Decompressive Craniectomy for Traumatic Brain Injury: Postoperative TCD Cerebral Hemodynamic Evaluation

Background: There are no studies describing the cerebral hemodynamic patterns that can occur in traumatic brain injury (TBI) patients following decompressive craniectomy (DC). Such data have potentially clinical importance for guiding the treatment. The objective of this study was to investigate the postoperative cerebral hemodynamic patterns, using transcranial Doppler (TCD) ultrasonography, in patients who underwent DC. The relationship between the cerebral circulatory patterns and the patients' outcome was also analyzed.Methods: Nineteen TBI patients with uncontrolled brain swelling were prospectively studied. Cerebral blood circulation was evaluated by TCD ultrasonography. Patients and their cerebral hemispheres were categorized based on TCD-hemodynamic patterns. The data were correlated with neurological status, midline shift on CT scan, and Glasgow outcome scale scores at 6 months after injury.Results: Different cerebral hemodynamic patterns were observed. One patient (5.3%) presented with cerebral oligoemia, 4 patients (21%) with cerebral hyperemia, and 3 patients (15.8%) with cerebral vasospasm. One patient (5.3%) had hyperemia in one cerebral hemisphere and vasospasm in the other hemisphere. Ten patients (52.6%) had nonspecific circulatory pattern. Abnormal TCD-circulatory patterns were found in 9 patients (47.4%). There was no association between TCD-cerebral hemodynamic findings and outcome.Conclusion: There is a wide heterogeneity of postoperative cerebral hemodynamic findings among TBI patients who underwent DC, including hemodynamic heterogeneity between their cerebral hemispheres. DC was proved to be effective for the treatment of cerebral oligoemia. Our data support the concept of heterogeneous nature of the pathophysiology of the TBI and suggest that DC as the sole treatment modality is insufficient

Genetic biomarkers in patients with aneurysmal subarachnoid hemorrhage in the Amazon patients

Hemorragia subaracnoidea aneurismática (HSAa) é considerada causa importante de morte e de sequelas neurológicas. A taxa de mortalidade desta doença pode alcançar 50% nos primeiros dois meses após sangramento de aneurisma encefálico. Apesar dos avanços científicos da modernidade, o resultado do tratamento da HSAa não mudou nos últimos anos. O presente estudo avaliou o papel de 14 biomarcadores genéticos, incluindo o polimorfismo (SNP) do gene eNOS, em pacientes da Amazônia com HSAa, para verificar as alterações alélicas associadas ao risco de vasoespasmo encefálico e déficit neurológico tardio. Avaliou-se a ancestralidade desta amostra de pacientes em que se utilizou 48 marcadores para identificar possível etnia associada à predisposição ao VE. Investigou-se 14 biomarcadores genéticos no tocante à resposta inflamatória encefálica na HSAa. Foram avaliados 265 doentes que foram divididos em dois grupos: grupo I (pacientes com vasoespasmo encefálico) e grupo 2 (pacientes sem vasoespasmo). A média das idades foi 51 anos, havia 224 mulheres (84%) e 124 pacientes (46,79%) apresentaram vasoespasmo encefálico (VE). A maior incidência de VE ocorreu na idade entre 50 e 59 anos. Tabagismo e hipertensão arterial sistêmica foram os fatores de risco mais associados à VE. Aneurismas encefálicos de tamanho pequeno e médio predominaram nesta casuística. As escalas amarela e vermelha do VASOGRADE associaram-se ao risco de VE (p < 0,001). Não houve variação na distribuição ancestral entre os grupos estudados e o que ocorre na população brasileira saudável na região Amazônica. O gene da eNOS com seus respectivos polimorfismos T-786C e 27VNTR4 correlacionaram-se com VE. Outros marcadores observados foram TP53, CASP8, ACE2, IL4 e XRCC1. O gene TP53 (modelo recessivo alelo 1) mostrou-se ser um fator protetor de VE, enquanto que genes com mutações INDEL CASP8 (modelo recessivo alelo 2) e o XRCC1 (modelo recessivo alelo 1) mostraram tendência ao desenvolvimento de VE com risco 2 vezes maior e 1,4 vezes maior que o grupo II (p < 0,001). Conclui-se que SNPs da eNOS se correlacionam com desenvolvimento de VE sintomático pós-HSAa. Este estudo também mostrou o papel dos marcadores inflamatórios na HSAa, o que auxiliaria na condução da terapia clínica.Aneurysmal subarachnoid hemorrhage (aSAH) is a leading cause of premature death and neurological disability. It is considered as a devastating condition that accounts to 50% of mortality during the first two months after a hemorrhagic event. Despite foremost advances in the clinical management of post-aSAH patients, the rates of mortality and morbidity have not changed in recent years. This study appraised the role of 14 genetic biomarkers, including the eNOS polymorphism (SNP) between Amazon\'s patients with aSAH, as means to document how variant alleles are related to a higher disposition to cerebral vasospasm (CV) and delayed cerebral ischemia (DCI). 265 patients were evaluated and then divided into two clusters: Group I (with symptomatic CV) and group II (presenting no symptomatic CV). The median ages of patients were 51.61 years of age, 224 (84.52%) were women and 124 patients (46.97%) had symptoms of cerebral vasospasm (CV). Tobacco smoking and systemic arterial hypertension are the risk factors most associated to CV. In the course of this research, most aneurysms found were small and medium-sized. The score VASOGRADE yellow and VASOGRADE red presented a high risk of CV (p < 0.001). We established a panel of 48 ancestry informative markers for estimating which ethnicity could present a predisposition to CV. There was no variation in the ancestral distribution between study groups and healthy brazilian folk over the Amazon region. The eNOS gene with its polymorphisms T-786C and 27 VNTR4 were correlated to CV. Other markers were accomplished: TP53, CASP8, ACE2, IL4, and XRCC1. The TP53 gene (recessive genetic model allele 1) supporting evidence of the protective role to CV. Whilst other genes with INDEL mutation like as CASP8 (recessive model allele 2) and the XRCC1 (recessive model allele 1) indicated a propensity to spread out CV with odds 2-fold higher, and 1.414 times greater than group II (p < 0.001). It follows that eNOS SNPs correlate to a positive association with a syntomatic CV post-aSAH. Also, this study showed up the role of inflammatory markers at aSAH to a further educated therapeutic choice for a better clinical respons

Intracranial hemorrhages in patients with COVID-19: a systematic review of the literature, regarding six cases in an Amazonian population

Background Coronavirus disease 2019 (COVID-19) has emerged as a public health emergency worldwide, predominantly affecting the respiratory tract. However, evidence supports the involvement of extrapulmonary sites, including reports of intracranial hemorrhages

Modificações da hemodinâmica e metabolismo cerebral na insuficiência hepatica fulminante

Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.O edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.PASCHOAL, E. H. A. Universidade Federal do Par

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure

ABSTRACT Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF

Embolic Signals during Routine Transcranial Doppler Ultrasonography in Aneurysmal Subarachnoid Hemorrhage

Introduction. Cerebral emboli may occur in subarachnoid hemorrhage (SAH) and intracranial aneurysm surgery. Although embolic signs (ES) have been reported in SAH, their origin remains unclear. The aim of this study was to report the detection of ES during routine TCD monitoring in patients with aneurysmal SAH. Methods. A total of 105 patients with aneurysmal SAH were submitted to TCD evaluation. Patients were monitored almost daily (5 times per week). In each monitoring session, one experienced operator performed TCD to detect or assess vasospasm and ES in arteries of the Willis polygon. Results. Four patients out of a total of 105 patients with aneurysmal SAH were found to present spontaneous cerebral embolization during routine TCD monitoring. The average age of the 4 patients (mean ± standard deviation) was 59.5 ± 8.34 years (range 49–68 ys); female patients predominated representing 75% (3/4) of subjects. Conclusion. Although detection of ES was relatively rare in this study, rates of emboli occurrence may be higher under systematic monitoring. The detection of ES after SAH surgery reinforces the need to study the role of embolus in this condition and may be an indicator for prophylactic antithrombotic treatment

Ventricular arteriovenous malformation bleeding: a rare cause of headache in children. Case report Hemorragia cerebral secundária a malformação artério-venosa ventricular: uma causa rara de cefaléia na infância. Relato de caso

Headache as a chief complaint is rare in the paediatric emergency room. Actually, very seldom cases secondary to life threatening conditions as non-traumatic subarachnoid haemorrhage have been reported. A child with severe headache and nuchal rigidity and no other abnormalities on the physical examination is reported. Magnetic resonance angiography and cerebral angiography disclosed a ventricular arteriovenous malformation in the choroid plexus, supplied by the anterior choroidal artery, classified according to Spetzler grading system as grade 3 (deep venous drainage: 1; eloquence area: 0 and size: 2). The differences in the clinical presentations of the central nervous system arteriovenous malformation between children and adults are discussed.Cefaléia como queixa principal raramente ocorre num serviço de emergência pediátrica. Quando isso acontece, casos de cefaléia secundária que trazem risco de vida, tais como a hemorragia subaracnóide são raramente relatados. Apresentamos o caso de uma criança que apresentou cefaléia de forte intensidade associada a rigidez de nuca, sem outras anormalidades no exame físico. A angioressonância e angiografia digital evidenciaram malformação arteriovenosa na topografia do plexo coróide do ventrículo lateral direito, nutrida pela artéria coroidéia anterior, grau III na classificação de Spetzler (drenagem venosa profunda: 1; área de eloqüência: 0 e tamanho: 2). Nós discutimos as diferenças na apresentação clínica das malformações arteriovenosas encefálicas nas crianças e adultos

TCD assessment in fulminant hepatic failure: Improvements in cerebral autoregulation after liver transplantation

Introduction and Objectives: Acute liver failure, also known as fulminant hepatic failure (FHF), includes a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction and hepatic encephalopathy. The objective of this study was to assess cerebral autoregulation (CA) in 25 patients (19 female) with FHF and to follow up with seventeen of these patients before and after liver transplantation. Patients and Methods: The mean age was 33.8 years (range 14–56, SD 13.1 years). Cerebral hemodynamics was assessed by transcranial Doppler (TCD) bilateral recordings of cerebral blood velocity (CBv) in the middle cerebral arteries (MCA). Results: CA was assessed based on the static CA index (SCAI), reflecting the effects of a 20–30 mmHg increase in mean arterial blood pressure on CBv induced with norepinephrine infusion. SCAI was estimated at four time points: pretransplant and on the 1st, 2nd and 3rd posttransplant days, showing a significant difference between pre- and posttransplant SCAI (p = 0.005). SCAI peaked on the third posttransplant day (p = 0.006). Categorical analysis of SCAI showed that for most patients, CA was reestablished on the second day posttransplant (SCAI > 0.6). Conclusions: These results suggest that CA impairment pretransplant and on the 1st day posttransplant was re-established at 48–72 h after transplantation. These findings can help to improve the management of this patient group during these specific phases, thereby avoiding neurological complications, such as brain swelling and intracranial hypertension

TCD assessment in fulminant hepatic failure: Improvements in cerebral autoregulation after liver transplantation

Introduction and Objectives Acute liver failure, also known as fulminant hepatic failure (FHF), includes a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction and hepatic encephalopathy. The objective of this study was to assess cerebral autoregulation (CA) in 25 patients (19 female) with FHF and to follow up seventeen of these patients before and after liver transplantation. Patients and Methods The mean age was 33.8 years (range 14–56, SD 13.1 years). Cerebral hemodynamics was assessed by transcranial Doppler (TCD) bilateral recordings of cerebral blood velocity (CBv) in the middle cerebral arteries (MCA). Results CA was assessed based on the static CA index (SCAI), reflecting the effects of a 20–30 mmHg increase in mean arterial blood pressure on CBv induced with norepinephrine infusion. SCAI was estimated at four time points: pretransplant and on the 1st, 2nd and 3rd posttransplant days showing a significant difference between pre- and posttransplant SCAI (p = 0.005). SCAI peaked on the third posttransplant day (p = 0.006). Categorical analysis of SCAI showed that for most patients, CA was reestablished on the second day posttransplant (SCAI > 0.6). Conclusions These results suggest that CA impairment pretransplant and on the 1st day posttransplant was re-established at 48–72 h after transplantation. These findings can help to improve the management of this patient group during these specific phases, thereby avoiding neurological complications, such as brain swelling and intracranial hypertension.</p