Normal Perfusion Pressure Research Articles

Novel Insights Into the Intratendinous Pressure Behavior of the Achilles Tendon in Athletes.

In contrast to other musculoskeletal tissues, the normal pressure behavior of the Achilles tendon is poorly understood. This study aimed to explore the normal intratendinous and perfusion pressures of the Achilles tendon at rest and during exercise, and investigate potential correlations with tendon load and morphology. Intratendinous and perfusion pressures of the Achilles tendon exhibit similarities to other musculoskeletal tissues and depend on tendon load and morphology. Observational study. Level 3. A total of 22 recreational athletes were enrolled. Demographics, activity level, and blood pressures were recorded. Achilles tendon thickness and echogenicity were assessed 25 mm proximal to the posterosuperior calcaneal border. In this region, intratendinous and perfusion pressures of the Achilles tendon were measured at rest and during isometric plantarflexion up to 50 N, using the microcapillary infusion technique. Linear mixed models were used to investigate the effects of plantarflexion force, tendon thickness, and echogenicity on intratendinous and perfusion pressures. At rest, intratendinous and perfusion pressures of the Achilles tendon were 43.8 ± 15.2 and 48.7 ± 18.4 mmHg, respectively. Intratendinous pressure increased linearly with plantarflexion force, reaching 101.3 ± 25.5 mmHg at 50 N (P < 0.01). Perfusion pressure showed an inverse relationship, dropping below 0 mmHg at 50 N (P < 0.01). Neither intratendinous nor perfusion pressures of the Achilles tendon correlated with tendon thickness or echogenicity. The normal intratendinous resting pressure of the Achilles tendon is higher than other musculoskeletal tissues, making it more susceptible to ischemia. During exercise, intratendinous pressure increases significantly to a level that lowers perfusion pressure, thereby compromising blood supply at already low plantarflexion forces. Given the potential role of ischemia in Achilles tendinopathy, our findings caution against intratendinous injections, as they may exacerbate high intratendinous resting pressure, and against prolonged postexercise tendon stretching, as the associated rise in intratendinous pressure may impair the required hyperemic response.

Abstract Number ‐ 121: Flow Diversion Jet: A Dangerous Mechanism in the Flow Diversion Treatment of Giant Intracranial Aneurysms

Introduction We present a patient with a giant vertebrobasilar system aneurysm. This case provides an in‐depth analysis of the pathologic mechanism resulting in catastrophic distal hemorrhage following stent deployment due to the shared effects of normal perfusion pressure breakthrough (NPPB) and the Windkessel phenomenon. The Windkessel phenomenon and NPPB occur before and after treatment of various vascular malformations, respectively. These phenomena are hypothesized to contribute to the loss of cerebrovascular autoregulation. High flow lesions and giant aneurysms reduce blood flow in downstream vessels, causing chronic distal vasodilation to protect against ischemia. Sudden restoration of normal pulsatile flow, following treatment, compromises the integrity of distal vessels leading to potential catastrophic intracerebral hemorrhage. Methods A retrospective review of the patient’s medical record was performed. Results A 60‐year‐old female initially presenting with pulsatile neck mass was found to have dolichoectasia of the right cervical internal carotid artery and two large, irregular, vertebrobasilar aneurysms. Managed conservatively for 10 years before developing gait ataxia, new imaging revealed growth of the now giant, more distal aneurysm. Flow diversion with partial coiling of the aneurysms was pursued. Following deployment, DynaCT demonstrated catastrophic thalamic and midbrain hemorrhage with intraventricular extension. A review of intra‐aneurysmal pressure measurements, angiography, MRI, and neuromonitoring data strongly suggests rupture of multiple deep perforators following the conversion to laminar flow when the flow diverting chain was finalized. This suggests giant aneurysms chronically depress the distal pulse pressure by acting as a Windkessel reservoir. Flow diversion bypasses the reservoir increasing pulse pressure distal to the aneurysm, exceeding autoregulatory capacity, leading to hemorrhage. Conclusions This is the first case in the literature to describe NPPB and the Windkessel phenomenon in the attempt to treat giant aneurysms with flow diversion. Flow diversion bypasses the reservoir, suddenly changing turbulent flow to laminar flow. The resultant dramatic rise in pulse pressure distal to the aneurysm can exceed the autoregulatory mechanisms of small distal vessels such as perforating branches. While demonstrating a poor outcome, awareness of these mechanisms and meticulous intra‐operative blood pressure management may reduce or prevent complications. Further modeling of flow dynamics both before and following treatment of these aneurysms may lead to altered guidelines in the temporality of treatment due to potential catastrophic sequelae.

Craniectomía descompresiva y compliance intracraneal en el traumatismo craneoencefálico grave pediátrico

ObjectiveTo show the effect of primary decompressive craniectomy on ICP, CPP, and intracranial compliance in a group of pediatric patients who suffered from severe head trauma. DesignDescriptive study. FrameworkPediatric intensive care. PatientsPediatric patients who underwent primary decompressive craniectomy due to severe head trauma, admitted to the pediatric intensive care unit of the “Roberto Rodríguez Fernandez” general teaching hospital in Morón, Ciego de Avila, Cuba between January 2003 and December 2017. ResultsDiffuse brain injury Grade IV, was the most frequent tomographic diagnosis at admission 18 (60%), with a predominance of shifts greater than 6mm in 24 cases (80%) and absent cisterns 15 (50%). Eighteen cases (60%) had normal ICP for their age after craniectomy, 20 (66.7%) cases showed normal cerebral perfusion pressure. There was a correlation between normal ICP and normal intracranial compliances. The pulse wave amplitude was used as a neuromonitoring method and qualitative representation of compliances. Twenty-two cases survived (73.3%), 18 (60%) of them without sequelae. Eight cases died (26.7%). ConclusionsPrimary DC was useful for the control of ICP and maintenance of CPP in the management of pediatric patients with severe TBI in the present study. The favorable effect of the procedure for the increase of intracranial compliance has been verified.

Intra- and post-operative acute hemorrhagic complications of Onyx embolization of brain arteriovenous malformations: A single-center experience.

BackgroundThe intra- and post-operative acute (within 72 h) hemorrhagic complications of endovascular treatment (EVT) for a brain arteriovenous malformation (BAVM) are disastrous. Thus, further experiential summaries are required to fully understand them.Materials and methodsThis was a retrospective study of 25 patients with consecutive BAVM who were treated via EVT with Onyx embolization and suffered intra- and post-operative acute hemorrhage. The clinical and imaging data of the patients were recorded, analyzed, and discussed.ResultTwenty-five patients were aged 11–70 years (mean, 37.2 ± 16.1 years), of whom 12 were female (48%, 12/25). Of the 25 hemorrhagic complications, 17 (68%, 17/25) were intraoperative, and 8 (32%, 8/25) were post-operative and occurred between 1 and 12 h after EVT. Of 17 intraoperative hemorrhages, 13 (76.5%, 13/17) were due to high-pressure Onyx casting. Of eight post-operative hemorrhages, six (75%, 6/8) were attributed to normal perfusion pressure breakthrough. The degree of nidus Onyx embolization was more than 2/3 or complete in seven (87.5%, 7/8) BAVMs. Draining vein occlusion was observed in eight (32%, 8/25) of 25 BAVMs. After hemorrhage, conservative treatment was administered in 12 (48%, 12/25) cases, and surgical management was performed in other cases. There were eight cases of mortality; the remaining 17 patients had follow-up data. Among them, 15 patients had good outcomes, with Glasgow Outcome Scale scores of 5 and 4, accounting for 60% (15/25).ConclusionIn EVT for BAVMs, intra- and post-operative acute hemorrhagic complications are disastrous; only 60% of patients have a good outcome. Therefore, high-pressure Onyx casting or casting too much Onyx at one time to pursue a high degree of nidus embolization should be performed cautiously, and primary draining vein occlusion should be avoided. In short, EVT needs to be performed carefully.

Examination of the Risk of Normal Perfusion Pressure Breakthrough and Occlusive Hyperemia after Cerebral Arteriovenous Malformation (AVM) Resection Using Intraoperative Cerebral Angiography

Examination of the Risk of Normal Perfusion Pressure Breakthrough and Occlusive Hyperemia after Cerebral Arteriovenous Malformation (AVM) Resection Using Intraoperative Cerebral Angiography

Normalization of Peri-Arteriovenous Malformation Hemodynamics Prior to Direct Microsurgery: 2-Dimensional Operative Video.

Arteriovenous malformations (AVMs) are highly complex vascular lesions characterized by abnormal connections between arteries and an intervening nidus. Definitive and safe treatment of AVMs may require the combination of multiple treatment modalities to address the various complex features of the AVM.1 Endovascular embolization can be used as an adjuvant to surgery in order to control deep feeders, reduce flow, and address high-risk features such as aneurysms. In addition, by progressively reducing the AVM flow, staged embolization can lead to normalization of peri-AVM hemodynamics and therefore may decrease the risk of postresection hemorrhage.2,3 In this operative video, we present a case of a 41-yr-old female who presented with progressively worsening left-sided hemiparesis. Magnetic resonance imaging (MRI) and angiography revealed a complex right fronto-parietal AVM with significant associated edema, likely due to the vascular steal phenomenon. The area of edema, which included the motor cortex, was thought to be at high risk for postoperative hemorrhage from normal perfusion pressure breakthrough. We therefore decided to proceed with staged presurgical embolization to gradually normalize the perilesional hemodynamics, and therefore possibly reduce the risk of postoperative morbidity. The patient underwent 3 embolization sessions at 6-wk intervals. An MRI after the last embolization showed near-complete resolution of the fluid-attenuated inversion-recovery (FLAIR) signal around the AVM. Microsurgical resection was performed on the day after the last embolization. The patient tolerated the procedure well and was discharged at her neurological baseline with mild contralateral hemiparesis, which has continued to improve at follow-up. Postoperative angiography showed complete resection of the AVM. The patient consented to the procedure as shown in this operative video and gave informed written consent for use of her images in publication.

Decoding the Onset of Intraoperative Normal Pressure Perfusion Breakthrough with Near-Infrared Spectroscopy and Jugular Venous Oxygen Saturation Catheter in a Case of Arteriovenous Malformation Surgery

AbstractMultimodal monitoring can be a useful tool to design an appropriate anesthesia technique in the intraoperative period during the surgical excision of an intracerebral arteriovenous malformation (AVM). Intraoperatively, hyperperfusion syndrome can be attributed to causes like insufficient blood pressure control, occlusion of venous drainage before complete resection of arterial feeders, or inadequate hemostatic control of distended capillaries receiving arterial flow. We would like to highlight the potential role of near-infrared spectroscopy and jugular venous oxygen saturation catheter in detection of intraoperative normal perfusion pressure breakthrough and take necessary measures to prevent further insult with the help of this case report.

Neuroprotective effect of indomethacin in normal perfusion pressure breakthrough phenomenon

Loss of cerebral autoregulation in normal perfusion pressure breakthrough (NPPB) phenomenon has been reported in other Central Nervous System diseases such as neonatal intraventricular haemorrhage. Several studies have demonstrated that low-dose indomethacin prevents this latter condition. A previous rat model was used to resemble NPPB phenomenon. Study animals were distributed in 4 groups that received 3 doses of indomethacin at different concentrations prior to fistula occlusion 60 days after its creation. Control animals received saline solution. Intracranial pressure (ICP) increased in all groups following fistula creation, whereas mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) decreased as a manifestation of cerebral hypoperfusion and intracranial hypertension. The administration of indomethacin was associated with raised MAP and CPP, as well as decreased ICP. Sodium fluorescein extravasation was slight in study animals when comparing with control ones. Histological analysis evidenced diffuse ischaemic changes with signs of neuronal apoptosis in all brain layers in control animals. These findings were only focal and slight in study animals. The results suggest the usefulness of indomethacin to revert, at least partially, the haemodynamic effects of NPPB phenomenon in this experimental model, as well as to reduce BBB disruption and histological ischemia observed in absence of indomethacin.

Experimental rat model of chronic cerebral hypoperfusion–reperfusion mimicking normal perfusion pressure breakthrough phenomenon

BackgroundNormal perfusion pressure breakthrough (NPPB) phenomenon is a major life-threatening complication that restricts the treatment of complex intracranial arteriovenous malformations. The aim of the study it to develop a rat model mimicking NPPB phenomenon that enables the evaluation of any therapy to prevent such complication. MethodsTwenty Wistar male rats were randomly assigned to either a study or a control group. Study animals underwent an end-to-side left external jugular vein-common carotid artery anastomosis and ligation of bilateral external carotid arteries. Control animals only underwent ligation of bilateral external carotid arteries. All animals were sacrificed sixty days after the procedure. Hemodynamic parameters [mean arterial pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP)], blood–brain barrier (BBB) permeability (measured by fluorescein staining) and histological features were then compared between both groups. ResultsA significant decrease in MAP and CPP was confirmed in the study group. An increase in ICP was also observed. A significant decrease in MAP and CPP was also present in the study group when comparing preoperative values with those recorded on days 0 (postoperative), 7 and 60. Fluorescein staining findings were consistent with signs of BBB disruption in study animals. Histological analysis demonstrated an increased number of pyknotic neurons in the ipsilateral hemisphere of rat brains included in the study group. ConclusionThese results confirm that this model mimics a vascular steal state with chronic cerebral hypoperfusion comparable to patients with AVMs behavior and disruption of the BBB after fistula closure comparable to NPPB phenomenon disorders.

Purulent pericarditis and mediastinal abscess in a young infant

A thriving, previously healthy 3-month-old girl presented with a 4-day history of fever, irritability and poor feeding. On admission, she was tachycardic, had cool peripheries with normal central perfusion, pulse...

An overview of management of intracranial hypertension in the intensive care unit.

Intracranial hypertension (IH) is a clinical condition commonly encountered in the intensive care unit, which requires immediate treatment. The maintenance of normal intracranial pressure (ICP) and cerebral perfusion pressure in order to prevent secondary brain injury (SBI) is the central focus of management. SBI can be detected through clinical examination and invasive and non-invasive ICP monitoring. Progress in monitoring and understanding the pathophysiological mechanisms of IH allows the implementation of targeted interventions in order to improve the outcome of these patients. Initially, general prophylactic measures such as patient’s head elevation, fever control, adequate analgesia and sedation depth should be applied immediately to all patients with suspected IH. Based on specific indications and conditions, surgical resection of mass lesions and cerebrospinal fluid drainage should be considered as an initial treatment for lowering ICP. Hyperosmolar therapy (mannitol or hypertonic saline) represents the cornerstone of medical treatment of acute IH while hyperventilation should be limited to emergency management of life-threatening raised ICP. Therapeutic hypothermia could have a possible benefit on outcome. To control elevated ICP refractory to maximum standard medical and surgical treatment, at first, high-dose barbiturate administration and then decompressive craniectomy as a last step are recommended with unclear and probable benefit on outcomes, respectively. The therapeutic strategy should be based on a staircase approach and be individualized for each patient. Since most therapeutic interventions have an uncertain effect on neurological outcome and mortality, future research should focus on both studying the long-term benefits of current strategies and developing new ones.

Experimental rat model of chronic cerebral hypoperfusion-reperfusion mimicking normal perfusion pressure breakthrough phenomenon.

Normal perfusion pressure breakthrough (NPPB) phenomenon is a major life-threatening complication that restricts the treatment of complex intracranial arteriovenous malformations. The aim of the study it to develop a rat model mimicking NPPB phenomenon that enables the evaluation of any therapy to prevent such complication. Twenty Wistar male rats were randomly assigned to either a study or a control group. Study animals underwent an end-to-side left external jugular vein-common carotid artery anastomosis and ligation of bilateral external carotid arteries. Control animals only underwent ligation of bilateral external carotid arteries. All animals were sacrificed sixty days after the procedure. Hemodynamic parameters [mean arterial pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP)], blood-brain barrier (BBB) permeability (measured by fluorescein staining) and histological features were then compared between both groups. A significant decrease in MAP and CPP was confirmed in the study group. An increase in ICP was also observed. A significant decrease in MAP and CPP was also present in the study group when comparing preoperative values with those recorded on days 0 (postoperative), 7 and 60. Fluorescein staining findings were consistent with signs of BBB disruption in study animals. Histological analysis demonstrated an increased number of pyknotic neurons in the ipsilateral hemisphere of rat brains included in the study group. These results confirm that this model mimics a vascular steal state with chronic cerebral hypoperfusion comparable to patients with AVMs behavior and disruption of the BBB after fistula closure comparable to NPPB phenomenon disorders.

Abstract 435: Controlled Sequential Elevation of the Head and Thorax Rapidly Achieves 50% of Baseline Cerebral Perfusion Pressure During Active Compression-Decompression Cardiopulmonary Resuscitation With an Impedance Threshold Device in a Swine Model of Cardiac Arrest

Introduction: Controlled sequential elevation of the head and thorax (CSE) during active compression-decompression (ACD) CPR with an impedance threshold device (ITD) has previously resulted in sustained nearly normal cerebral perfusion pressures (CerPP) of 75 mmHg. However, the optimal speed of CSE remains unknown. It is also unknown if some CPR is needed to ‘prime the system’ prior to maximal CSE. Hypothesis: An optimized CSE will achieve 50% of baseline (50% BL) CerPP in &lt;3 minutes from the start of CPR. Methods: Female farm pigs were intubated and anesthetized. Central vascular and intracranial access were obtained. After 8 min of untreated ventricular fibrillation, pigs were placed in a customized elevation device (CED). After 2 min of ACD+ITD CPR at the lowest CED level to prime the circulation, pigs were randomized to CSE over 1) 4-min or 2) 10-min until the CED reached its highest level. ACD ITD CPR was performed for a total of 19 minutes. Based upon initial results, two additional groups of pigs were studied: one with a CSE over 2-min after the 2 min ‘priming’ step, and the other with CSE over 24-sec without priming. The primary outcome was time in minutes to achieve 50% BL of CerPP values. Results: There were six pigs per study group (4-min, 10-min, 2-min and 24-sec). The 4-min CSE group achieved 50% BL CerPP faster (min ± SD) than the 10-min CSE group (2.53 ± 1.26 vs 5.98 ± 3.16 , p=0.04, Figure 1). The 2-min CSE group CerPP was similar to the 4-min group (2.36 ± 2.18, p=0.92). The time to 50% BL CerPP trended 4 min faster in the 2-min CSE group versus the 24-sec CSE group (6.6 ± 6.73, p=0.16), as shown in the figure. With CSE, CerPPs increased over time in all groups. All pigs were resuscitated. Conclusions: A 50% BL CerPP value was achieved in &lt;3 minutes by combining a priming step and 2-min CSE time together with ACD+ITD CPR. This optimized approach is more advantageous than the 24-sec or 10-min elevation times.

Abstract 565: Response of the Ischemic Myocardium to Adrenergic Stimulation as Detected by Hyperpolarized [1- 13 C]pyruvate

Metabolic imaging by nuclear methods is widely used to access ischemic myocardium but provide limited information about individual enzyme-catalyzed reactions. 13 C hyperpolarization methods are sensitive to flux in specific key enzymes such as lactate dehydrogenase and pyruvate dehydrogenase. We tested the hypothesis that LDH flux is increased while PDH flux is abolished in low-flow ischemia. Metabolism of HP [1- 13 C]pyruvate was studied in four groups: (1) normal perfusion pressure (NPP), 100 cm H 2 O; (2) NPP with epinephrine; (3) low-perfusion pressure (LPP), 25 cm H 2 O; (4) LPP with epinephrine. Hearts excised from male Sprague-Dawley rats were perfused (37°C) at an initial pressure of 100 cm H 2 O using standard Langendorff method with Krebs-Henseleit buffer containing 0.75% bovine serum albumin, 0.4 mM non-labeled free fatty acid, 5.5 mM [U- 13 C]glucose, 1 mM [3- 13 C]pyruvate, 0.1 mM [3- 13 C]lactate. Perfusion pressure was reduced to 25 cm H 2 O after 30 min of perfusion for ischemia group and epinephrine added at 50 th min of perfusion. HP [1- 13 C]pyruvate was injected to heart and subsequently, 13 C NMR spectra were acquired. The freeze clamped heart tissues were extracted with perchloric acid and analyzed by high-resolution 1 H and 13 C NMR (14.1 T). The 31 P NMR spectroscopy confirmed significant myocardial ischemia under LPP conditions, demonstrated by a marked increase in the [Pi]/[ATP] ratio. Surprisingly, increased LDH flux was observed in the ischemic hearts (+18.4%) while the metabolism of HP [1- 13 C]pyruvate by PDH remained unchanged as indicated by bicarbonate production. To investigate the oxidative capacity of mitochondria, epinephrine was used to stimulate hearts. As anticipated, epinephrine increased heart rate (+23%) and coronary flow (+11%) under NPP. Epinephrine increased heart rate (-60%) but did not alter coronary flow under LPP. We found that epinephrine had no effect on the rate of bicarbonate production under LPP. The study demonstrated that the conversion of pyruvate to lactate increased in ischemic hearts but the degree of pyruvate oxidation was not affected by the low-flow ischemia. Adrenergic stimulation did not increase PDH flux in these ischemic hearts. Translation to human is likely to provide new data from low-flow myocardium.

Effects of surgical position on cerebral oxygen saturation and its regulation

Background Regional cerebral oxygen saturation (rSO2) is an important parameter to evaluate cerebral perfusion, brain metabolism, brain oxygen supply and demand, and to prevent postoperative neurological complications. Cerebral perfusion and rSO2 vary with different surgical positions. Objective This article reviews the characteristics and underlying mechanisms of the relationship between rSO2 values and surgical positions, and the clinical practices in preventing intraoperative brain ischemia and hypoxia in patients with different surgical positions. This review aims to provide an insight for the prevention of neurological complications associated with general anesthesia. Content Real-time quantification of oxygen supply and consumption is essential in operative monitoring. Insufficient blood and oxygen supply in the brain during operation may result in ischemia, hypoxia, and even postoperative cognitive dysfunction, depression and stroke. Monitoring rSO2 and maintaining it in normal ranges can prevent these postoperative complications. The rSO2 decreases in some surgical positions, including beach chair position, prone position, lateral position, and Trendelenburg position. In these situations, efforts should be made to maintain normal cerebral perfusion pressure and to improve lung ventilation. Trend Using near infrared spectroscopy to monitor rSO2 is valuable to efficiently recognize the adverse effects of altered surgical positions on cerebral oxygen supply, and to timely make efforts to prevent postoperative complications. Key words: Cerebral oxygen saturation; Surgical position; Anesthesia management

Increased perfusion pressure enhances the expression of endothelin (ETB) and angiotensin II (AT1) receptors in rat basilar artery smooth muscle cells

Background: It is known that the endothelin and angiotensin receptors ETA/ETB and AT1 on smooth muscle cells induce contraction and stimulate proliferation and cell hypertrophy. In hypertensive animals and in situations of altered blood flow, e.g. in stroke, there is an up-regulation of ET- and AT-receptors due to de novo transcription. In order to simulate this situation we hypothesized that changes in perfusion pressure may result in altered expression of protein encoding for the receptors ETA, ETB, AT1, and AT2 in the rat basilar artery. Methods: Segments of the rat basilar artery (n = 6) were cannulated with glass micropipettes, pressurized and luminally perfused in a perfusion chamber. After exposure to normal (80/70 mm Hg) or high (140/130 mm Hg) pressure at constant flow for 16 hours the vessel segments were immersed in a fixative solution, dehydrated, frozen, cut in a cryostat and immunohistology-stained for ET- and AT-receptor protein. Results: ETB- and AT1-receptor proteins were significantly up-regulated after high perfusion pressure compared to normal perfusion pressure at 16 hours (p < 0.05). Immunohistochemistry showed that the up-regulated proteins were located mainly in the smooth muscle cells in the arterial wall. Conclusion: The results from our rat perfusion model show significant up-regulation of ETB- and AT1-receptor proteins after high perfusion pressure. Since the increased protein expression was located in the smooth muscle layer, the results of our study have suggested a shift in the role of the endothelin and angiotensin system towards a worsening of the pathophysiology in the early stages of hypertension.

Pediatric traumatic brain injury—a review of management strategies

Management of traumatic brain injury (TBI) in children varies due to differing physician practices and availability of resources. Optimizing treatment to meet the physiologic demands of the wounded brain is crucial to achieve maximal recovery and minimize secondary injury. This review aims to discuss and update the different aspects of acute care in a child with TBI. A literature search for relevant original and review articles was carried out via PubMed. Relevant literatures from adult studies were included where there was a lack of pediatric data. Case reports and non-English articles were excluded. Acute airway management with carefully chosen sedative agents, appropriate ventilation and hyperosmolar therapy strategies are targeted at maintaining normal cerebral perfusion pressure (CPP). The goal of temperature control and glycemic control is to maintain normal ranges to optimize outcomes. Decisions for neuroimaging and initiation of anticonvulsants are weighed against potential complications. Achieving a beneficial neurological outcome for pediatric patients with TBI depends on effective management from the onset of injury. More high quality collaborative prospective research is required to develop individualized management strategies for our pediatric TBI patients in the acute setting.

Hunt-Hess 5 subarachnoid haemorrhage presenting with cardiac arrest is associated with larger volume bleeds

AimsThe mechanism, effects, and outcomes of cardiac arrest (CA) caused by subarachnoid haemorrhage (SAH) remain unclear. We compared SAH patients presenting with CA to other high-grade SAH patients presenting without CA in order to better understand (1) the cause of CA, (2) cerebral pathophysiology following CA, and (3) outcomes of CA in patients with SAH. MethodsWe performed a retrospective analysis of a prospectively collected observational cohort. 31 Hunt-Hess 5 patients that presented with CA were compared to 146 Hunt-Hess 5 patients that presented without CA. Clinical and imaging findings were predefined and adjudicated. Cerebral physiology measures were available for a subset of patients, matched 1:1 by age. ResultsTwenty-two (71%) CA patients had pulseless electrical activity/asystole compared to 2 (6%) with a shockable rhythm. The CA patients were younger (OR 0.96, 95% CI 0.93-0.99, p=0.009), had more SAH on CT (OR 1.07, 95% CI 1.01-1.13, p=0.02), and had higher in-hospital mortality (87% vs. 58%, OR 6.2 (2.1–26.6), p=0.004). There were no differences in aneurysm location, cerebral herniation, or ictal seizures. Despite similar cerebral perfusion pressure, CA patients had pathologically lower brain tissue oxygenation, lower glucose, and higher lactate to pyruvate ratios. ConclusionsCA in SAH is associated with larger volume bleeds. Despite normal cerebral perfusion pressures, CA patients show compromised cerebral physiology.

Diameter of fluorescent microspheres determines their distribution throughout the cortical watershed area in mice

A hemodynamic mechanism has long been assumed to play an important role in watershed infarction. In recent years, however, clinical evidence has indicated that an embolic mechanism is involved. The mechanism by which emboli are trapped preferentially in watershed areas remains unclear. In the present study, we developed a mouse embolus model using fluorescent microspheres with different diameters and evaluated the role of the microspheres’ diameters in the generation of a watershed-patterned distribution. We injected fluorescent microspheres of four different diameters (i.e., 13, 24, 40, and 69 μm) into the internal carotid artery of C57BL/6 mice either (1) without ligation of the common carotid artery (normal perfusion pressure model: NPPM) or (2) with ligation of the common carotid artery (low perfusion pressure model: LPPM). Left common carotid artery ligation induced reductions in local cerebral blood flow in both the periphery and the core area of the left middle cerebral artery. A greater reduction in the border-zone area between the left anterior cerebral artery and the middle cerebral artery was also noted. After 24 h, the brains were removed and the distribution of the microspheres in the brain was evaluated using a fluorescence microscope. The 24-μm microspheres were distributed in the watershed area more frequently than the other microsphere sizes (P < .05, ANOVA followed by Tukey’s test). Meanwhile, the distribution rates were similar between the NPPM and LPPM models for all microsphere sizes. This study suggested that the distribution pattern of the microspheres was only affected by the microspheres’ diameters.

Calcified Chronic Subdural Hematoma: A Case Report and Literature Review

Calcified chronic subdural hematoma (CCSDH) is a rare disease that accounts for approximately 0.3%–2.7% of all chronic subdural hematomas (CSDHs). The clinical features of CCSDH are very similar to those of noncalcified CSDH and include headache, decreased alertness, weakness, numbness, gait disturbance, seizures, memory impairment, confusion, and unconsciousness. All symptomatic CCSDH should be treated surgically. Majority of these patients recover well following surgery. In this report, we present the case of a patient with CCSDH who developed severe cerebral edema following its removal, necessitating decompressive craniectomy. Although there were no abnormal findings in laboratory blood tests, and no signs of brain herniation or epilepsy was found the following day after surgery, the patient's family refused all treatment and a postoperative brain computed tomography (CT) scan. The patient was discharged and died at home. Cerebral hematoma and normal perfusion pressure breakthrough (NPPB) may cause severe cerebral edema following the total removal of a CCSDH.