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A child undergoing routine transcatheter patent arterial duct closure developed severe transient ischemic changes in the electrocardiogram (Pardee waves) while the aortic retention skirt of the Amplatzer™ Duct Occluder was pulled against the duct orifice. The occluder was then released, and the delivery system was pulled back to inferior caval vein which led to electrocardiogram normalisation. Aortic root angiography showed a single coronary artery originating from the right sinus of Valsalva with the left coronary stem wedged behind the posterior aspect of the right ventricular outflow tract. We believe that the left coronary artery was compressed while applying tension on the occluder delivery system.
This prospective study aimed to evaluate the relationship between serum ischaemia-modified albumin levels and Bell's palsy severity.
The study included 30 patients diagnosed with Bell's palsy and 30 healthy individuals. The patients were separated into three disease severity groups (grades 2, 3 and 4) according to House–Brackmann classification. Blood samples were collected from all participants and the results compared between groups.
Significant differences in serum ischaemia-modified albumin were found between the study and control groups (p < 0.001); values were significantly higher in the study group than in the control group.
The significantly higher levels of serum ischaemia-modified albumin in the study group suggest that Bell's palsy pathogenesis is associated with oxidative stress.
Introduction: Vasopressors are routinely utilized to treat systemic shock, a significant source of morbidity and mortality in the pediatric population. Local tissue ischemia has been classically implicated with peripheral use of these medications. However, peripheral administration (PVC) has theoretical benefits, and avoids many of the risks associated with central venous catheter (CVC) placement. There appears to be paucity of literature in pediatrics examining this subject. We conducted a systematic review investigating local tissue complications and extravasations of both PVC and CVC administration in the pediatric population. Specifically we examined the type of vasopressor used, the site used, the duration of the infusion, and finally the overall outcome for patients. Methods: A systematic search was conducted using PubMed, Embase, Cochrane, and CINAHL databases. Terms for IV administration, specific vasopressor use, complication of interest, and pediatric population were combined. We included studies that satisfied our predetermined criteria. All search results were imported into Covidence software where the primary author conducted an initial title and abstract review. Papers that met the pre-identified criteria were selected for full text review. Papers selected for full text review were independently reviewed by two of the authors. Agreement between the authors was measured utilizing a κ statistic. Results: Our search yielded 14784 results, of which 237 were assessed for full text review. The κ between the authors is pending. 13 studies were selected for final inclusion. There were 14 patients with 15 total events. 13 were from PVC use while 2 occurred with CVC's. 11 of the 13 complications associated with PVC administration occurred through extravasation, with 2 events from local ischemia. 9 children were administered dopamine, 1 norepinephrine, and 14 were on multiple vasopressors. 3/13 events were “proximal” or occurring at or above the AC or popliteal fossa while 10/13 events were “distal”. The average time to ischemic injury or extravasation peripherally was 56.1 hours with a range of 1.5 to 360 hours. 9 of the total patients did not have any long-term sequelae. One patient had toe amputations, while two others died because of illness. One CVC patient died as a result extravasation leading to asphyxiation. Conclusion: There is a lack of significant literature reporting serious adverse events related to peripheral or central administration of vasopressors in the pediatric population.
Background: We have previously shown that low-intensity ultrasound (LIUS), a noninvasive mechanical stimulus, inhibits brain edema formation induced by oxygen and glucose deprivation (OGD) or treatment with glutamate, a mediator of OGD-induced edema, in acute rat hippocampal slice model in vitro. Methods: In this study, we treated the rat hippocampal slices with N-methyl-d-aspartic acid (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) to determine whether these different glutamate receptor agonists induce edema. The hippocampal slices were then either sonicated with LIUS or treated with N-methyl-d-aspartic acid receptor (NMDAR) antagonists, namely, MK-801 and ketamine, and observed their effects on edema formation. Results: We observed that treatment with NMDA, an agonist of ionotropic glutamate receptors, induced brain edema at similar degrees compared with that induced by OGD. However, treatment with DHPG, an agonist of metabotropic glutamate receptors, did not significantly induce brain edema. Treatment with the NMDAR antagonists MK-801 or ketamine efficiently prevented brain edema formation by both OGD and NMDA in a concentration-dependent manner. N-Methyl-d-aspartic acid-induced brain edema was alleviated by LIUS in an intensity-dependent manner when ultrasound was administered at 30, 50, or 100 mW/cm2 for 20 minutes before the induction of the edema. Furthermore, LIUS reduced OGD- and NMDA-induced phosphorylation of NMDARs at Y1325. Conclusion: These results suggest that LIUS can inhibit OGD- or NMDA-induced NMDAR activation by preventing NMDAR phosphorylation, thereby reducing a subsequent brain edema formation. The mechanisms by which LIUS inhibits NMDAR phosphorylation need further investigation.
The purpose of this study was to investigate the 10-year impact of Hurricane Katrina on the incidence of acute myocardial infarction (AMI) along with contributing risk factors and any alteration in chronobiology of AMI.
A single-center, retrospective, comparison study of AMI incidence was performed at Tulane University Health Sciences Center from 2 years before Hurricane Katrina to 10 years after Hurricane Katrina. A 6-year, pre-Katrina and 10-year, post-Katrina cohort were also compared according to pre-specified demographic, clinical, and chronobiological data.
AMI incidence increased from 0.7% (150/21,079) to 2.8% (2,341/84,751) post-Katrina (P<0.001). The post-Katrina cohort had higher rates of coronary artery disease (36.4% vs. 47.9%, P=0.01), diabetes mellitus (31.3% vs. 39.9%, P=0.04), hyperlipidemia (45.4% vs. 59.3%, P=0.005), smoking (34.4% vs. 53.8%, P<0.001), drug abuse (10.2% vs. 15.4%, P=0.02), psychiatric illness (6.7% vs. 14.9%, P<0.001), medication non-adherence (7.3% vs. 15.3%, P<0.001), and lack of employment (7.2% vs. 16.4%, P<0.001). The post-Katrina group had increased rates of AMI during nights (29.8% vs. 47.8%, P<0.001) and weekends (16.1% vs. 29.1%, P<0.001).
Even 10 years after the storm, Hurricane Katrina continues to be associated with increased incidence of AMI, higher prevalence of traditional cardiovascular and psychosocial risk factors, and an altered chronobiology of AMI toward nights and weekends. (Disaster Med Public Health Preparedness. 2019;13:217–222)
Background: Cross-clamp ischemia during carotid endarterectomy can be prevented with carotid bypass shunts in vulnerable patients identified by cerebral monitoring for ischemia. We compared transcranial cerebral oximetry (TCO) with carotid stump pressure measurements for selective shunt use. Methods: We prospectively collected data on 300 consecutive patients operated on under general anesthesia between 2009 and 2016. Shunts were inserted for a 10% or greater drop in cerebral saturations and/or a mean stump pressure less than 40 mmHg. Results: Seventy-five patients, 25% of the study population, were shunted. The indication was a combined desaturation and stump pressure in 38 (50% of the shunted group), desaturation alone in 11 patients (15%), and a low stump pressure alone in 26 patients (35%). There were no significant differences in baseline characteristics between those patients who were or were not shunted, except angiographic collateral blood supply, which was more commonly identified in patients who were not shunted. A watershed infarct occurred in just one patient with borderline TCO and stump pressure measurements in whom a shunt was not used. Conclusions: There was poor concordance between TCO and stump pressures, but using both in determining the need for shunt use almost eliminated cross-clamp ischemia in this series of 300 carotid endarterectomy patients.
Development of collateral vessels, arteriogenesis, may protect against tissue ischemia, however, quantitative data on this process remain scarce. We have developed a technique for replicating the entire arterial network of ischemic rat hindlimbs in three dimensions (3D) based on vascular casting and automated sequential cryo-imaging. Various dilutions of Batson’s No. 17 with methyl methacrylate were evaluated in healthy rats, with further protocol optimization in ischemic rats. Penetration of the resin into the vascular network greatly depended on dilution; the total length of casted vessels below 75 µm was 13-fold higher at 50% dilution compared with the 10% dilution. Dilutions of 25–30%, with transient clamping of the healthy iliac artery, were optimal for imaging the arterial network in unilateral ischemia. This protocol completely filled the lumina of small arterioles and collateral vessels. These appeared as thin anastomoses in healthy legs and increasingly larger vessels during ligation (median diameter 1 week: 63 µm, 4 weeks: 127 µm). The presented combination of quality casts with high-resolution cryo-imaging enables automated, detailed 3D analysis of collateral adaptation, which furthermore can be combined with co-registered 3D distributions of fluorescent molecular imaging markers reflecting biological activity or perfusion.
Objective: The purpose of this article is to provide a systematic review of the evidence supporting the use of milrinone for the management of delayed cerebral ischemia (DCI) following subarachnoid hemorrhage (SAH). Design: Primary outcomes were functional neurological status and the incidence of cerebral infarction. Search strategies adapted to the different databases were developed by a professional librarian. Medline, EMBASE, the Cochrane Library database, Web of Science, SCOPUS, BIOSIS, Global Health, Health Star, Open SIGLE, Google Scholar and the New York Academy of Medicine Gray Literature were searched as well as clinical trials databases and the proceedings of several scientific meetings. Quality of the evidence for these outcomes across studies was adjudicated using the GRADE Working Group criteria. Results: The search resulted in 284 citations after elimination of duplicates. Of those 9 conference proceedings and 15 studies met inclusion criteria and consisted of case reports, case series and two comparative studies: one non-randomized study with physiological outcomes only and a case series with historical controls. There was considerable variation in dosing and in co-interventions and no case control or randomized controlled studies were found. Conclusion: There is currently only very low quality evidence to support the use of milrinone to improve important outcomes in patients with delayed cerebral ischemia secondary to subarachnoid hemorrhage. Further research is needed to clarify the value and risks of this medication in patients with SAH.
Cerebral vasospasm is a prolonged but reversible narrowing of cerebral arteries beginning days after subarachnoid hemorrhage. Progression to cerebral ischemia is tied mostly to vasospasm severity, and its pathogenesis lies in artery encasement by blood clot, although the complex interactions between hematoma and surrounding structures are not fully understood. The delayed onset of vasospasm provides a potential opportunity for its prevention. It is disappointing that recent randomized, controlled trials did not demonstrate that the endothelin antagonist clazosentan, the cholesterol-lowering agent simvastatin, and the vasodilator magnesium sulfate improve patient outcome. Minimizing ischemia by avoiding inadequate blood volume and pressure, administering the calcium antagonist nimodipine, and intervention with balloon angioplasty, when necessary, constitutes current best management. Over the past two decades, our ability to manage vasospasm has led to a significant decline in patient morbidity and mortality from vasospasm, yet it still remains an important determinant of outcome after aneurysm rupture.
Early locomotor exercise after stroke has attracted a great deal of attention in clinical and animal research in recent years. A series of animal studies showed that early locomotor exercise poststroke could protect against ischemic brain injury and improve functional outcomes through the promotion of angiogenesis, inhibition of acute inflammatory response and neuron apoptosis, and protection of the blood-brain barrier. However, to date, the clinical application of early locomotor exercise poststroke was limited because some clinicians have little confidence in its effectiveness. Here we review the current progress of early locomotor exercise poststroke in animal models. We hope that a comprehensive awareness of the early locomotor exercise poststroke may help to implement early locomotor exercise more appropriately in treatment for ischemic stroke.
It is controversial to observe or close symptomatic congenital coronary artery fistula in infants. We herein describe a medium-sized symptomatic congenital coronary artery fistula that underwent rapid spontaneous closure in an infant aged <3 months.
This chapter discusses the diagnosis, evaluation and management of aortic dissection. In addition to chest pain, patients may present with focal neurological deficits secondary to the physical obstruction of either one of the carotid arteries by an intimal flap, or false lumen propagation. Vascular obstruction and ischemia may occur at any level, leading to syncope, stroke symptoms, acute myocardial infarction (frequently from right coronary artery compromise), mesenteric ischemia, paraplegia (from hypoperfusion of the spinal arteries), or limb ischemia. Cardiogenic shock may also arise as a complication of dissection into the pericardium resulting in cardiac tamponade. Beck's triad of hypotension, muffled heart sounds, and jugular venous distension can sometimes be found. Electrocardiogram (ECG) findings rarely aid in the diagnosis, though ST elevations may be present in as many as 20% of patients due to ostial coronary involvement.
This chapter discusses the diagnosis, evaluation and management of small bowel obstruction (SBO). It details the specific types of small bowel obstruction. Common causes of small bowel obstruction include hernias, neoplasms, intussusception, and others. Thorough history should be taken, with particular attention paid to prior SBOs, abdominal surgeries, hernias, cancer, and opiate use. The vital signs of SBO are: fever, tachycardia, hypotension, and tachypnea. The examination of the abdomen is performed by visually inspecting the abdomen for scars and distension. Rectal examination is considered with evaluation for occult blood, although diagnostic yield may below and classically the rectal vault will be empty. In laboratory evaluation findings are not specific to bowel obstruction. Results may show evidence of dehydration, acidosis, renal failure, and leukocytosis. Antibiotics are indicated with evidence of ischemia, perforation, or severe disease, although there is no good evidence supporting or refuting the use of empiric broad-spectrum antibiotics.
This chapter discusses the diagnosis, evaluation and management of acute mesenteric ischemia. The diagnosis should be considered in those older than 50 years, presenting with nonspecific abdominal pain and risk factors for the disease. The physician must have a high index of suspicion as the history of the disease may be difficult to obtain. The chapter lists clinical presentations of the subtypes of mesenteric ischemia. Emergent laparotomy is indicated, especially if signs of peritonitis are present. Surgery is generally the standard of care for mesenteric arterial embolism and thrombosis. Surgery is done to determine the extent of damage, to find the underlying cause, to revascularize viable bowel, and to resect infarcted bowel. Second-look procedures are often performed 24-48 hours after the initial surgery in order to restore continuity and assess extension of ischemia to ensure that at-risk or ischemic bowel is not used for the final anastomosis.
The sleep apnea syndrome occurs in 4% of adult men and 2% of adult women. Inflammation and hypoxia are intertwined at the molecular, cellular, and clinical levels. Sleep apnea influences heart rate variability, during sleep and during wakefulness. It is also an independent risk factor for stroke. Sleep apnea may also lead to cognitive dysfunction from the effects of chronic hypoxia and sympathetic stress associated with small-vessel disease in the brain, white matter ischemia, and lacunar strokes. This syndrome is a modifiable risk factor and therefore efforts to control this condition in patients at risk of vascular disease is a clinical endeavor that should be pursued vigorously, even though clinical research needs to persist in its quest to answer pressing pathophysiological questions. Emerging evidence suggests that restless legs syndrome (RLS) and periodic limb movements of sleep (PLMS) represent risk factors for cardio- and cerebrovascular disease, even leading to stroke.
Transient monocular visual loss is the most important visual symptom of arteriosclerotic vascular disease, arteritis and states of altered coagulability, and thrombocytosis. In most patients, the visual abnormality during each individual attack of visual loss is stereotypic. Visual loss occurrence is divided into four types. Type I is due to transient retinal ischemia, type II to retinal vascular insufficiency, and type III to vasospasm. Type IV occurs in association with antiphospholipid antibodies but includes cases of unknown etiology. Sudden monocular blindness is the major symptom of an ocular stroke causing permanent visual loss. The ocular strokes discussed are: central retinal artery (CRA) occlusion, ophthalmic artery (OA) occlusion, branch retinal artery (BRA) occlusion, and ischemic optic neuropathy (ION), which is the result of infarction of the optic nerve. Blindness can result from infarction of the retina or the optic nerve.
Anterior choroidal artery (AChA) territory infarcts represent the second most common infarct in the territory of the deep perforators of the carotid artery system. The classical pattern of clinical signs attributed to AChA territory infarction is hemiplegia, hemianesthesia, and homonymous hemianopia, often associated with neuropsychological signs. Aphasia, spatial neglect, attention disorder, executive functioning impairment, and delayed memory are reported to be less severe than when due to thalamic or cortical infarctions. The high prevalence of arterial hypertension or diabetes mellitus as an isolated risk factor of stroke in small-sized AChA infarcts suggests that small artery disease is a common etiology of AChA territory infarcts. The clinical syndromes, vascular risk factor profile, presumed etiology of stroke, and prognosis allow consideration of small and large AChA territory infarcts in the differential diagnosis of patients with brain ischemia.
This chapter talks about Mary who was admitted to Tertiary Hospital in early June of 2003 having stumbled to the ground being unable to get up. CT of her head confirmed general parenchymal volume loss with decreased attenuation periventricularly. No significant areas of ischemia or space-occupying lesions were noted. PET scan was suggestive of a neurodegenerative process of Alzheimer's type. No scan evidence of frontal lobe dementia. The diagnosis prior to the PET scan being performed was frontotemporal dementia. The final clinical diagnosis after the PET scan and on discharge was that of Alzheimer's type dementia. She was not started on acetylcholine esterase therapy. She was discharged to a low level residential facility. This case is interesting in that it does not on face value fit into one category of neurodegenerative disorders. False beliefs related to misinterpretation of the environment due to significant visual impairment is known as Charles-Bonnet syndrome.
Subcortical hyperintensities (SH) on neuroimaging are a prominent feature of vascular dementia (VaD) and SH severity correlates with cognitive impairment in this population. Previous studies demonstrated that SH burden accounts for a degree of the cognitive burden among VaD patients, although it remains unclear if individual factors such as cognitive reserve influence cognitive status in VaD. To address this issue, we examined 36 individuals diagnosed with probable VaD (age = 77.56; education = 12). All individuals underwent MMSE evaluations and MRI brain scans. We predicted that individuals with higher educational attainment would exhibit less cognitive difficulty despite similar levels of SH volume, compared to individuals with less educational attainment. A regression analysis revealed that greater SH volume was associated with lower scores on the MMSE. Additionally, education moderated the relationship between SH volume and MMSE score, demonstrating that individuals with higher education had higher scores on the MMSE despite similar degrees of SH burden. These results suggest that educational attainment buffers the deleterious effects of SH burden on cognitive status among VaD patients. (JINS, 2011, 17, 531–536)