Significant Brain Swelling Research Articles

Pathophysiology, clinical presentation, and treatment of coma and acute kidney injury complicating falciparum malaria.

Purpose of reviewCerebral impairment and acute kidney injury (AKI) are independent predictors of mortality in both adults and children with severe falciparum malaria. In this review, we present recent advances in understanding the pathophysiology, clinical features, and management of these complications of severe malaria, and discuss future areas of research.Recent findingsCerebral malaria and AKI are serious and well recognized complications of severe malaria. Common pathophysiological pathways include impaired microcirculation, due to sequestration of parasitized erythrocytes, systemic inflammatory responses, and endothelial activation. Recent MRI studies show significant brain swelling in both adults and children with evidence of posterior reversible encephalopathy syndrome-like syndrome although targeted interventions including mannitol and dexamethasone are not beneficial. Recent work shows association of cell-free hemoglobin oxidation stress involved in the pathophysiology of AKI in both adults and children. Paracetamol protected renal function likely by inhibiting cell-free-mediated oxidative stress. It is unclear if heme-mediated endothelial activation or oxidative stress is involved in cerebral malaria.SummaryThe direct causes of cerebral and kidney dysfunction remain incompletely understood. Optimal treatment involves prompt diagnosis and effective antimalarial treatment with artesunate. Renal replacement therapy reduces mortality in AKI but delayed diagnosis is an issue.

Management of Hemispheric Infarction and Ischemic Swelling.

This article provides an overview of large territory hemispheric infarction, with an emphasis on recent developments and practical issues related to its evaluation, diagnosis, monitoring, and treatment. Swelling after large infarction results in severe morbidity and often death. Early vigilance for the development of swelling is critical to optimize patient outcome. Comprehensive management is highly dependent on a strong multidisciplinary, collaborative approach. Several advances in the last decade have led to an increasingly standardized approach to the patient with significant brain swelling after stroke. In particular, early identification of patients with large stroke at high risk for deterioration, and decompressive craniectomy as an important treatment option, are two significant advances. Effective management of hemispheric ischemic stroke and swelling requires a team skilled in the neurologic examination of critically ill patients and a broad understanding of the natural history of brain swelling after stroke.

Pediatric traumatic brain injury and elevated intracranial pressure

Dr. Jagannathan and colleagues provide a detailed review of the management of severe pediatric head injury in 96 patients in whom intracranial pressure (ICP) was elevated when first measured and who were followed-up for a minimum of 2 years in almost every case. The present paper follows a previous study from the same investigative group on decompressive craniectomy1 but adds considerable new information. This new study appropriately excludes patients with nonaccidental trauma and includes only those patients in whom the initial CT scan result was abnormal. These investigators used a definition of ICP as . 20 mm Hg as their cutoff point for elevated ICP. Although it is a retrospective review, this study is one of the largest patient series of pediatric head injury specifically focusing on intracranial hypertension and its influence on outcome, and is particularly important given the long-term follow-up aspect of the study. Using a standardized protocol with a bias toward using early decompressive craniectomy, ICP could be controlled in 82 of the patients (85%) in this study. Medical therapy was effective in 35% of the patients, which was defined as using sedation, intermittent hyperventilation, and muscle relaxation. When ventriculostomy was used, 24% of the patients also attained ICP control. Fourteen patients underwent either an attempt or successful evacuation of a mass lesion; ICP could still not be controlled in 2 patients after this procedure, and both patients died. Decompressive craniectomy was performed in 25 patients and ICP was controlled in 16 of these patients (64%). In the 9 cases in which ICP control could not be achieved after decompressive craniectomy, all the patients died. This paper provides a number of very important observations, but also raises some questions. First, it appears that the means to ICP control is less important than the method in which ICP can be brought below 20 mm Hg. The authors’ bias toward using early decompressive craniectomy appears, in part, to reflect dissatisfaction with the rate of infection following placement of a ventricular drain. Clearly, decompressive craniectomy is a much more invasive procedure, and although the infection rate after ventriculostomy in this study (~ 8%) is consistent with rates in other studies, it is possible that changes in the technique of ventricular drain placement might reduce the frequency of infection. The recent focus on reducing catheter-related sepsis has resulted in dramatic reductions in such infections and perhaps a much more vigorous approach to sterility when a ventricular catheter is placed might yield similar benefits. Nevertheless, the authors should not be criticized for attempting decompressive craniectomy at a relative early time period because it is fairly clear that a late decompressive craniectomy, when all other measures have failed, is likely to result in very unsatisfactory outcomes. One particularly attractive feature of the study is the long-term follow-up aspect. As the authors note in the paper, this feature is probably particularly important in the pediatric population, in which substantial plasticity and microcellular reshaping of the brain is occurring at a time in these patients when the brain is severely traumatized. The brain is literally “pruning itself” in its day-to-day evolution to optimize neuronal connections, and therefore improved outcomes in children and young adults are not terribly surprising. Nevertheless, permitting adequate cerebral perfusion by reducing ICP as Juul and colleagues2 have demonstrated appears to be the appropriate approach in a critical care environment. Of interest is the observation that vascular injuries were present in ~ 4% of the patients. This indicates that these impairments of cerebral perfusion may be more common than previously believed, and given modern interventional techniques these injuries might be amenable to treatment if they could be recognized early. It would be of interest to know the authors’ view on this subject. It would also be helpful for the authors to clarify what they did in those patients who underwent operative intervention for hematoma without a decompressive craniectomy, who developed significant brain swelling in the operating room following evacuation of the mass lesion. Under those circumstances, many neurosurgeons would have already turned a large flap or would enlarge the intracranial opening to provide a large decompression. In Table 6 one notes that in patients with diffuse injury

Diffuse brain injury complicated by acute subdural hematoma and secondary insults in the rodents: the effect of surgical evacuation.

Head Trauma associated with acute sudural hematoma (SDH) and complicated by secondary insult is a grave clinical combination with complex pathophysiology. The aim of this study was to develop a clinically relevant injury model, which can be used to study the interaction between injury mechanisms. We present a novel model of SDH combined with diffuse brain injury (DBI) and a hypoxic secondary insult, and investigate the effects of surgical evacuation. Adult Sprague-Dawley rats were given a 300 microliters SDH and 20 minute-hypoxia following Impact Acceleration DBI. Hematoma was evacuated at one hour post-injury. Physiological parameters were measured for 5 hours, together with assessment of brain water content. Secondary insult after traumatic SDH was associated with significant brain swelling and stimulated refractory rise in ICP. In traumatic SDH complicated by secondary insult, brain swelling is exacerbated by surgical evacuation.

Volumetric Quantification of Brain Swelling after Hypobaric Hypoxia Exposure

We applied a novel MR imaging technique to investigate the effect of acute mountain sickness on cerebral tissue water. Nine volunteers were exposed to hypobaric hypoxia corresponding to 4572 m altitude for 32 h. Such an exposure may cause acute mountain sickness. We imaged the brains of the volunteers before and at 32 h of hypobaric exposure with two different MRI techniques with subsequent data processing. (1) Brain volumes were calculated from 3D MRI data sets by applying a computerized brain segmentation algorithm. For this specific purpose a novel adaptive 3D segmentation program was used with an automatic correction algorithm for RF field inhomogeneity. (2) T2 decay rates were analyzed in the white matter. The results demonstrated that a significant brain swelling of 36.2 ± 19.6 ml (2.77 ± 1.47%, n = 9, P < 0.001) developed after the 32-h hypobaric hypoxia exposure with a maximal observed volume increase of 5.8% (71.3 ml). These volume changes were significant only for the gray matter structures in contrast to the unremarkable changes seen in the white matter. The same study repeated 3 weeks later in 6 of 9 original subjects demonstrated that the brains recovered and returned approximately to the initially determined sea-level brain volume while hypobaric hypoxia exposure once again led to a significant new brain swelling (24.1 ± 12.1 ml, 1.92 ± 0.96%, n = 6, P < 0.005). On the contrary, the T2 mapping technique did not reveal any significant effect of hypobaria on white matter. We present here a technique which is able to detect reversible brain volume changes as they may occur in patients with diffuse brain edema or increased cerebral blood volume, and which may represent a useful noninvasive tool for future evaluations of antiedematous drugs.

Influence of ischemia and reperfusion on the course of brain tissue swelling and blood-brain barrier permeability in a rodent model of transient focal cerebral ischemia.

Brain swelling is a serious complication associated with focal ischemia in stroke and severe head injury. Experimentally, reperfusion following focal cerebral ischemia exacerbates the level of brain swelling. In this study, the permeability of the blood-brain barrier has been investigated as a possible cause of reperfusion-related acute brain swelling. Blood-brain barrier disruption was investigated using Evans Blue dye and [14C]aminoisobutyric acid autoradiography in a rodent model of reversible middle cerebral artery (MCA) occlusion. Acute brain swelling and cerebral blood flow (CBF) during ischemia and reperfusion were analyzed from double-label CBF autoradiograms after application of the potent vasoconstrictor peptide endothelin-1 to the MCA. Ischemia was apparent within ipsilateral MCA territory, 5 min after endothelin-1 application to the exposed artery. Reperfusion, examined at 30 min and 1, 2, and 4 h, was gradual but incomplete within this time frame in the core of middle cerebral artery territory and associated with significant brain swelling. Ipsilateral hemispheric swelling increased over time to a maximum (>5%) at 1-2 h after endothelin-1 but was not associated with a significant increase in the ipsilateral transfer constant for [14C]aminoisobutyric acid over this time frame. These results indicate that endothelin-1 induced focal cerebral ischemia is associated with an acute but reversible hemispheric swelling during the early phase of reperfusion which is not associated with a disruption of the blood-brain barrier.

Disturbed cerebrospinal fluid circulation after subarachnoid hemorrhage and acute aneurysm surgery

In 138 patients with ruptured cerebral aneurysms operated on within 48 to 72 hours after subarachnoid hemorrhage, an external ventricular drainage catheter was inserted before craniotomy and was used intermittently during the first week after surgery. In 51 patients, intracranial pressure (ICP) was measured intraoperatively. The majority of patients showed increased ICP intraoperatively irrespective of the preoperative Hunt and Hess grade and the amount of subarachnoid blood accumulation or intraventricular blood clot. Intraoperative drainage of cerebrospinal fluid allowed easy access for aneurysm dissection by making the brain slack in more than 90% of patients. Postoperative ICP measurements revealed that significant brain swelling did not occur in the majority of patients. In 7 patients, persistently elevated ICP (greater than 20 mm Hg) was recorded. Nine patients (8%) developed shunt-dependent hydrocephalus; all of these patients had suffered an intraventricular hemorrhage. Measurements of the volumes of cerebrospinal fluid drained did not allow prediction of shunt-dependent hydrocephalus.

Disturbed Cerebrospinal Fluid Circulation after Subarachnoid Hemorrhage and Acute Aneurysm Surgery

Abstract In 138 patients with ruptured cerebral aneurysms operated on within 48 to 72 hours after subarachnoid hemorrhage, an external ventricular drainage catheter was inserted before craniotomy and was used intermittently during the first week after surgery. In 51 patients, intracranial pressure (ICP) was measured intraoperatively. The majority of patients showed increased ICP intraoperatively irrespective of the preoperative Hunt and Hess grade and the amount of subarachnoid blood accumulation or intraventricular blood clot. Intraoperative drainage of cerebrospinal fluid allowed easy access for aneurysm dissection by making the brain slack in more than 90% of patients. Postoperative ICP measurements revealed that significant brain swelling did not occur in the majority of patients, In 7 patients, persistently elevated ICP (&amp;gt;20 mm Hg) was recorded. Nine patients (8%) developed shunt-dependent hydrocephalus; all of these patients had suffered an intraventricular hemorrhage. Measurements of the volumes of cerebrospinal fluid drained did not allow prediction of shunt-dependent hydrocephalus.