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Traumatic brain injury (TBI) is a very common occurrence in both human and veterinary medicine and carries a high rate of morbidity and mortality. Notice to pet owners & publicThis website has been created as an educational resource for the veterinary community. Ana Sofia Cruz,Sonia Menezes,Maria Silva Brazilian Journal of Anesthesiology. Ana Sofia Cruz,Sonia Menezes,Maria Silva Brazilian Journal of Anesthesiology (English Edition).
Anteroposterior chest radiograph shows bilateral alveolar opacities in a patient with subarachnoid hemorrhage who developed neurogenic pulmonary edema.
Axial, contrast-enhanced computed tomography (CT) scan shows alveolar and interstitial pulmonary edema. The correct diagnosis relies on clinical and radiologic findings, despite some overlap in the clinical and imaging findings between the different causes.
An initial and rapid increase in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury. Two major components contribute to the pathogenesis of NPE: elevated intravascular pressure and pulmonary capillary leak. Whether the hemodynamic changes produce a pulmonary capillary leak through pressure-induced mechanical injury to the pulmonary capillaries or whether some direct nervous system control over pulmonary capillary permeability exists remains uncertain.
Gadolinium-based MRI contrast agents has been associated with several adverse effects, some of which can be serious. In conjunction with the clinical presentation, radiographic findings are generally sufficient to arrive at a diagnosis of NPE.
The specificity of chest radiographs, particularly portable, anteroposterior (AP) images, is low, and it may not be possible to differentiate the various causes of lung parenchymal shadowing on radiographs alone.
Most patients with NPE are generally ill, and there may be transportation problems to computed tomography (CT) scanning and magnetic resonance imaging (MRI) units.
The heart is usually enlarged in cardiogenic pulmonary edema, but it may be normal in lung injury and NPE. The infiltrates of cardiogenic pulmonary edema are usually diffuse, and air bronchograms are rare. One of 3 patterns is seen: a normal chest, bilateral perihilar pulmonary edema, or generalized pulmonary edema. Another feature that may be seen is cardiac enlargement, in cases of previous cardiac failure. NPE is a known complication of lung transplantation.[2, 3] Herman and colleagues, however, found chest radiography to be helpful, but not definitive, in distinguishing problems after bilateral lung transplantation and found CT scanning to be excellent for the demonstration of airway problems.
The reimplantation response (NPE due to ischemia, trauma, denervation, and lymphatic interruption) occurred in 12 patients and usually consisted of bilateral perihilar and basal consolidation. Radiographic findings associated with the reimplantation response and rejection were nonspecific and were mimicked by fluid overload and infection.
The 3 principal features found were the distribution of pulmonary flow, the distribution of pulmonary edema, and the width of the vascular pedicle. A study by Liebman et al indicated that it is hazardous to accept a portable radiographic diagnosis of congestive heart failure as a cause of pulmonary edema. CT scanning is seldom used in assessing patients with NPE and ARDS, mostly because of problems in transporting and monitoring these severely ill individuals.
Tagliabue and colleagues reviewed the findings of 74 patients with ARDS who underwent chest CT scanning.[9] Lung opacities were bilateral in almost all patients and in most cases (86%) were dependent. In contrast with previous reports, pleural effusion was a frequent finding (50%) that did not worsen the patients' prognosis. Gattinoni and co-authors examined 10 patients with full-blown ARDS who were receiving mechanical ventilation with positive end-expiratory pressure (PEEP) and who underwent lung CT scanning.[10] Seven healthy subjects also were included in the study. Stark and colleagues described the CT scan features of 28 patients with ARDS.[11] Diffuse lung consolidation, lobar or segmental disease, and multifocal, patchy involvement were observed.
Research indicates that a variety of nuclear imaging techniques can be used to diagnose NPE.
Raijmakers and co-investigators concluded that a 67Ga pulmonary leak index can be used in distinguishing ARDS from hydrostatic pulmonary edema. According to a study by Chen and Schuster, fluorodeoxyglucose (FDG)a€“positron emission tomography (PET) FDG-PET scanning may be useful for studying neutrophil kinetics during oleic acida€“induced lung injury.
Iodine-123 meta-iodobenzylguanidine (MIBG) results can be considered indicators of pulmonary endothelial cell function.
Koizumi and colleagues studied serial scintigraphic assessment of 123I MIBG lung uptake in a patient with high-altitude pulmonary edema.[15] The initial evaluation was performed 7 days after the patient's admission. Medscape's clinical reference is the most authoritative and accessible point-of-care medical reference for physicians and healthcare professionals, available online and via all major mobile devices.
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Stroke is the third most common cause of death in the Western World and is a condition seen by Neurologists, General Physicians and Primary Care Physicians.
We describe a case of basilar thrombosis treated with intra-arterial thrombolysis where prone ventilation was employed to treat neurogenic cardio-pulmonary complications. This resulted in rapid resolution of neurogenic pulmonary edema and patient recovery after recanulation of the basilar artery by intra-arterial urokinase. This technique of prone positioning for ventilation is of importance to physicians who manage stroke and its complications. Neurogenic pulmonary edema (NPE) is a relatively rare form of pulmonary edema caused by an increase in pulmonary interstitial and alveolar fluid. The pathogenesis of neurogenic pulmonary edema (NPE) is not completely understood.[1] Because the most common neurological events are associated with increased intracranial pressure, intracranial hypertension is considered a key etiologic factor. Within the central nervous system, the sites responsible for the development of neurogenic pulmonary edema are not fully elucidated. The medulla is believed to activate sympathetic components of the autonomic nervous system.
An acute neurological crisis, accompanied by a marked increase in intracranial pressure, may stimulate the hypothalamus and the vasomotor centers of the medulla. A central nervous system event produces a dramatic change in Starling forces, which govern the movement of fluid between capillaries and the interstitium. Factors leading to the development of neurogenic pulmonary edema in patients with subarachnoid hemorrhage. Alterations in pulmonary vascular pressures appear to be the most likely Starling force to influence the formation of neurogenic pulmonary edema. An increase in left atrial pressure may occur because of increases in sympathetic tone and venous return. Pulmonary venoconstriction occurs with sympathetic stimulation, which may increase the capillary hydrostatic pressure and produce pulmonary edema without affecting left atrial or pulmonary capillary wedge pressures.
An increase in capillary permeability can result in neurogenic pulmonary edema without elevation of pulmonary capillary hydrostatic pressure, because causative hemodynamic alteration is inconsistent. An initial and rapid rise in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury.
As many as one third of patients with status epilepticus may have evidence of neurogenic pulmonary edema.[8] More than half the patients with severe, blunt, or penetrating head injury have associated neurogenic pulmonary edema. A series of 457 patients with subarachnoid hemorrhage reported a 6% prevalence of severe neurogenic pulmonary edema.[11] Solenski et al reported in 1995 that increased age and a worse clinical grade of subarachnoid hemorrhage were associated with neurogenic pulmonary edema.
No data suggest differences in the international incidence of neurogenic pulmonary edema compared with the experience in the United States. Data regarding morbidity and mortality following neurogenic pulmonary edema (NPE) have not been well documented, given the relatively low prevalence and likely underdiagnosis. The individuala€™s sex is not associated with the development of neurogenic pulmonary edema.
Age is not a specific risk factor for neurogenic pulmonary edema, other than the increased risk for neurologic events and cardiovascular abnormalities associated with increasing age. Progression of neurogenic pulmonary edema in the same patient in the image above, with subdural hematoma (day 2). The site contains images and videos that may be considered graphic to non-medical individuals.
If you have any questions about the information contained within, especially as to any decisions you wish to make concerning the health or well-being of your pet, please contact your regular veterinarian. Acute intraoperative neurogenic pulmonary edema during endoscopic ventriculoperitoneal shunt revision. Postictal neurogenic pulmonary edema during uncal herniation-a case report and literature review. Pulmonary vascular response to increase in intracranial pressure: Role of sympathetic mechanisms. Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits.
Effects of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure. Influence of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure in patients with acute stroke. Severe subarachnoid hemorrhage with pulmonary edema successfully treated by intra-aneurysmal embolization using Guglielmi detachable coils-Two case reports.
Ventriculoperitoneal shunt dysfunction in a patient presenting with neurogenic pulmonary edema.
The latter, noncardiogenic pulmonary edema (NPE), is caused by changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult (see the images below).
An increase in vascular permeability consequently results in edema formation, as suggested by the frequent observation of pulmonary hemorrhage in NPE (ie, the blast theory). The neuro-effector site for nervous systema€“induced pulmonary edema appears to be relatively well established in regions about the caudal medulla, where nuclei regulating systemic arterial pressure, as well as afferent and efferent pathways to and from the lungs, are located.
The use of chest radiography and other tests is key to establishing the diagnosis and to distinguishing between the 2 types of pulmonary edema. It has extremely rare life-threatening systemic complications, which can lead to bronchospasm, hypersensitivity reactions, and cardiovascular arrest. Conventional chest radiography is readily and universally available, and it has the added advantage of portability; chest radiography is the examination of choice. Moreover, because these patients may be restless, sedation may be required to obtain images that are not degraded by motion artifacts. However, the heart may also be of normal size in cardiogenic edema after acute myocardial infarction.



Infiltrates in nephrogenic pulmonary edema are classically described as having a bat-wing distribution, whereas those in lung injury tend to be more peripheral. The early signs of pulmonary edema (interstitial edema) are the septal lines (Kerley B lines), which are horizontal lines seen laterally in the lower zones.
In their study, the authors reviewed the postoperative chest radiographic and CT scan findings in 13 patients who underwent bilateral lung transplantation.[4] Portable chest radiography was performed daily for about 10 days, after which upright posteroanterior studies were performed daily for about 10 days and then as clinically required. Twelve episodes of acute rejection, an imprecise clinical diagnosis, occurred in 10 patients.
The cause of the pulmonary edema can be determined with a high degree of accuracy by paying careful attention to certain radiographic features. The ancillary features were pulmonary blood volume, peribronchial cuffing, septal lines, pleural effusions, air bronchograms, lung volume, and cardiac size.
In their report, the authors assessed the usefulness of portable chest radiographs in defining the amount of physiologic shunting and the severity of NPE.[6, 7] Ten of their 11 patients had acute respiratory failure. High-resolution CT (HRCT) scanning demonstrates widespread airspace consolidation, which may have predominant distribution in the dependent lung regions. Large lung cysts and small cysts producing a Swiss-cheese appearance of the parenchyma were detected. In their study, the investigators examined the effectiveness of a noninvasive, bedside, dual-radionuclide method (67Ga circulating transferrin and technetium-99m [99mTc]a€“labeled RBCs) of measuring pulmonary microvascular permeability, in differentiating between hydrostatic pulmonary edema and pulmonary edema due to ARDS.[13] Patients in the study suffered from respiratory insufficiency and bilateral, alveolar pulmonary edema, as demonstrated on chest radiographs.
With various definitions, a supranormal pulmonary leak index for ARDS had a sensitivity of 100%, while its specificity ranged from 46-75%.
The investigators measured neutrophil glucose uptake with FDGa€“PET scanning in anesthetized dogs after intravenous, oleic acida€“induced, acute lung injury (n = 6) or after low-dose, intravenous endotoxin (which is known to activate neutrophils without causing lung injury) followed by oleic acid (n = 7).
Lung transplantation: indications, donor and recipient selection, and imaging of complications.
Limitations of portable roentgenography of the chest in patients with acute respiratory failure. Adult respiratory distress syndrome due to pulmonary and extrapulmonary causes: CT, clinical, and functional correlations. Positron emission tomography with [18F]fluorodeoxyglucose to evaluate neutrophil kinetics during acute lung injury. Serial scintigraphic assessment of iodine-123 metaiodobenzylguanidine lung uptake in a patient with high-altitude pulmonary edema.
Topics are richly illustrated with more than 40,000 clinical photos, videos, diagrams, and radiographic images. The articles assist in the understanding of the anatomy involved in treating specific conditions and performing procedures. Check mild interactions to serious contraindications for up to 30 drugs, herbals, and supplements at a time. Plus, more than 600 drug monographs in our drug reference include integrated dosing calculators. Neurogenic pulmonary edema can complicate the management of large strokes and cerebral hemorrhage. They do not and should not be interpreted as being representative or endorsed by the Uniformed Services University, U.S. Neurogenic pulmonary edema develops within a few hours after a neurologic insult, and diagnosis requires exclusion of other causes of pulmonary edema (eg, high-altitude pulmonary edema).
Animal studies suggest that hypothalamic lesions, stimulation of the vasomotor centers of the medulla, elevated intracranial pressure, and activation of the sympathetic system have potential roles.[2, 3] Cervical spinal cord nuclei also may have a role. Experimentally, bilateral lesions of the nuclei in the medulla produce profound pulmonary and systemic hypertension and pulmonary edema. This, in turn, initiates a massive autonomic discharge mediated by preganglionic centers within the cervical spine.
Both hemodynamic (cardiogenic) and nonhemodynamic (noncardiogenic) components contribute to edema formation. Left ventricular performance may deteriorate secondary to the direct effects of catecholamines and other mediators, as well as transient systemic hypertension. However, evidence shows that alpha-adrenergic blockade can protect against neurogenic pulmonary edema. Patients with neurologic events often have multiple other comorbidities, which may obscure or mimic the diagnosis of neurogenic pulmonary edema.
Approximately 71% of fatal cases of subarachnoid hemorrhage are complicated by neurogenic pulmonary edema.
However, note that epidemiologic data on this entity in general are very sparse because of the difficulties in recognition and diagnosis and lack of a standardized definition. Overall, patient outcome is usually determined by the underlying neurological insult that led to neurogenic pulmonary edema.
Transpulmonary Thermodilution-Based Management of Neurogenic Pulmonary Edema After Subarachnoid Hemorrhage. Electrocardiographic abnormalities predict neurogenic pulmonary edema in patients with subarachnoid hemorrhage. Hypoxia mediated pulmonary edema: potential influence of oxidative stress, sympathetic activation and cerebral blood flow. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Medical complications after subarachnoid hemorrhage: new strategies for prevention and management.
Clinical significance of elevated natriuretic peptide levels and cardiopulmonary parameters after subarachnoid hemorrhage.
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractClassical inflammation is a well-characterized secondary response to many acute disorders of the central nervous system. These components often work in concert, as in pulmonary edema after epileptic convulsions or intracranial pressure elevation.
Pulmonary vascular plethora often occurs with upper lobe blood diversion in cardiogenic cases; vessels of the upper lobe are balanced to cephalic in fluid overload but are normal in lung injury. Although the peripheral infiltrate is fairly specific for lung injury, the diffuse variety is seen with equal frequency in lung injury. The septal lines arise from the pleural surface and are typically 1 mm thick and 10 mm long; unlike blood vessels, these reach the edge of the lung.
However, over the course of 24-48 hours following the onset of tachypnea, dyspnea, and hypoxia, ARDS becomes more widespread and uniform. Radiographic changes consisted of bibasal (n = 2) and right middle and lower (n = 2) or left basal consolidation (n = 1); no changes were observed in 7 episodes. In general, chest radiography was inaccurate in the assessment of these complications, and CT scanning was accurate in such assessments. Differing constellations of these features, each characteristic of a specific type of edema, were found. Radiographic assessment of the amount of pulmonary edema and the severity of left ventricular failure was compared with the physiologic shunt fraction, tracer-measured lung water, and pulmonary arterial wedge pressure.
Therefore, the radiographic findings were predictive for the shunt value of the preceding day. The most consistent morphologic finding in ARDS was attenuating in the dependent regions of the lung. On receiver operating characteristic curves, the pulmonary leak index performed best when ARDS and hydrostatic pulmonary edema were defined only on the basis of risk factors.
The authors concluded that the rate of FDG uptake in the lungs during lung injury reflects the state of neutrophil activation. Customize your Medscape account with the health plans you accept, so that the information you need is saved and ready every time you look up a drug on our site or in the Medscape app. While the principles of management of this type of pulmonary edema are similar to the more common cardiogenic pulmonary edema, placing a patient in the prone position may be a helpful maneuver facilitating recovery. Both hypothalamic lesions (paraventricular and dorsomedial nuclei) and stimulation of the vasomotor centers of the medulla (A1 and A5, nuclei of solitary tract, and area postrema, medial reticulated nucleus, and the dorsal motor vagus nucleus in the medulla oblongata) can increase output along the sympathetic trunk. Alpha-adrenergic blockade (with phentolamine) and spinal cord transection at the C7 level prevent the formation of neurogenic pulmonary edema, suggesting an important role for sympathetic activation. Factors leading to the development of edema in patients with subarachnoid hemorrhage are illustrated in the flowchart below; however, these can be extrapolated to other types of central nervous system insults. Epinephrine, norepinephrine, and even a release of secondary mediators may directly increase pulmonary vascular permeability. The lack of a standardized definition for neurogenic pulmonary edema also makes defining its epidemiology difficult. Morbidity related to neurogenic pulmonary edema is reported to be in the range of 40-50%, and reported mortality from neurogenic pulmonary edema is low, at approximately 7%.
However, in recent years, the role of neurogenic inflammation in the pathogenesis of neurological diseases has gained increasing attention, with a particular focus on its effects on modulation of the blood-brain barrier BBB.
The hemodynamic component is relatively brief and may unmask pure NPE, such as that seen in experimental seizures. As the edema progresses, alveolar edema is observed in a butterfly pattern characterized by the central predominance of shadows, with a clear zone at periphery lobes. A useful characteristic for differentiating cardiac pulmonary edema from NPE, as well as from pneumonia and other widespread exudates, is the amount of time it takes for the edema to develop and to vanish. Following the intravenous administration of steroids, radiographic resolution occurred in 4 cases. The radiographic scores for edema were not predictive for the shunt fraction or for the tracer-measured lung water. Pulmonary air cysts (30%), always multiple and mostly bilateral, were associated with a mortality rate (55%) higher than that of the whole study group (35%). Assuming that the 3 levels were a representative sample of the whole lung, the authors computed lung weight from the mean CT scan number and lung gas volume. The index was better than hemodynamic measures, and its performance equaled that of ventilatory variables in discriminating between edema types (if definitions were based primarily on hemodynamic and ventilatory variables, respectively). Easily compare tier status for drugs in the same class when considering an alternative drug for your patient. Whether the capillary leak is produced by pressure-induced mechanical injury because of the elevated capillary hydrostatic pressure or because of some direct nervous system control over the pulmonary capillary permeability remains uncertain. The neuropeptide substance P has been shown to increase blood-brain barrier permeability following acute injury to the brain and is associated with marked cerebral edema. Presence of preoperative NPE presents a dilemma to the neuroanesthetist due to the divergent goals of management of raised intracranial pressure and pulmonary edema and also the possible adverse interaction of the two conditions when they co-exist. Septal lines indicative of interstitial edema are more frequent with cardiogenic causes than with others.
If substantial improvement occurs within 24 hours, this is virtually diagnostic of cardiac pulmonary edema.
The highest accuracy was obtained in distinguishing capillary permeability edema from all other varieties (91%). The radiographic score for congestive heart failure was correlated with the wedge pressure but not well enough to be clinically useful. Compared with chest radiography, CT scanning often yielded additional information (66%), with direct influence on patient treatment in 22% of cases. We report a patient with acute obstructive hydrocephalus due to cerebellar metastatic lesion who presented with NPE that resolved on placement of the ventriculoperitonial (VP) shunt. The lowest accuracy (81%) was obtained in distinguishing chronic cardiac failure from renal failure. Accordingly, blocking substance P NK1 receptors may provide a novel alternative treatment to ameliorate the deleterious effects of neurogenic inflammation in the central nervous system. In 15 patients, CT scans provided additional information not obvious on bedside chest radiographs and led to a change in care for 5 patients. The purpose of this paper is to provide an overview of the role of substance P and neurogenic inflammation in acute injury to the central nervous system following traumatic brain injury, spinal cord injury, stroke, and meningitis.1.
Pape, “Patterns of mortality and causes of death in polytrauma patients-Has anything changed?” Injury, vol.


Her magnetic resonance imaging (MRI) brain revealed fourth ventricular obstruction with obstructive hydrocephalus. IntroductionAcute disorders of the central nervous system (CNS), including traumatic brain injury (TBI), spinal cord injury (SCI), stroke, and meningitis, account for a significant disease burden worldwide, with CNS injury being the leading cause of death after trauma [1].
As the patient was drowsy though responding to verbal commands and oriented, an emergency VP shunt was planned. These acute neurological conditions affect individuals of all ages and both sexes alike resulting in significant morbidity and mortality.
She had an unremarkable past history with no previous history of tuberculosis or respiratory illness. Despite the prevalence of these conditions, current treatments remain limited and largely inadequate.
New therapies are urgently required in order to reduce the death and disability associated with these conditions. As such, targeting this aspect of the injury cascade is likely to produce beneficial outcomes in each of these conditions. Recent reports on the role of the neuropeptide substance P (SP) and neurogenic inflammation in BBB dysfunction and genesis of cerebral edema following acute brain injury suggest that this pathway provides a novel target for therapeutic intervention.
The current paper will provide an overview of the BBB and vasogenic edema, followed by a discussion of the role of SP and neurogenic inflammation in CNS injury.2.
Chest X-ray showed slight haziness in the right lung suggestive of pulmonary edema- [Figure1]. It is the interface between the blood and the brain, separating the brain parenchyma from the blood within cerebral capillaries, and involves the interactions between endothelial cells, astrocytes, pericytes, and the capillary basement membrane.
Within the spinal cord, the blood-spinal cord barrier (BSCB) is similar in function to the BBB [2] and serves to protect the spinal cord by modulating the entry of blood-borne substances.
Noble, “Vascular events after spinal cord injury: contribution to secondary pathogenesis,” Physical Therapy, vol. The SpO 2 increased to 92% on administration of 100% oxygen through the face mask of the anesthetic circuit. The fundamental structures of the BBB and BSCB are the same although there are some specific differences in the BSCB including glycogen deposits, decreased P-glycoprotein transporters, and decreased expression of tight junctional protein expression [3].
As there was no other cause for the respiratory dysfunction such as infection, aspiration, or previous respiratory illness, a diagnosis of NPE was considered.
The gate function of the BBB and BSCB is afforded by tight and adherens junctions, comprised of a complex network of transmembrane and cytosolic proteins [4, 5]. Anesthesia was maintained with air and oxygen mixture, adjusting the FiO 2 to maintain an arterial saturation of >90%, and 1% isoflurane along with atracurium and fentanyl infusions.
Specifically, claudins, occludins, junctional adhesion molecules (JAMs), and zona occludens (ZOs) are the proteins that make up this network.
Tight junctions are located on the most apical region of the cleft between cerebral capillary endothelial cells and form a seal to prevent substances from passing between them [6]. Claudins, predominately caludin-5, are involved in the primary makeup or backbone of tight junctions, forming dimers which interact with opposing claudin molecules to form the primary seal of the tight junction [6, 7]. Patient remained hemodynamically stable and mean arterial blood pressure (MAP) was maintained at 80 mmHg. JAM has a single transmembrane segment, which initiates cell-to-cell attachment and is able to mediate permeability through this avenue [7]. Positive end expiratory pressure affects regional distribution of ventilation differently in supine and prone sheep.
Occludin has four transmembrane segments and is present in higher concentrations in endothelial cells of the BBB than in those in systemic capillary endothelial cells.
A further obstacle to prevent the entry of unwanted substances into the brain is provided by the basement membrane of the BBB, which is made up of proteins found within the extracellular matrix including collagens, vitronectin, fibronectin, tenascin, and proteoglycans [9]. These components provide stability to the structure of the blood vessels and a surface upon which cerebral capillary endothelial cells can rest. Their end feet surround 99% of BBB endothelial cells and act to support and enhance the tight junctions between them [7, 10]. Furthermore, astrocytes mediate the connection between neurones and endothelial cells [11], and the gap junctions between astrocytes allow for quick transfer of substances and information [12]. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. The main function of pericytes is thought to be blood flow regulation, particularly in the precapillary arterioles that supply the brain with blood [14]. The structure of pericytes makes them ideal for this function, as they are contractile and express the smooth muscle actin isoform [13].
Johnson, “Induction of blood brain barrier tight junction protein alterations by CD8 T cells,” PLoS ONE, vol.
A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome. Collagen type IV glycosaminoglycans and laminin are also synthesised in pericytes to be used in formation of the basement membrane [13]. They have the ability to regulate endothelial cell proliferation, survival, migration, and differentiation [7]. Prone ventilation reduces lung stress and strain in severe acute respiratory distress syndrome. EdemaOf the secondary injury factors that occur in the setting of CNS injury, edema within the brain or spinal cord is of particular concern given its association with increased mortality and morbidity [15, 16]. The treatment is mainly supportive using mechanical ventilation and alpha-adrenergic blocking agents for managing increased pulmonary arterial pressure.Anesthetic management of patient with NPE has not been reported widely. Förster, “Differential susceptibility of cerebral and cerebellar murine brain microvascular endothelial cells to loss of barrier properties in response to inflammatory stimuli,” Journal of Neuroimmunology, vol. Klatzo [17] was the first to classify edema into two broad categories based upon the integrity of the BBB: cytotoxic and vasogenic edema.
It is characterized by a shift of water from the extracellular compartment to the intracellular compartment, accompanied by shrinkage of the extracellular space. Therefore, maintenance of adequate depth of anesthesia and attenuation of neuroendocrine response to intubation are important.The use of PEEP in neurosurgical patients is limited by conflicting reports on its effect on intracranial pressure. The reduced lung compliance and high intrathoracic pressure during mechanical ventilation in the presence of pulmonary edema may also pose a problem for providing brain relaxation.The cerebrogenic autonomic and neurohumoral dysregulation due to intracranial hypertension may cause intraoperative hemodynamic dysfunction. There is a strong correlation between extravasation of proteins into the extracellular space and the development of vasogenic edema [21, 22].
Lo, “Junctional complexes of the blood-brain barrier: permeability changes in neuroinflammation,” Progress in Neurobiology, vol.
The temporal profile of edema pathogenesis after injury varies greatly with injury type and severity [23] and has been extensively studied in order to characterize the period in which anti-inflammatory pharmacological interventions may be effective. In a mouse model of cerebral contusion, permeability of the BBB to large proteins was resolved by approximately 5 hours following injury, whereas smaller molecules of 10 kDa were still able to pass through the BBB for up to 4 days [24].
A thorough understanding of the patho-physiological mechanisms behind the development of NPE helps in the management of these patients, thus preventing further complications. Furthermore, in ischemic stroke, it has been shown that edema continues to develop for up to 7 days, with the initial cytotoxic edema being followed by vasogenic edema [27]. NPE after aneurismal sub-arachnoid haemorrage was shown to resolve after endovascular coiling. Further studies are required to elucidate the exact mechanisms of barrier disruption and subsequent edema pathogenesis to develop targeted therapeutic agents.
The development of edema is associated with significant mortality and morbidity in the setting of CNS injury.
Anesthetic management must be carefully titrated considering the divergent goals of NPE and intracranial hypertension. Such outcomes are related to the ability of vasogenic edema to lead to an increase in pressure within the cranium or spinal canal.
Given that the skull is rigid structure, any increase in the intracranial contents (blood, brain, and cerebral spinal fluid) must be compensated by a decrease in the volume of the other components. Kanmogne, “Blood-brain barrier: structural components and function under physiologic and pathologic conditions,” Journal of Neuroimmune Pharmacology, vol. Within both the brain and the spinal cord, there is limited capacity for compensation through reductions in blood or cerebrospinal fluid volume to accommodate for an increase in the intracranial volume. When such compensatory mechanisms fail, profound increases in intracranial pressure (ICP) or intrathecal pressure (ITP) may result.
With the mortality of malignant cerebral edema approaching 80% [18], the reduction of cerebral edema and its associated rise in ICP is now widely recognised as an important clinical management target. Current treatments seek to reduce brain swelling and ICP though administration of hyperosmotic agents and barbiturates, induction of hyperventilation or hypothermia, and surgical interventions such as cerebrospinal fluid (CSF) drainage, or in severe cases, decompressive craniectomy [23, 30, 32, 33]. Prone position delays the progression of ventilator induced lung injury in rats: does lung strain distribution play a role. In the case of hemorrhage, evacuation of space occupying lesions like hematomas may be warranted [34]. The use of steroids in an attempt to minimize SCI-induced edema and inflammation is common, despite the controversy surrounding their effectiveness and safety [35]. With respect to patient morbidity and mortality, current clinical treatment regimens for acute disorders of the CNS have proven somewhat ineffective, mainly because they do not address the specific mechanisms that are associated with the genesis of edema in cerebral ischemia.
Recent studies have identified substance P (SP) release as a feature of acute CNS injury and have delineated a critical role for SP in increased BBB permeability and the development of vasogenic edema. Stanimirovic, “Post-ischemic hypothermia attenuates loss of the vascular basement membrane proteins, agrin and SPARC, and the blood-brain barrier disruption after global cerebral ischemia,” Brain Research, vol. Neurogenic InflammationNeurogenic inflammation is a neurally elicited, local inflammatory response characterized by vasodilation, increased vascular permeability, mast cell degranulation, and the release of neuropeptides including SP and calcitonin gene-related peptide (CGRP) [37]. Neurogenic inflammation has been demonstrated in tissue receiving trigeminal innervation and may be stimulated by many agents including prostanoids, leukotrienes, histamine, and serotonin, as well as by changes in the extracellular environment such as decreased pH, increased osmolarity, heat, inflammatory conditions, and tissue (mechanical) injury [39, 40]. The changes in blood vessel size and permeability that occur with neurogenic inflammation lead to edema formation within the tissue [21, 22]. Perhaps the most important factor in this response is SP, having been identified as the most potent initiator of neurogenic inflammation [41, 42].Neurogenic inflammatory mediators such as SP and CGRP and their respective receptors are found in abundance in both the rodent and human CNSs, and whilst neurogenic inflammation and classical inflammation are both inflammatory processes, neurogenic inflammation in the brain differs from classical inflammation in that neurogenic inflammation is neurally elicited and results in an increased permeability of the BBB through the release of neuropeptides. In contrast, classical inflammation involves the accumulation and proliferation of microglia, perivascular macrophages, and other inflammatory cells (Figure 1) [43, 44].
Abbott, “All vertebrates started out with a glial blood-brain barrier 4-500 million years ago,” GLIA, vol. These cells subsequently release classical inflammatory mediators like bradykinin, which drive vascular changes [45]. Nevertheless, there is an interaction between the two processes as many of the factors within each cascade may initiate or potentiate the other.
For example, the classical inflammatory mediator bradykinin causes release of the neurogenic inflammatory mediator SP, which in turn is well known to cause mast cell degranulation along with bradykinin and nitric oxide release by endothelial cells and thus potentiation of classical inflammation (Figure 1).
Inflammation in the brain may play many roles, including the maintenance of tissue homeostasis, although when these processes are unable to be controlled, tissue damage occurs. Thus, this paper focuses on the pharmacological blockade of neurogenic inflammation for the treatment of acute disorders of the CNS. It is well documented, using both animal models and isolated neurons in vitro, that capsaicin, heat, protons, bradykinin, and tryptase are upstream regulators of the intracellular calcium influx, which results in inflammatory neuropeptide release [46–48].
In contrast, it is thought that prostaglandins E2 and I2, cytokines, interleukin-1, interleukin-6, and tumor necrosis factor do not cause neurotransmitter release themselves, but rather excite sensory neurons and thus lower the threshold for firing and cause augmented release of neuropeptides [48, 49].
While neurogenic inflammation has been extensively studied and well documented in peripheral tissues [50, 51], until recently the concept of neurogenic inflammation within the CNS has remained largely unexplored. Bonvento, “Targeted activation of astrocytes: a potential neuroprotective strategy,” Molecular Neurobiology, vol.




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  5. Sexual weak spot they'll take.