Moderate Traumatic Brain Injury in Adult Population: The Latin American Brain Injury Consortium Consensus for Definition and Categorization.

Moderate traumatic brain injury (TBI) is a diagnosis that describes diverse patients with heterogeneity of primary injuries. Defined by a Glasgow Coma Scale between 9 and 12, this category includes patients who may neurologically worsen and require increasing intensive care resources and/or emergency neurosurgery. Despite the unique characteristics of these patients, there have not been specific guidelines published before this effort to support decision-making in these patients. A Delphi consensus group from the Latin American Brain Injury Consortium was established to generate recommendations related to the definition and categorization of moderate TBI. Before an in-person meeting, a systematic review of the literature was performed identifying evidence relevant to planned topics. Blinded voting assessed support for each recommendation. A priori the threshold for consensus was set at 80% agreement. Nine PICOT questions were generated by the panel, including definition, categorization, grouping, and diagnosis of moderate TBI. Here, we report the results of our work including relevant consensus statements and discussion for each question. Moderate TBI is an entity for which there is little published evidence available supporting definition, diagnosis, and management. Recommendations based on experts' opinion were informed by available evidence and aim to refine the definition and categorization of moderate TBI. Further studies evaluating the impact of these recommendations will be required.

Effects of Tranexamic Acid in Patients with Subarachnoid Hemorrhage in Brazil: A Prospective Observational Study with Propensity Score Analysis.

BACKGROUND: Rebleeding from a ruptured aneurysm increases the risk of unfavorable outcomes after subarachnoid hemorrhage (SAH) and is prevented by early aneurysm occlusion. The role of antifibrinolytics before aneurysm obliteration remains controversial. We investigated the effects of tranexamic acid on long-term functional outcomes of patients with aneurysmal SAH (aSAH). METHODS: This was a single-center, prospective, observational study conducted in a high-volume tertiary hospital in a middle-income country from December 2016 to February 2020. We included all consecutive patients with aSAH who either received or did not receive tranexamic acid (TXA) treatment. Multivariate logistic regression analysis using propensity score was used to evaluate the association of TXA use with long-term functional outcomes, measured by the modified Rankin Scale (mRS) at 6 months. RESULTS: A total of 230 patients with aSAH were analyzed. The median (interquartile range) age was 55 (46-63) years, 72% were women, 75% presented with good clinical grade (World Federation of Neurological Surgeons grade 1-3), and 83% had a Fisher scale of 3 or 4. Around 80% of patients were admitted up to 72 h from ictus. The aneurysm occlusion method was surgical clipping in 80% of the patients. A total of 129 patients (56%) received TXA. In multivariable logistic regression using inverse probability treatment weighting, the long-term rate of unfavorable outcomes (modified Rankin scale 4-6) was the same in the TXA and non-TXA groups (61 [48%] in TXA group vs. 33 [33%] in non-TXA group; odds ratio [OR] 1.39, 95% confidence interval [CI] 0.67-2.92; p = 0.377). The TXA group had higher in-hospital mortality (33 vs. 11% in non-TXA group; OR 4.13, 95% CI 1.55-12.53, p = 0.007). There were no differences between the groups concerning intensive care unit length of stay (16 ± 11.22 days in TXA group vs. 14 ± 9.24 days in non-TXA group; p = 0.2) or hospital (23 ± 13.35 days in TXA group vs. 22 ± 13.36 days in non-TXA group; p = 0.9). There was no difference in the rates of rebleeding (7.8% in TXA group vs. 8.9% in non-TXA group; p = 0.31) or delayed cerebral ischemia (27% in TXA group vs. 19% in non-TXA group; p = 0.14). For the propensity-matched analysis, 128 individuals were selected (64 in TXA group and 64 in non-TXA group), and the rates of unfavorable outcomes at 6 months were also similar between groups (45% in TXA group and 36% in non-TXA group; OR 1.22, 95% CI 0.51-2.89; p = 0.655). CONCLUSIONS: Our findings in a cohort with delayed aneurysm treatment reinforce previous data that TXA use before aneurysm occlusion does not improve functional outcomes in aSAH.

Intracranial Pressure Monitoring in Moderate Traumatic Brain Injury: A Systematic Review and Meta-Analysis.

BACKGROUND: The principal aim of this study was to determine the prevalence of intracranial pressure (ICP) monitoring and intracranial hypertension (IHT) in patients treated for moderate traumatic brain injury (TBI). A secondary objective was to assess factors associated with ICP monitoring. METHODS: We conducted a systematic review of the literature to identify studies that assessed ICP monitoring in moderate TBI. The meta-analysis was performed by using a random-effects model. RESULTS: A total of 13 studies comprising 116,714 patients were pooled to estimate the overall prevalence of ICP monitoring and IHT (one episode or more of ICP > 20 mm Hg) after moderate TBI. The prevalence rate for ICP monitoring was 18.3% (95% confidence interval 8.1-36.1%), whereas the proportion of IHT was 44% (95% confidence interval 33.8-54.7%). Three studies were pooled to estimate the prevalence of ICP monitoring according to Glasgow Coma Scale (GCS) (≤ 10 vs. > 10). ICP monitoring was performed in 32.2% of patients with GCS ≤ 10 versus 15.2% of patients with GCS > 10 (p = 0.59). Both subgroups were highly heterogeneous. We found no other variables associated with ICP monitoring or IHT. CONCLUSIONS: The prevalence of ICP monitoring in moderate TBI is low, but the prevalence of IHT is high among patients undergoing ICP monitoring. Current literature is limited in size and quality and does not identify factors associated with ICP monitoring or IHT. Further research is needed to guide the optimal use of ICP monitoring in moderate TBI.

How to manage traumatic brain injury without invasive monitoring?

PURPOSE OF REVIEW: Severe traumatic brain injury (TBI) is an extremely serious health problem, especially in low-middle income countries (LMICs). The prevalence of severe TBI continues to increase in LMICs. Major limitations in the chain of care for TBI patients are common in LMICs including suboptimal or nonexistent prehospital care, overburdened emergency services, lack of trained human resources and limited availability of ICUs. Basic neuromonitoring, such as intracranial pressure, are unavailable or underutilized and advanced techniques are not available. RECENT FINDINGS: Attention to fundamental principles of TBI care in LMICs, including early categorization, prevention and treatment of secondary insults, use of low-cost technology for evaluation of intracranial bleeding and neuromonitoring, and emphasis on education of human resources and multidisciplinary work, are particularly important in LMICs. Institutional collaborations between high-income and LMICs have developed evidence focused on available resources. Accordingly, an expert group have proposed consensus recommendations for centers without availability of invasive brain monitoring. SUMMARY: Severe TBI is very prevalent in LMIC and neuromonitoring is often not available in these environments. When intracranial pressure monitors are not available, careful attention to changes on clinical examination, serial imaging and noninvasive monitoring techniques can help recognize intracranial hypertension and effectively guide treatment decisions.

Acute Intracranial Hypertension During Pregnancy: Special Considerations and Management Adjustments.

Pregnancy is associated with a number of pathophysiological changes (including modification of vascular resistance, increased vascular permeability, and coagulative disorders) that can lead to specific (eclampsia, preeclampsia) or not specific (intracranial hemorrhage) neurological complications. In addition to these disorders, pregnancy can affect numerous preexisting neurologic conditions, including epilepsy, brain tumors, and intracerebral bleeding from cerebral aneurysm or arteriovenous malformations. Intracranial complications related to pregnancy can expose patients to a high risk of intracranial hypertension (IHT). Unfortunately, at present, the therapeutic measures that are generally adopted for the control of elevated intracranial pressure (ICP) in the general population have not been examined in pregnant patients, and their efficacy and safety for the mother and the fetus is still unknown. In addition, no specific guidelines for the application of the staircase approach, including escalating treatments with increasing intensity of level, for the management of IHT exist for this population. Although some of basic measures can be considered safe even in pregnant patients (management of stable hemodynamic and respiratory function, optimization of systemic physiology), some other interventions, such as hyperventilation, osmotic therapy, hypothermia, barbiturates, and decompressive craniectomy, can lead to specific concerns for the safety of both mother and fetus. The aim of this review is to summarize the neurological pathophysiological changes occurring during pregnancy and explore the effects of the possible therapeutic interventions applied to the general population for the management of IHT during pregnancy, taking into consideration ethical and clinical concerns as well as the decision for the timing of treatment and delivery.

Management of severe traumatic brain injury in regions with limited resources.

IMPORTANCE: Severe traumatic brain injury (sTBI) is a critical health problem in regions of limited resources (RLRs). Younger populations are among the most impacted. The objective of this review is to analyze recent consensus-based algorithms, protocols and guidelines proposed for the care of patients with TBI in RLRs. OBSERVATIONS: The principal mechanisms for sTBI in RLRs are road traffic injuries (RTIs) and violence. Limitations of care include suboptimal or non-existent pre-hospital care, overburdened emergency services, lack of trained human resources, and surgical and intensive care. Low-cost neuromonitoring systems are currently in testing, and formal neurotrauma registries are forming to evaluate both long-term outcomes and best practices at every level of care from hospital transport to the emergency department (ED), to the operating room and intensive care unit (ICU). CONCLUSIONS AND RELEVANCE: The burden of sTBI is highest in RLRs. As working-age adults are the predominantly affected age-group, an increase in disability-adjusted life years (DALYs) generates a loss of economic growth in regions where economic growth is needed most. Four multi-institutional collaborations between high-income countries (HICs) and LMICs have developed evidence and consensus-based documents focused on capacity building for sTBI care as a means of addressing this substantial burden of disease.

Neurological Prognostication After Cardiac Arrest in the Era of Target Temperature Management.

PURPOSE OF REVIEW: The purpose of this study is to provide an updated review on neurological prognostication in comatose patients after cardiac arrest in light of current targeted temperature management (TTM) strategies. RECENT FINDINGS: With improved pre-hospital and hospital care, death due to cardiac arrest is decreasing. Yet, most survivors have poor neurological outcomes. While TTM has demonstrated to improve neurological outcomes, it may cloud our prognostic accuracy. A multimodal approach is currently used to diminish prognostic uncertainty. The neurological examination remains the mainstay for prognosis after cardiac arrest. The combination electroencephalogram, somatosensory evoked potentials, and neuron-specific enolase improve prognostic accuracy, mostly in patients who underwent TTM. Quantitative analysis of pupillary reaction and EEG background variability, neuroimaging (CT perfusion and DWI-MRI), and middle/long-latency evoked potentials are promising methods that may further improve the precision of outcome prognostication.

Paroxysmal sympathetic hyperactivity syndrome caused by fat embolism syndrome. / Síndrome de hiperatividade simpática paroxística causada por síndrome da embolia gordurosa.

Paroxysmal sympathetic hyperactivity represents an uncommon and potentially life-threatening complication of severe brain injuries, which are most commonly traumatic. This syndrome is a clinical diagnosis based on the recurrent occurrence of tachycardia, hypertension, diaphoresis, tachypnea, and occasionally high fever and dystonic postures. The episodes may be induced by stimulation or may occur spontaneously. Underdiagnosis is common, and delayed recognition may increase morbidity and long-term disability. Trigger avoidance and pharmacological therapy can be very successful in controlling this complication. Fat embolism syndrome is a rare but serious complication of long bone fractures. Neurologic signs, petechial hemorrhages and acute respiratory failure constitute the characteristic presenting triad. The term cerebral fat embolism is used when the neurological involvement predominates. The diagnosis is clinical, but specific neuroimaging findings can be supportive. The neurologic manifestations include different degrees of alteration of consciousness, focal deficits or seizures. Management is supportive, but good outcomes are possible even in cases with very severe presentation. We report two cases of paroxysmal sympathetic hyperactivity after cerebral fat embolism, which is a very uncommon association.

A hiperatividade simpática paroxística representa uma complicação incomum, com potencial risco à vida, de lesões cerebrais graves, mais comumente de origem traumática. Seu diagnóstico clínico se baseia na manifestação recorrente de taquicardia, hipertensão, diaforese, taquipneia e, às vezes, febre, além de posturas distônicas. Os episódios podem ser induzidos por estímulos ou ocorrer de forma espontânea. É comum que ocorra subdiagnóstico desta síndrome, e o retardamento de seu reconhecimento pode aumentar a morbidade e a incapacidade em longo prazo. Evitar os desencadeantes e a farmacoterapia podem ter muito sucesso no controle desta complicação. A síndrome da embolia gordurosa é uma complicação rara, mas grave, das fraturas de ossos longos. Sinais neurológicos, petéquias hemorrágicas e insuficiência respiratória aguda são as características que constituem seu quadro clínico. O termo "embolia gordurosa cerebral" é estabelecido quando predomina o envolvimento neurológico. O diagnóstico é clínico, porém achados específicos de neuroimagem podem confirmá-lo. As manifestações neurológicas incluem diferentes graus de alteração da consciência, défices focais ou convulsões. Seu tratamento é de suporte, porém são possíveis desfechos favoráveis, mesmo nos casos com apresentação grave. Relatamos dois casos de hiperatividade simpática paroxística após embolia gordurosa cerebral, uma associação muito incomum.

Síndrome de hiperatividade simpática paroxística causada por síndrome da embolia gordurosa / Paroxysmal sympathetic hyperactivity syndrome caused by fat embolism syndrome

RESUMO A hiperatividade simpática paroxística representa uma complicação incomum, com potencial risco à vida, de lesões cerebrais graves, mais comumente de origem traumática. Seu diagnóstico clínico se baseia na manifestação recorrente de taquicardia, hipertensão, diaforese, taquipneia e, às vezes, febre, além de posturas distônicas. Os episódios podem ser induzidos por estímulos ou ocorrer de forma espontânea. É comum que ocorra subdiagnóstico desta síndrome, e o retardamento de seu reconhecimento pode aumentar a morbidade e a incapacidade em longo prazo. Evitar os desencadeantes e a farmacoterapia podem ter muito sucesso no controle desta complicação. A síndrome da embolia gordurosa é uma complicação rara, mas grave, das fraturas de ossos longos. Sinais neurológicos, petéquias hemorrágicas e insuficiência respiratória aguda são as características que constituem seu quadro clínico. O termo "embolia gordurosa cerebral" é estabelecido quando predomina o envolvimento neurológico. O diagnóstico é clínico, porém achados específicos de neuroimagem podem confirmá-lo. As manifestações neurológicas incluem diferentes graus de alteração da consciência, défices focais ou convulsões. Seu tratamento é de suporte, porém são possíveis desfechos favoráveis, mesmo nos casos com apresentação grave. Relatamos dois casos de hiperatividade simpática paroxística após embolia gordurosa cerebral, uma associação muito incomum.

ABSTRACT Paroxysmal sympathetic hyperactivity represents an uncommon and potentially life-threatening complication of severe brain injuries, which are most commonly traumatic. This syndrome is a clinical diagnosis based on the recurrent occurrence of tachycardia, hypertension, diaphoresis, tachypnea, and occasionally high fever and dystonic postures. The episodes may be induced by stimulation or may occur spontaneously. Underdiagnosis is common, and delayed recognition may increase morbidity and long-term disability. Trigger avoidance and pharmacological therapy can be very successful in controlling this complication. Fat embolism syndrome is a rare but serious complication of long bone fractures. Neurologic signs, petechial hemorrhages and acute respiratory failure constitute the characteristic presenting triad. The term cerebral fat embolism is used when the neurological involvement predominates. The diagnosis is clinical, but specific neuroimaging findings can be supportive. The neurologic manifestations include different degrees of alteration of consciousness, focal deficits or seizures. Management is supportive, but good outcomes are possible even in cases with very severe presentation. We report two cases of paroxysmal sympathetic hyperactivity after cerebral fat embolism, which is a very uncommon association.

Cerebral Fat Embolism: Recognition, Complications, and Prognosis.

Fat embolism syndrome (FES) is a rare syndrome caused by embolization of fat particles into multiple organs including the brain. It typically manifests with petechial rash, deteriorating mental status, and progressive respiratory insufficiency, usually occurring within 24-48 h of trauma with long-bone fractures or an orthopedic surgery. The diagnosis of FES is based on clinical and imaging findings, but requires exclusion of alternative diagnoses. Although there is no specific treatment for FES, prompt recognition is important because it can avoid unnecessary interventions and clarify prognosis. Patients with severe FES can become critically ill, but even comatose patients with respiratory failure may recover favorably. Prophylactic measures, such as early stabilization of fractures and certain intraoperative techniques, may help decrease the incidence and severity of FES.

First-Ever Stroke and Transient Ischemic Attack Incidence and 30-Day Case-Fatality Rates in a Population-Based Study in Argentina.

BACKGROUND AND PURPOSE: Epidemiological data about stroke are scarce in low- and middle-income Latin-American countries. We investigated annual incidence of first-ever stroke and transient ischemic attack (TIA) and 30-day case-fatality rates in a population-based setting in Tandil, Argentina. METHODS: We prospectively identified all first-ever stroke and TIA cases from overlapping sources between January 5, 2013, and April 30, 2015, in Tandil, Argentina. We calculated crude and standardized incidence rates. We estimated 30-day case-fatality rates. RESULTS: We identified 334 first-ever strokes and 108 TIAs. Age-standardized incidence rate per 100 000 for Segi's World population was 76.5 (95% confidence interval [CI], 67.8-85.9) for first-ever stroke and 25.1 (95% CI, 20.2-30.7) for first-ever TIA, 56.1 (95% CI, 48.8-64.2) for ischemic stroke, 13.5 (95% CI, 9.9-17.9) for intracerebral hemorrhage, and 4.9 (95% CI, 2.7-8.1) for subarachnoid hemorrhage. Stroke incidence was slightly higher for men (87.8; 95% CI, 74.6-102.6) than for women (73.2; 95% CI, 61.7-86.1) when standardized for the Argentinean population. Thirty-day case-fatality rate was 14.7% (95% CI, 10.8-19.5) for ischemic stroke, 24.1% (95% CI, 14.2-36.6) for intracerebral hemorrhage, and 1.9% (95% CI, 0.4-5.8) for TIA. CONCLUSIONS: This study provides the first prospective population-based stroke and TIA incidence and case-fatality estimate in Argentina. First-ever stroke incidence was lower than that reported in previous Latin-American studies, but first-ever TIA incidence was higher. Thirty-day case-fatality rates were similar to those of other population-based Latin-American studies.

Moderate Traumatic Brain Injury: The Grey Zone of Neurotrauma.

Moderate traumatic brain injury (MTBI) is poorly defined in the literature and the nomenclature "moderate" is misleading, because up to 15 % of such patients may die. MTBI is a heterogeneous entity that shares many aspects of its pathophysiology and management with severe traumatic brain injury. Many patients who ''talk and died'' are MTBI. The role of neuroimaging is essential for the proper management of these patients. To analyze all aspects of the pathophysiology and management of MTBI, proposing a new way to categorize it considering the clinical picture and neuroimaging findings. We proposed a different approach to the group of patients with Glasgow Coma Scale (GCS) ranging from 9 through 13 and we discuss the rationale for this proposal. Patients with lower GCS scores (9-10), especially those with significant space-occupying lesions on the CT scan, should be managed following the guidelines for severe traumatic brain injury, with ICU observation, frequent serial computed tomography (CT) scanning and ICP monitoring. On the other hand, those with higher range GCS (11-13) can be managed more conservatively with serial neurological examination and CT scans. Given the available evidence, MTBI is an entity that needs reclassification. Large-scale and well-designed studies are urgently needed.

Is a second cycle of immunoglobulin justified in axonal forms of Guillain-Barré syndrome?

Objective In certain situations, severe forms of Guillain-Barré syndrome (GBS) show no response or continue to deteriorate after intravenous immunoglobulin (IVIg) infusion. It is unclear what the best treatment option would be in these circumstances.Method This is a case report on patients with severe axonal GBS in whom a second cycle of IVIg was used.Results Three patients on mechanical ventilation who presented axonal variants of GBS, with autonomic dysfunction, bulbar impairment and Erasmus score > 6, showed no improvement after IVIg infusion of 400 mg/kg/d for 5 days. After 6 weeks, we started a second cycle of IVIg using the same doses and regimen as in the previous one. On average, 5 days after the second infusion, all the patients were weaned off mechanical ventilation and showed resolution of their blood pressure and heart rate fluctuations.Conclusions A second cycle of IVIg may be an option for treating severe forms of GBS.

Is a second cycle of immunoglobulin justified in axonal forms of Guillain-Barré syndrome? / É justificável utilizar um segundo ciclo de imunoglobulina para as formas axonais da síndrome de Guillain-Barré?

Objective In certain situations, severe forms of Guillain-Barré syndrome (GBS) show no response or continue to deteriorate after intravenous immunoglobulin (IVIg) infusion. It is unclear what the best treatment option would be in these circumstances.Method This is a case report on patients with severe axonal GBS in whom a second cycle of IVIg was used.Results Three patients on mechanical ventilation who presented axonal variants of GBS, with autonomic dysfunction, bulbar impairment and Erasmus score > 6, showed no improvement after IVIg infusion of 400 mg/kg/d for 5 days. After 6 weeks, we started a second cycle of IVIg using the same doses and regimen as in the previous one. On average, 5 days after the second infusion, all the patients were weaned off mechanical ventilation and showed resolution of their blood pressure and heart rate fluctuations.Conclusions A second cycle of IVIg may be an option for treating severe forms of GBS.

Objetivo Em determinadas situações, as formas graves da síndrome de Guillain-Barré (GBS) não mostram resposta ou continuam a deteriorar após a infusão endovenosa de imunoglobulina (IVIg). Não está claro qual seria a melhor opção de tratamento nestas circunstâncias.Método Este é o relato de caso de pacientes com grave comprometimento axonal em GBS, nos quais um segundo ciclo de IVIg foi utilizado.Resultados Três pacientes em ventilação mecânica que apresentavam variantes de GBS com disfunção autonômica, comprometimento bulbar e valores de Erasmus > 6, não mostraram melhora após infusão de IVIg 400 mg/kg/d por 5 dias. Após 6 semanas, foi iniciado um segundo ciclo de IVIg utilizando as mesmas doses e esquema feitos previamente. Em média, após 5 dias da segunda infusão, todos os pacientes haviam sido retirados da ventilação mecânica e mostravam resolução de suas flutuações de pressão arterial e frequência cardíaca.Conclusões O segundo ciclo de IVIg pode ser uma alternativa para tratamento de formas graves de GBS.