale scores ranging from 3 to 15, were evaluated with transcranial Doppler ultrasound monitoring. Blood flow velocity was determined in the middle cerebral artery (MCA) and the intracranial portion of the internal carotid artery (ICA) in all patients. Because proximal flow in the extracranial ICA declines in velocity when arterial narrowing becomes hemodynamically significant, the extracranial ICA velocity was concurrently monitored in 19 patients. To assess cerebral perfusion, cerebral blood flow (CBF) measurements obtained with the intravenous 133Xe technique were completed in 16 patients. Vasospasm, designated as MCA velocity exceeding 120 cm/sec, was found in eight patients (26.7%). Severe vasospasm, defined as MCA velocity greater than 200 cm/sec, occurred in three patients, and was confirmed by angiography in all three. Subarachnoid hemorrhage (SAH) was documented by computerized tomography in five (62.5%) of the eight patients with vasospasm. All cases of severe vasospasm were associated with subarachnoid blood. The time course of vasospasm in patients with traumatic SAH was similar to that found in patients with aneurysmal SAH; in contrast, arterial spasm not associated with SAH demonstrated an uncharacteristically short duration (mean 1.25 days), suggesting that this may be a different type of spasm. A significant correlation (p less than 0.05) was identified between the lowest CBF and highest MCA velocity in patients during the period of vasospasm, indicating that arterial narrowing can lead to impaired CBF. Ischemic brain damage was found in one patient who had evidence of cerebral infarction in the territories supplied by the arteries affected by spasm. These findings demonstrate that delayed cerebral arterial spasm is a frequent complication of closed head injury and that the severity of spasm is, in some cases, comparable to that seen in aneurysmal SAH. This experience suggests that vasospasm is an important secondary posttraumatic insult that is potentially treatable.
Using transcranial doppler ultrasonography, cerebral blood flow velocity was measured daily from both middle cerebral arteries in 121 patients who had suffered minor (n = 55), moderate (n = 16), or severe (n = 50) brain injury. Serial computed tomographic scans were performed to identify noncontusion-related infarction (NCI). Cerebral perfusion pressure was monitored continuously in 41 patients who had severe head injury; of these, 22 had continuous measurement of arterial and jugular bulb venous oxygen (SJO2) saturation. Abnormally high mean flow velocity (greater than 100 cm/s) was observed in 23 patients (minor injury, n = 3; moderate injury, n = 3; severe injury, n = 17), but was recorded only when cerebral perfusion pressure exceeded 60 mm Hg (P less than 0.0001). Fourteen patients who underwent SJO2 monitoring developed increased mean flow velocity (MFV). In 6, the arterial-jugular venous oxygen content difference (AVDO2) was below 4 ml/dl, indicating global cerebral hyperemia. All had bilateral elevation of MFV, and 6 of the 8 nonhyperemic patients (AVDO2, 4-9 ml/dl) had a unilateral increase of MFV (P = 0.018). Four of the 23 patients with increased MFV developed NCI, as compared with none of the patients without elevated MFV (P = 0.015). All patients with NCI had suffered severe brain injury, had unilateral elevation of MFV in the terriory of the relevant cerebral vessel, and had received therapy to correct reduced cerebral perfusion pressure (P = 0.008). NCI did not occur in any patient with increased MFV that was associated with global hyperemia.
Thirty-five patients were admitted to the hospital with Glasgow coma scale scores of 4 to 7 after severe, blunt head injury. Blood flow velocities of the middle cerebral artery (MCA) and the ipsilateral internal carotid artery (ICA), high in the neck, were recorded noninvasively by Doppler ultrasonography. Serial examinations were begun within 48 hours of trauma and continued until the patient either died or was discharged. Spasm of the MCA was assumed if the ratio of the velocity of blood flow in the MCA (VMCA) to the velocity of blood flow in the ICA (VICA) exceeded 3 (normal value, 1.7 +/- 0.4). In cases of severe MCA spasm, this ratio is higher because of increased flow velocity in the MCA and reduced flow in the ICA due to increased cerebrovascular resistance. Higher MCA velocities with VMCA/VICA above 3, consistent with MCA spasm, were found in 14 of the 35 patients (40%). The increase began as early as 48 hours after injury, reached a maximum between Days 5 and 7, and lasted until 2 weeks after injury. There was a significant correlation between the occurrence of vasospasm and the quantity of cisternal or intracerebral blood seen on a computed tomographic scan. No correlation was found with the age of the patients, the Glasgow coma scale score at admission, the intracranial pressure, or the functional outcome 6 months after injury. The occurrence of a secondary infarction in a patient with severe MCA spasm suggests that, at least in some cases, spasm may influence the prognosis.
In this prospective multicenter study, the authors have examined data derived from the initial computerized tomography (CT) scans of 753 patients with severe head injury. When the CT findings were related to abnormal intracranial pressure and to death, the most important characteristics of the scans were: midline shift: compression or obliteration of the mesencephalic cisterns: and the presence of subarachnoid blood. Diffuse hemispheric swelling was also found to be associated with an early episode of either hypoxia or hypotension.
In 39 patients with a proven subarachnoid hemorrhage (SAH), the clinical status, the amount of subarachnoid blood on a computerized tomography scan obtained within 5 days after SAH, and the flow velocities (FV's) in both middle cerebral arteries (MCA's) measured by transcranial Doppler sonography were recorded daily and correlated. All patients had pathological FV's over 80 cm/sec between Day 4 and Day 10 after SAH. The side of the ruptured aneurysm showed higher FV's than did the unaffected side in cases of laterally localized aneurysms. Increase in FV preceded clinical manifestation of ischemia. A step early increase of FV's portended severe ischemia and impending infarction. Maximum FV's in the range of 120 to 140 cm/sec were not critical and in no case led to brain infarction. Maximum FV's over 200 cm/sec were associated with a tendency for ischemia, but the patients may remain clinically asymptomatic. In cases of no or only a little blood in the basal cisterns, mean FV's in both MCA's increased only moderately whereas, with thick clots of subarachnoid blood, there was a steeper and higher increase of mean FV's.
Acht Patienten mit schwerem Schädel-Hirn-Trauma (Glasgow Coma Scale 3-5) wurden wegen eines traumatischen zerebralen Gefäßspasmus mit dem Kalzium-Einstrom-Blocker Nimodipine (2-3 mg/h) behandelt. Der Spasmus betraf in allen Fällen den vorderen Bereich des Circulus arteriosus Willisi mit den beiden ersten Segmenten der Arteria cerebri anterior und media. 6 Kontroll-angiographien bei 6 Patienten zeigten ein erweitertes oder normalisiertes Gefäßlumen der bei der Erstangiographie spastischen Gefäße.
Der intrakranielle und der mittlere arterielle Druck bleiben durch Nimodipine unbeeinflußt, bei gleichzeitiger Anwendung neurochirurgischer Intensivtherapie (Dexamethason, Mannit, Relaxation und Beatmung für 2-3 Tage).
Die Kontrolle der somato-sensiblen-evozierten Potentiale (SEP) zeigten eine deutliche Besserung der kortikalen Antwort innerhalb von 7 Tagen.
Ein Patient verstarb 8 Tage nach dem Unfall an einer Sepsis und einer blieb im vegetativen Stadium. Die restlichen Patienten erreichten innerhalb 8,6 ± 2,2 Tagen GCS 13,0 ± 1,1 von anfänglich 4,4 ± 0,8. Ein Jahr nach dem Unfall waren alle Patienten voll in den Arbeitsprozeß wieder eingegliedert. Die Überlebensqualität war demnach besser als in der Literatur angegeben.
Wir schließen aus diesen vorläufigen Ergebnissen, daß Kalzium-Einstrom-Blocker in der Therapie von traumatischen Gefäßspasmen und auch von schweren Schädel-Hirn-Traumen erfolgreich bei Patienten eingesetzt werden können. Eine Studie mit einer größeren Anzahl von Patienten ist derzeit im Gange.
A clinical scale has been evolved for assessing the depth and duration of impaired consciousness and coma. Three aspects of behaviour are independently measured—motor responsiveness, verbal performance, and eye opening. These can be evaluated consistently by doctors and nurses and recorded on a simple chart which has proved practical both in a neurosurgical unit and in a general hospital. The scale facilitates consultations between general and special units in cases of recent brain damage, and is useful also in defining the duration of prolonged coma.
✓ The authors describe fibrous structures they name “chordae” that stabilize the position of arteries in cerebral subarachnoid spaces. The innervation of these structures and their relation to the innervation apparatus of the arterial wall is discussed. Animal experiments and human autopsy material were used to study the role of the stabilizing structures in the pathogenesis of arterial spasm following the rupture of saccular aneurysms. Mechanical stimuli produced short-term but not prolonged arterial spasm.
✓ Arteriography in 350 patients with a moderate to severe head injury, including repeated studies in 40 patients, revealed narrowing of one or more of the intracranial arteries in 65 patients (18.6%). Narrowing of the intracranial portion of the internal carotid artery and the first part of the anterior and middle cerebral arteries was found in 18 patients and was believed to be responsible for the clinical symptoms in some. Narrowing of the branches of the cerebral arteries at the site of the cerebral contusion was seen in 33 patients and diffuse narrowing of the intracranial arteries in 12. In two additional patients with gunshot wounds of the brain, there was narrowing of the cerebral artery adjoining a torn vessel. The evidence suggests that vascular spasm is responsible for the narrowing in some patients, while contusion and hemorrhage in the arterial wall is the cause in others. Whatever the mechanism, the occurrence and significance of cerebral arterial narrowing in association with acute head inju...
Two cases of spasm of the internal carotid and one of the middle cerebral artery are reported after cranio-cerebral injury. The mechanism of spasm, the Symptomatologic polymorphism, and the prognosis are discussed with reference to the data in literature. Positive diagnosis can only be established by carotid angiography. Rapid recovery was observed during conservative therapy.
Cerebral vasospasm occurs frequently after head injury. Correlation between neurological deterioration and vasospasm has been reported previously, but delayed neurological deterioration secondary to vasospasm in head injury is a rare occurrence. We report the case of a 57-year-old man who, after a motorcycle accident, developed an acute subdural hematoma and a thick subarachnoid deposition of blood in the left sylvian-insular cistern. After surgical evacuation of the hematoma, the patient improved until the 10th postoperative day, when he developed aphasia and a right hemiparesis. Angiography demonstrated multitapering spasm, and a computed tomographic (CT) scan showed persistence of the cisternal deposition of blood. Despite therapy with hypervolemia, the patient improved only slightly. The association of head injury with substantial subarachnoid hemorrhage producing vasospasm has been considered rarely. Delayed posttraumatic vasospasm secondary to blood degradation products seems to play some role in the vasospasm after head injury. CT scanning may be useful in predicting vasospasm in such patients, and digital subtraction angiography might be useful in demonstrating it.
Antifibrinolytic therapy remains a controversial issue in the management of subarachnoid hemorrhage (SAH). The relationship of antifibrinolytic therapy with mortality, rebleeding, ischemia, hydrocephalus, and clotting abnormalities was studied in 672 patients in the International Cooperative Study on the Timing of Aneurysm Surgery. The patients with antifibrinolytic therapy had a significantly lower rebleeding rate, but higher rates of ischemic deficits and hydrocephalus. The net result was no difference in mortality in the 1st month following the initial SAH. Further clinical trials are needed to determine the overall effects of antifibrinolytic therapy.
The effect of removal of subarachnoid blood clots on the prevention of delayed ischemic deficit was evaluated in 239 consecutive patients with ruptured supratentorial non-giant aneurysms. All patients were hospitalized within 24 hours after subarachnoid hemorrhage (SAH) and were classified in Grades 1 to 4 according to the system of Hunt and Hess; classification was made immediately preoperatively in patients operated on within 48 hours after SAH, or 48 hours after SAH in patients for whom delayed operation was planned. Delayed ischemic deficit causing permanent disability or death occurred in 11 (25%) of 44 patients in whom surgery was planned to be delayed for 10 days or more, in 26 (27.7%) of 94 patients in whom the aneurysms were obliterated and blood clots adjacent to them were removed within 48 hours of SAH, and in 11 (10.9%) of 101 patients in whom the aneurysms were obliterated and extensive and aggressive removal of thick subarachnoid clots lying along the arteries (identified on computerized tomographic scan) was performed within 48 hours of SAH. Accordingly, early operation is an effective and reliable method to reduce the occurrence of severe delayed ischemic deficit only when subarachnoid blood clots are removed extensively and aggressively along the arteries within 48 hours of SAH.
We report a case of severe posttraumatic arterial vasospasm treated with repetitive intraarterial papaverine infusions. The salient features of the mechanism of action of papaverine are included.
Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO2; loss of CO2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO2. This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO2, the estimated blood volume change per torr change of PCO2 was calculated by the following equation: BVR = PVI x delta log(ICP)/delta PCO2, where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO2, thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.
Eighty-six patients with head injuries with an admission Glasgow Coma Scale score between 3 and 12 were studied sequentially by transcranial and cervical Doppler sonography. On a subset of 26 patients, sequential autoregulation and CO2 reactivity testing was also performed. Patient characteristics and hemodynamic data were correlated and analyzed with respect to the final outcome. The internal carotid artery (ICA) and middle cerebral artery flow velocities followed a typical pattern. Both were depressed during the first 3 days after the trauma and then increased to a maximum between Days 5 and 7. The increase of the middle cerebral artery flow velocities was more pronounced than the increase of the ICA flow velocities, thus indicating some degree of vasospasm. The amount of subarachnoid hemorrhage on the initial computed tomography correlated with the average middle cerebral artery/ICA flow velocity ratio (r = 0.5). Subarachnoid hemorrhages on computed tomography and, to a lesser degree, subdural and intracerebral hematomas were correlated with an unfavorable outcome. Vasospasm remained subcritical, and no negative relationship to outcome could be identified. Hyperperfusion, as based on ICA flow velocities, and vasospasm were correlated with diminished vasoreactivity. However, disturbed vasoreactivities, particularly during the first days, were common and did not necessarily predict an unfavorable outcome.
- Pasqualin A