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By: Rasheed Adebayo Gbadegesin, MBBS

  • Professor of Pediatrics
  • Professor in Medicine
  • Affiliate of Duke Molecular Physiology Institute

https://medicine.duke.edu/faculty/rasheed-adebayo-gbadegesin-mbbs

Presence arteria obstruida effective micardis 20mg, communication pulse pressure stroke volume buy online micardis, and culture heart attack female 40mg micardis mastercard, can all be grouped as social factors all being related to blood pressure joint pain buy micardis american express the visibility of the library within the community and its social visibility blood pressure under stress discount micardis. Leadership arrhythmia and chest pain generic micardis 40 mg amex, investment and strategy are all strategic issues that will drive the direction of the service and decision making. Staff, access and service are all service factors that are enabling factors making the service visible within the community. Performance indicators or systems checks could be set at the sub-factor level to support performance assessment against critical areas and to assure attention to critical factors. The idea is that when attention is needed and given to these areas, performance will increase, having a positive impact on the success of the service. They are usually focussed down to a small number, maybe six, the few areas within an organisation it is critical for the organisation to get right in order to ensure success. Key performance indicators can be established at any level in order to assess achievement within those critical areas. This model is data driven, and is grounded in the analysis of the data collected within the case study. Conclusions the findings of this study address the complexity of the service situation in the public sector library, avoiding an overly reductionist approach. Once confirmed, the critical success factors are the issues that the service must give attention to. Indicators and measures can be established in these areas, and reviewed to ensure continued success. This study is a single exploratory qualitative case study and as such the results are not generalisable. However, the model and main lessons from this research could be of interest to other libraries and public sector services. To take a reductionist approach, and ignore complexity may mean that critical issues are ignored and likely to have severe implications for the success of a service. Determining organizational information needs: the Critical Success Factors approach. The critical success factors for school and community joint use libraries in New Zealand. Market orientation and alternative strategic orientations: a longitudinal assessment of performance implications. Chief executives define their own data needs, Harvard Business Review, 57(2) 81-93. Conferences Pprovide opportunities to explore current trends, report on research and share new ideas or best practices. Presentation at conferences is viewed as a preliminary step to publication; research presented at conferences that is not published in the formal literature is effectively lost to future professionals. Establishing a benchmark of scholarly contribution through publication is an important measure of evidence production in a particular discipline or field. A Cochrane systematic review analyzed 79 biomedical research studies that examined publication rates post conference presentation. The average time from presentation to publication was 21 months with papers taking 26 months, posters 19 months, panel presentations took 17 months to publish and roundtable discussion took 21 months. From 442 abstracts of papers and posters presented at the two meetings, a publication rate of 27. Harvey & Wandersee report that the greatest barrier to publication as perceived by conference presenters was a lack of time. Harvey & Wandersee suggest library science posters and papers presented at meeting are often designed to share successful projects and many not always follow strict research design (Harvey, Wandersee 2010, p. Scholarly communication is often mentioned as a new and future area of opportunity for academic and bioscience librarianship, which includes supporting researchers in the knowledge of metrics and data, and other areas in the publication lifecycle. As librarianship assumes this mantle, it is important to develop a composite of comparative research to definitively establish a measure that librarians can compare to other disciplines. To contribute to the comparative evidence, the authors replicated the Harvey & Wandersee study in the Canadian health sciences librarian context. As secondary outcomes, the authors conducted a bibliometric and altmetric analysis to determine impact level and factors influencing impact. In order to collect an adequate sample size we used 6 years of conference proceedings. The date range allowed for 3 years to publish from the last conference chosen to the beginning of the study. Some authors had more than one abstract in the years study resulting in 150 unique first authors. Publication rate was calculated using two different methods, a literature search and an author survey. Each conference abstract title was searched in each database checking for authors last name and potential title keywords. A survey was sent to first authors to confirm publication rates and discover reasons that may affect their choice to publish. Author emails were collected from conference programs, university directories and websites, 120 email addresses were found for the 150 first authors 30 email address could not be located. Authors were asked to respond based on the first paper/poster presented chronologically in the year range. Respondents were to provide a citation if they had published as a check against the literature search. Using Fluid Survey in July of 2012 first authors were emailed a survey link to complete, 12 email addresses bounced back leaving 108 surveys successfully sent. If they choose not to publish, abstract authors were asked to indicate a primary and secondary reason for not publishing. All citations were compiled into a spreadsheet and identified by publication type (ie journal article, book chapter etc). A bibliometric analysis consisting of Bradfords Law of Scatter, impact factor, and times cited was conducted on the sample. For a majority of titles the impact factor was unavailable and the analysis by impact factor was abandoned. Google was used to collect times cited counts as other sources, such as Scopus and Web of Science, did not index a majority of the titles in the sample. Times cited counts were collated by journal title and descriptive statistics performed. In February 2013 an altmetric analysis on the journal citation sample was performed using Altmetrics. Results Literature search and bibliometrics analysis the publication rate found by the literature search was calculated as 31. In total, there were 80 publications found from the abstract sample: 76 journal articles, 2 journal letters, 1 dissertation and 1 book chapter. In this analysis, all publication types were included in the rate, regardless of the timing of the publication, pre or post conference presentation, so long as the topic of the paper closely paralleled the topic or title of the conference abstract. The focus for the bibliometric and altmetric analysis was restricted to journal articles and letters only, as other publication types (eg dissertation) did not warrant their inclusion due to their low number. Google Times Cited was sought for all citations whose journal title was represented 2 or more times in the sample. As shown in Figure 2, 4 out of the 6 titles had averages within a 2-point spread; there was no statistical variance found between any of the titles (F-score=2. For a majority of library science titles in the sample, Google Times Cited was the only consistent available count, although its reliability is debatable at the present time. Using ImpactStory, 29 of 71 citations had at least 1 kind of metric reporting (41%). Mendeley counts were used to determine the degree of correlation between the counts provided by Altmetrics. Mendeley counts can be used as an indicator of scholarly community uptake of a given publication. In the survey conference presenters were asked to choose the main reason they did not submit their presentation for publication, 43% (15 out of 37) of respondents selected time restriction as the main reason for not publishing. Time restriction was also chosen as the secondary reason for not publishing by 36% of the respondents. The second most common primary reason for not publishing was a belief that the abstract was unworthy of further publication. Comments from survey respondents illustrate this belief Not sure there is a paper in it since it was a presentation on a database project; not a research project; Topic did not warrant a full article; it was a how I do this type of abstract not really worthy of further publication. However the majority of medical librarians publishing are from the academic area with 59% of the respondents from universities or university hospitals, and another 14% in teaching hospitals. Survey respondents showed no difference in publication rate by years in the profession. The largest educational classification was 77% (43 out of 56) with a Masters of Library Science or equivalent qualification, 11% (6 out of 56) had other Masters level degrees, 7% (4 out of 56) had PhDs and 6% (3 out of 56) had Bachelor level or diplomas. Among the commonalities are similar rates of publication, common publication choices, similar reasons for not publishing and demographics. Harvey & Wandersee established a publication benchmark for librarians presenting at Medical Library Association conferences of 27. This rate is although comparable to that found by Harvey & Wandersee is significantly less than the 44. To regard 29% as a satisfactory bar would be detrimental to our profession as the majority of new research and ideas presented at conferences is lost to the vast majority of library science professionals. It is not surprising that the official publications of each national health library association are the leading publication for each respective nation. The main reasons for not publishing, including lack of time and confidence in the presentation material, present significant barriers to improving publication rate. The lack of confidence reason is a form of self-censorship as it results in a seeming reluctance to engage the publication process, denying peer review its work to determine what is of value to the broader community. Further, to address the issue of time, some academic institutions allow for protected research time and resource support. A national examination and collation of institutional policy around protected research time to raise awareness, and then the development of an official statement of support around such policies, would be an appropriate advocacy of this issue. The publishing demographics in this study shows a bias in health librarian research toward academic health librarianship practice as academic health sciences librarians do the majority of publishing. This may have implications for the future of the smaller health libraries if the body of knowledge does not reflect the culture, practices and conditions of those libraries and the professionals who practice in them. More research is required to determine what specific advocacy on the part of organizations can be done to assist and encourage non-academic librarians to engage and complete the research lifecycle in their own practice. The secondary outcomes of this study illuminate issues in publication quality in the library literature. Todays librarians need to demonstrate the impact of their services and their work just as their research counterparts. Traditional bibliometrics and new altmetrics measurements are methods used by academics to quantify impact in their curriculum vitae and performance reviews. The decision to publish is primarily influenced by two factors, time and authors confidence. As librarians continue to embrace evidence based librarianship the need for a robust pool of evidence found in the published literature is paramount. If librarians are to demonstrate value to the disciplines they serve, then publication with demonstrated impact through traditional bibliometrics such as times cited and new measures found in altmetrics are methods to be employed. Jiscs considerable work on activity data has highlighted the lack of tools and services for libraries to exploit this data. The project aims to help libraries effectively manage collections and services as well as delivering pre-emptive indicators and actionable insights to help identify new trends, personalise services and improve efficiencies, economies and effectiveness (student attainment and satisfaction and institutional reputation, for example). The project builds on the Library Impact Data Project at the University of Huddersfield and the work of the Copac Activity Data and Collections Management tools. The paper will deliver a case study of the project, its progress to date, the challenges of such an approach and the implications the service has for academic libraries. A description of the approach adopted by the project, and the vision and goals of the project 2. In particular the challenges around accessing and sharing the data, warehousing and data infrastructure considerations and the design challenge of visualising the data sources in a useful and coherent way 3. Findings this paper will report on the initial findings of the project, which will run from January 2013 to December 2013. In particular it will consider the issues surfaced through the close engagement with the academic library community (through the projects community advisory and planning group) and the institutional early-adopters around data gathering and analysis. While there are a number of recognised and well understood use-cases for library analytics these tend to revolve around usage and collection management. Yet, the potential of a shared analytics service is in uncovering those links and indicators across diverse data sets. The paper will consider a number of practical impacts: l Performance: benchmarking, student attainment, research productivity l Design: fine tuning services, personalised support l Trends: research landscape, student marketplace, utilisation of resources. The case study will explore these practical implications for libraries and what they mean for the future of the library within the academy. Originality and value of the proposal the paper will present a case study of a unique service that currently fills an important gap within the library analytics space. The paper will focus on the services potential to transform both the way the library works and how it is perceived by its users, as well as its role and relationship within the broader institution. Uncontrolled keywords Library usage, student attainment, low use, non-use, academic libraries, undergraduate students, achievement background the 10th Northumbria International Conference on Performance Measurement in Libraries and Information Services is testament that libraries have been collecting and analysing data for many years. The variety and scope of this data has ranged from transactional data, such as catalogue searches, book issues and returns, access to electronic resources and entry through the library gates to the manual collection of statistics on space usage, student satisfaction and external visitors to the library and library spend. Jisc has been working in this area through the Jisc Activity Data programme (Jisc, 2012), which has provided a significant body of evidence and practical guidance to make a library analytics service feasible. This phase used continuous rather than categorical data, which allowed the project to do more with the data. Using students final grades as a percentage, rather than a class, also allowed phase two to demonstrate a correlation in the phase one hypothesis in addition to the statistical significance found in phase one.

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The neurocognitive impairments do not occur exclusively during the course of a delir ium and persist beyond the usual duration of intoxication and acute withdrawal blood pressure goal jnc 8 generic micardis 80 mg with visa. The involved substance or medication and duration and extent of use are capable of producing the neurocognitive impairment hypertension nos 4019 order cheap micardis online. The temporal course of the neurocognitive deficits is consistent with the timing of sub stance or medication use and abstinence hypertension kidney infection buy 20 mg micardis visa. The neurocognitive disorder is not attributable to blood pressure medication used for withdrawal buy online micardis another medical condition or is not better explained by another mental disorder arrhythmia certification generic 20mg micardis amex. If a mild substance use disorder is comorbid with the sub stance-induced neurocognitive disorder pulse pressure pv loop buy 40mg micardis overnight delivery, the 4th position character is 1 andthe clinician should record mild [substance] use disorderbefore the substance-induced neurocognitive disorder. If a moderate or severe substance use disorder is comorbid with the substanceinduced neurocognitive disorder, the 4th position character is 2,and the clinician should record moderate [substance] use disorderor severe [substance] use disorder,depending on the severity of the comorbid substance use disorder. If there is no comorbid substance use disorder, then the 4th position character is 9,and the clinician should record only the substance-induced neurocognitive disorder. Behav ioral disturbance cannot be coded but should still be indicated in writing. The name of the substance/medication-induced neurocognitive disorder be gins with the specific substance/medication. For substances that do not fit into any of the classes, the code for "other substance" should be used; and in cases in which a substance is judged to be an etiological factor but the specific class of substance is unknown, the cat egory "unknown substance" should be used. For example, in the case of persistent amnestic-confabulatory symptoms in a man with a severe alcohol use disorder, the diagnosis is 291. If the substance/medi cation-induced neurocognitive disorder occurs without a comorbid substance use disorder. The name of the substance/medication-induced neurocognitive disorder begins with the specific substance. For substances that do not fit into any of the classes, the code for "other sub stance" should be used; and in cases in which a substance is judged to be an etiological fac tor but the specific class of substance is unknown, the category "unknown substance" should be used. When recording the name of the disorder, the comorbid substance use disorder (if any) is listed first, followed by the word "with," followed by the name of the disorder. For example, in the case of persistent amnestic-confabulatory symptoms in a man with a severe alcohol use disorder, the diagnosis is F10. If the substance-induced neurocognitive disorder occurs without a comorbid substance use dis order. Initially, these manifestations can reflect slow recovery of brain functions from a period of prolonged substance use, and improvements in neurocognitive as well as brain imaging indicators may be seen over many months. The given substance and its use must be known to be capable of causing the observed impairments (Criterion C). While nonspecific decrements in a range of cognitive abilities can occur with nearly any substance of abuse and a variety of medications, some patterns occur more frequently with selected drug classes. In addition to or independent of the more common neurocognitive symptoms related to methamphetamine use. There may also be loss of emotional control, including aggressive or inappropriate affect, or apathy. In the case of methamphetamine, cerebrovascular disease can also occur, resulting in diffuse or focal brain injury that can be of mild or major neu rocognitive levels. With cannabis, intoxication is accompanied by various neurocognitive disturbances, but these tend to clear with abstinence. Development and Course Substance use disorders tend to commence during adolescence and peak in the 20s and 30s. Earlier commencement of abuse, particularly of alcohol, may lead to defects in later neural development. Mag netic resonance spectroscopy may reveal reduction in N-acetylaspartate, and increase in markers of inflammation. Many of these brain imaging changes and neurocognitive manifestations reverse following suc cessful abstinence. D ifferential Diagnosis Individuals with substance use disorders, substance intoxication, and substance withdrawal are at increased risk for other conditions that may independently, or through a compounding effect, result in neurocognitive disturbance. These include history of traumatic brain injury and infections that can accompany substance use disorder. Comorbidity Substance use disorders, substance intoxication, and substance withdrawal are highly comorbid with other mental disorders. Comorbid posttraumatic stress disorder, psychotic disorders, depressive and bipolar disorders, and neurodevelopmental disorders can con tribute to neurocognitive impairment in substance users. Severe, long-term alcohol use disorder can be associated with major organ system disease, including cerebrovascular disease and cirrhosis. The neurocognitive disorder is not attributable to another medical condition and is not better explained by a mental disorder. Language difficulties, such as aphasia, are uncommon, although reductions in fluency may be observed. There may be loss of emotional control, includ ing aggressive or inappropriate affect or apathy. A subcortical neurocognitive profile may interact with age over the life course, when psychomotor slowing and motor impairments such as slowed gait may occur as a consequence of other age-related condi tions so that the overall progression may appear more pronounced in later life. Chronic exposure to antiret roviral drugs also raises the possibility of neurotoxicity, although this has not been defin itively established. Specialized techniques such as diffusion tensor imaging may reveal damage to specific white matter tracts. Thus, impaired executive abilities and slowed information processing may substantially interfere with the complex disease management decisions required for ad herence to the combined antiretroviral therapy regimen. D ifferentiai Diagnosis In the presence of comorbidities, such as other infections. Among older adults, onset of neurocognitive decline related to cerebrovascular disease or neurodegeneration. Because more severe im munodeficiency can result in opportunistic infections of the brain. There are motor features of prion disease, such as myoclonus or ataxia, or biomarker evidence. The neurocognitive disorder is not attributable to another medical condition and is not better expiated by another mental disorder. Coding note: For major neurocognitive disorder due to prion disease, with behavioral dis turbance, code first 046. For major neu rocognitive disorder due to prion disease, without behavioral disturbance, code first 046. However, many individuals with the dis order may have atypical presentations, and the disease can be confirmed only by biopsy or at autopsy. Prodromal symptoms of prion disease may include fatigue, anx iety, problems with appetite or sleeping, or difficulties with concentration. After several weeks, these symptoms may be followed by incoordination, altered vision, or abnormal gait or other movements that may be myoclonic, choreoathetoid, or ballistic, along with a rapidly progressive dementia. The disease typically progresses very rapidly to the major level of impairment over several months. Cross-species transmission of prion infections, with agents that are closely related to the human form, has been demonstrated. Transmission by comeal transplantation and by human growth factor injection has been documented, and anecdotal cases of transmission to health care workers have been reported. There is a genetic component in up to 15% of cases, associ ated with an autosomal dominant mutation. Diagnostic iVlarlcers Prion disease can be definitively confirmed only by biopsy or at autopsy. In some individuals, the electroencephalogram reveals periodic sharp, often triphasic and synchronous dis charges at a rate of 0. Major or Mild Neurocognitive Disorder Due to Parkinsons Disease Diagnostic Criteria A. The neurocognitive disorder is not attributable to another medical condition and is not better explained by another mental disorder. Major or mild neurocognitive disorder probably due to Parkinsons disease should be diagnosed if 1 and 2 are both met. The Parkinsons disease clearly precedes the onset of the neurocognitive disorder. Coding note: For major neurocognitive disorder probably due to Parkinsons disease, with behavioral disturbance, code first 332. For major neurocognitive disorder probably due to Parkinsons disease, without behavioral disturbance, code first 332. Associated Features Supporting Diagnosis Frequently present features include apathy, depressed mood, anxious mood, hallucina tions, delusions, personality changes, rapid eye movement sleep behavior disorder, and excessive daytime sleepiness. This distinction is based sub stantially on the timing and sequence of motor and cognitive symptoms. Motor symptoms and frequent co-occurrence of depression or apathy can make functional impairment worse. Major or Mild Neurocognitive Disorder Due to Huntingtons Disease Diagnostic Criteria A. There is clinically established Huntingtons disease, or risk for Huntingtons disease based on family history or genetic testing. Coding note: For major neurocognitive disorder due to Huntingtons disease, with behav ioral disturbance, code first 333. For major neurocognitive disorder due to Huntingtons disease, without behav ioral disturbance, code first 333. Cognitive and associated behavioral changes often precede the emergence of the typical motor abnormalities of bradykinesia. The disease is gradually progressive, with median survival approximately 15 years after motor symptom diagnosis. Psychiatric and cognitive abnormalities can predate the motor abnormality by at least 15 years. Initial symptoms requiring care often include irritabity, anxiety, or depressed mood. Other behavioral disturbances may include pronounced ap athy, disinhibition, impulsivity, and impaired insight, with apathy often becoming more progressive over time. Early movement symptoms may involve the appearance of fidget iness of the extremities as well as mild apraxia. As the disorder progresses, other motor problems in clude impaired gait (ataxia) and postural instability. Motor impairment eventually affects speech production (dysarthria) such that the speech becomes very difficult to understand. End-stage motor disease impairs motor control of eating and swallowing, typically a major contributor to the death of the individual from aspiration pneumonia. Some individuals with a positive family history request genetic testing in a presymptomatic stage. Associated features may also include neuroimaging changes; volume loss in the basal ganglia, particularly the caudate nucleus and putamen, is well known to occur and progresses over the course of illness. Other structural and functional changes have been observed in brain imaging but remain research measures. Cognitive deficits that contribute most to functional decline may include speed of processing, initi ation, and attention rather than memory impairment. As the disease progresses, disability from problems such as impaired gait, dysarthria, and impulsive or irritable behaviors may substantially add to the level of impairment and daily care needs, over and above the care needs attributable to the cognitive decline. Severe choreic movements may substantially interfere with provision of care such as bathing, dressing, and toileting. Major or Mild Neurocognitive Disorder Due to Another Medical Condition Diagnostic Criteria A. There is evidence from the history, physical examination, or laboratory findings that the neurocognitive disorder is the pathophysiological consequence of another medical condition. The cognitive deficits are not better explained by another mental disorder or another specific neurocognitive disorder. Coding note: For major neurocognitive disorder due to another medical condition, with behavioral disturbance, code first the other medical condition, followed by the major neu rocognitive disorder due to another medical condition, with behavioral disturbance. For major neurocognitive disorder due to an other medical condition, without behavioral disturbance, code first the other medical condition, followed by the major neurocognitive disorder due to another medical condition, without behavioral disturbance. Behavioral distur bance cannot be coded but should still be indicated in writing. Unusual causes of central nervous system injury, such as electrical shock or intracranial radiation, are generally evident from the history. Diagnostic certainty regarding this relationship may be increased if the neuro cognitive deficits ameliorate partially or stabilize in the context of treatment of the medical condition. Diagnostic iVlarlcers Associated physical examination and laboratory findings and other clinical features de pend on the nature and severity of the medical condition. If cog nitive deficits persist following successful treatment of an associated medical condition, then another etiology may be responsible for the cognitive decline. Major or Mild Neurocognitive Disorder Due to Multiple Etiologies Diagnostic Criteria A. There is evidence from the history, physical examination, or laboratory findings that the neurocognitive disorder is the pathophysiological consequence of more than one etio logical process, excluding substances. Note: Please refer to the diagnostic criteria for the various neurocognitive disorders due to specific medical conditions for guidance on establishing the particular etiologies. The cognitive deficits are not better explained by another mental disorder and do not occur exclusively during the course of a delirium. Coding note: For major neurocognitive disorder due to multiple etiologies, with behavioral disturbance, code 294. All of the etiological medical conditions (with the exception of vascular disease) should be coded and listed separately immediately before major neurocognitive disorder due to multiple etiologies.

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There is a progressive loss of muscle power arrhythmia murmur purchase micardis 20 mg without prescription, especially in the external eye muscles and other muscles of the face hypertension goals cheap micardis 20 mg on-line. A charley horse is an enlargement of the first joint of the great describes muscular strain and soreness arrhythmia unspecified icd 9 code buy 80mg micardis with amex, espetoe with bursitis at the joint prehypertension nhs buy cheap micardis line. The term comes from common from the word bony heart attack cafe discount micardis online master card, changed to hypertension prevention order micardis amex bunny, and use of the name Charley for old lame horses that used to mean a bump on the head and then a were kept around for family use when they could swelling on a joint. Wryneck, called a corn because it is a hardened or horny technically torticollis, uses the word wry meanthickening of the skin in an area of friction or ing twisted or turned, as in the word awry pressure. The lactic acid leads to muscle fatigue, after which it is gradually removed from the tissues. The goal of occupational therapy is to increase the patients independence and quality of daily life. Exercise, massage, and other therapeutic methods are used to restore proper movement. Biceps femoris Deltoid Gastrocnemius 1 Gluteus maximus Latissimus dorsi 5 2 Peroneus longus Semimembranosus 3 6 Semitendinosus Sternocleidomastoid 7 Teres major Teres minor 4 Trapezius Triceps brachii 8 1. The neurotransmitter released at the neuromuscular junction is . A muscle that produces flexion at a joint is called a(n) . The number of origins (heads) in the biceps brachii muscle is . The sheath of connective tissue that covers a muscle is called . A band of connective tissue that attaches a muscle to a bone is a(n) . The strong, cordlike tendon that attaches the calf muscle to the heel is the . Movement toward the midline of the body is termed . Write a word that has the opposite meaning of each of the following terms as they pertain to muscles: 51. After anesthesia induction and positioning in a semisitting (beach chair) position, the surgeon made an anterosuperior deltoid incision (the standard deltopectoral approach) and divided the coracoacromial ligament at the acromial attachment. The rotator cuff was identifled after the deltoid was retracted and the clavipectoral fascia was incised. After incision of the capsule, inspection showed a large pouch inferiorly in the capsule, consistent with laxity (instability). The torn edges of the capsule were anchored to the rim of the glenoid fossa with heavy nonabsorbable sutures. A flap from the subscapularis tendon was transposed and sutured to the supraspinatus and infraspinatus muscles to bridge the gap. He had atrophy over the supraspinatus and infraspinatus muscles and also subluxation of his shoulder and atrophy of the deltoid. With middle trunk brachial plexus injury, damage to the subscapular nerve will interrupt conduction to the subscapularis and teres major muscles. Damage to the long thoracic nerve prevents conduction to the serratus anterior muscles. A neuromonitoring technologist placed the electrodes and attended the computer monitor throughout the case. During the procedure, selected muscle groups were stimulated with 15 to 40 milliamps (mA) of current to test the nerves and muscles. Feedback data into the computer conflrmed the neuromuscular integrity and status of the spinal flxation of the instrumentation and implants. After the pedicle screws, hooks, and wires were in place and the spinal rods were cinched down to straighten the spine, L. She was given commands to move her feet, straighten her legs, and wiggle her toes to test all neuromuscular groups that could be affected by misplaced or compressed spinal flxation devices. Dorsiflexion cleared the tibialis anterior muscles; plantar flexion cleared the gastrocnemius muscles. Knee flexion cleared the hamstring muscle group, and knee extension determined function of the quadriceps group. The surgical instruments and tables were kept sterile until after all of the monitored muscle groups were tested and showed voluntary movement. The joint motion characterized by elevating the toes toward the anterior ankle is: a. Adjective for a type of muscle contraction crease function and independence in daily life: 20. Its color, texture, and resilience reveal much, as does the condition of the hair and nails. This body-covering system protects against infection, dehydration, ultraviolet radiation, and injury. Extensive damage to the skin, such as by burns, can result in a host of dangerous complications. Anatomy of the Skin the outermost portion of the skin is the epidermis, consisting of 4 to 5 layers (strata) of epithelial cells (Fig. As these cells gradually rise toward the surface, they die and become fllled with keratin, a protein that thickens and toughens the skin. The outermost (horny) layer of the epidermis, the stratum corneum, is composed of flat, dead, protective cells that are constantly being shed and replaced. Some of the cells in the epidermis produce melanin, a pigment that gives color to the skin and protects against sunlight. The subcutaneous tissue beneath the dermis is composed mainly of connective tissue and fat. The sebaceous glands release an oily fluid, sebum, that lubricates the hair and skin and prevents drying. Each hair develops within a sheath or hair follicle and grows from its base within the deep layers of the skin. The study of the skin and diseases of the skin is dermatology, but careful observation of the skin, hair, and nails should be part of every physical examination. It should be palpated to evaluate its texture, temperature, moisture, flrmness, and any tenderness. Wounds Wounds are caused by trauma, such as in cases of accidents or attacks, or by surgery and other therapeutic or diagnostic procedures. Infection and hemorrhage may complicate wounds, as do dehiscence, disruption of the wound layers, and evisceration, protrusion of internal organs through the lesion. This drainage, called exudate, may be clear, bloody (sanguinous), or pus-containing (purulent). Proper wound healing depends on cleanliness and care of the lesion and also on proper circulation, good general health, and good nutrition. Various types of dressings are used to protect wounded areas and promote healing. This may be accomplished by cutting or scrubbing away the dead tissue or by means of enzymes. Contrecoup in French means from Latin and Greek; others are derived from counter blow. Sometimes a foreign word is ing pain along the path of the trigeminal nerve in used as is. They may also be caused by electrical malfunctions, contact with harmful chemicals, or abrasion. Depth of tissue destruction is categorized as follows: Superflcial partial-thickness, which involves the epidermis and perhaps a portion of the dermis. The above classiflcation replaces an older system of ranking burns as flrst-, second-, and third-degree according to the depth of tissue damage. Infection is a common complication of burns because a major defense against invasion of microorganisms is damaged. Treatment of burns includes respiratory care, administration of fluids, wound care, and pain control. Monitoring for cardiovascular complications, infections, and signs of posttraumatic stress are also important. The pressure interrupts circulation, leading to thrombosis, ulceration, and death of tissue. Poor general health, malnutrition, age, obesity, and infection contribute to the development of pressure ulcers. If ignored, they may penetrate the skin and underlying muscle, extending even to bone, and may require months to heal. Pads or mattresses to relieve pressure, regular cleansing and drying of the skin, frequent change in position, and good nutrition help to prevent pressure ulcers. Both of these terms refer to lying down in bed, although pressure ulcers may appear in anyone with limited movement, not only those who are conflned to bed. A chronic allergic form of this disorder that appears early in childhood is called eczema or atopic dermatitis. Although its exact cause is unknown, atopic dermatitis is made worse by allergies, infection, temperature extremes, and skin irritants. Other forms of dermatitis include contact dermatitis, caused by chemical irritants; seborrheic dermatitis, which involves areas with large numbers of sebaceous glands such as the scalp and face; and stasis dermatitis, caused by poor circulation. Psoriasis Psoriasis is a chronic overgrowth (hyperplasia) of the epidermis, producing large, erythematous (red) plaques with silvery scales (Fig. The cause is unknown but there is sometimes a hereditary pattern, and autoimmunity may be involved. Autoimmune Disorders the diseases discussed below are caused, at least in part, by autoimmune reactions. Rupture of these lesions leaves deeper areas of the skin unprotected from infection and fluid loss, much as in cases of burns. It is seen as rough, raised, violet-tinted papules, usually limited to the face and scalp. There may also be a butterfly-shaped rash across the nose and cheeks that is typical of this disease. The skin lesions of lupus are worsened by exposure to the ultraviolet radiation in sunlight. Scleroderma is a disease of unknown cause that involves thickening and tightening of the skin. A very early sign of scleroderma is Raynaud disease, in which blood vessels in the flngers and toes constrict in the cold, causing numbness, pain, coldness, and tingling. Its rate has been increasing in recent years, mainly because of the mutation-causing effects of the ultraviolet rays in sunlight. Malignant melanoma results from an overgrowth of melanocytes, the pigment-producing cells in the epidermis. It is the most dangerous form of skin cancer because of its tendency to metastasize. This cancer appears as a lesion that is variable in color with an irregular border (Fig. It may spread superflcially for up to 1 or 2 years before it begins to invade the deeper tissues of the skin and to metastasize through blood and lymph. The prognosis for cure is good if the lesion is recognized and removed surgically before it enters this invasive stage. Squamous cell carcinoma and basal cell carcinoma are both cancers of epithelial cells. Squamous cell carcinoma appears as a painless, flrm, red nodule or plaque that may develop surface scales, ulceration, or crusting (Fig. It is treated by surgical removal and sometimes with x-irradiation or chemotherapy. Because these cancers are easily seen and do not metastasize, the cure rate after excision is greater than 95%. Squamous cell carcinoma shown on the face and the back of the hand, sun-exposed areas that are commonly affected. An initial translucent nodule spreads, leaving a depressed center and a flrm, elevated border. Actinic keratosis is caused by exposure to sunlight and may lead to squamous cell carcinoma. Beau lines, transverse depressions in the nails associated with acute severe illness. Depigmented macules appear on the skin and may merge into large areas that lack melanin. The brown pigment seen in the illustration is the persons normal skin color; the pale areas are caused by vitiligo. The skin and its associated structures make up the system. The layer of the skin under the epidermis is the . The protein that thickens the skin and makes up hair and nails is . The lesion had been present for about 2 months when she consulted a dermatologist. She thought the lump might have been triggered by the regular tanning salon sessions she had used to retain her tan because it did not resemble the acne pustules, blackheads, or resulting scars of her adolescent years. Although dermabrasion had removed the obvious acne scars and left several areas of dense skin, this lump was brown-pigmented and different. On examination, the dermatologist noted a small pearly-white nodule at the lower portion of the left ala (outer flared portion of the nostril). A plastic surgeon excised the lesion and was able to re-approximate the wound edges without a fullthickness skin graft.

Malouf syndrome

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Dry cough: Pleural disorders hypertension 2014 guidelines generic micardis 20mg line, interstitial lung disease hypertension yahoo discount micardis online, Copious sputum production upon changes in posture mediastinal lesions is seen in bronchiectasis and lung abscess blood pressure medication used for hot flashes discount micardis 80 mg. Short cough: It is seen in upper respiratory tract Large amount of colourless sputum is present in alveolar cell infections (common cold) carcinoma heart attack kurt buy micardis 80mg low cost. Brassy cough: Cough with metallic sound produced by compression of the trachea by intrathoracic space Chronology occupying lesions Chronic bronchitis: Sputum production is more in the 5 blood pressure normal low discount micardis 80 mg without a prescription. Bovine cough: Cough with loss of its explosive nature blood pressure food buy micardis online pills, early morning for many years. Prolonged and paroxysmal cough: It is present in chronic Bronchial asthma: Sputum production is more either in bronchitis and whooping cough the morning or at night. Barking cough: It is found in epiglottal involvement production signifies severe infection. Green or yellow coloured thick sputum indicates intrathoracic pressure, which reduces venous return to bacterial infections. The green colour to sputum is the heart, thereby diminishing cardiac output, resulting imparted by the enzyme myeloperoxidase (verdoin cerebral hypoperfusion and syncope. It is seen in bronchoMassive > 500 ml blood loss per day (or) rate of alveolar carcinoma. It may be pink, as occurs in blood loss > 150 ml/hr (or) 100 ml blood pulmonary oedema. Mucoid: It is clear, greyish white or black in colour and If there is > 500 ml blood loss per day, aggressive frothy. It may be seen in conditions like chronic bronintervention (rigid bronchoscopy or surgery) is advochitis and chronic asthma. If the blood loss is submassive, after subsidence of haemoptysis, fibreoptic bronchoscopy is indicated. Mucopurulent or purulent: Yellowish or greenish brown in colour, seen in bacterial infection. Bronchial asthma: Macroscopically the sputum is worm Causes of Haemoptysis like, which are remnants of casts of bronchus. Differences between Haemoptysis and Haematemesis Odour of Sputum Haemoptysis Haematemesis Offensive and foetid: a. Malaena absent Malaena present It is defined as expectoration of blood, or bloody sputum. Previous history of Previous history of Types of Haemoptysis respiratory disease peptic ulcer disease Frank haemoptysis: It is the expectoration of blood only. Diagnosed by bronchoscopy Diagnosed by gastroscopy Massive and fatal blood loss may occur. Spurious haemoptysis: Haemoptysis present secondary Cardiovascular Disorders to upper respiratory tract infection, above the level of larynx. Endemic haemoptysis: Present in infection with Paragonimus westermani (lung fluke). J receptors, situated at the alveolo-capillary junction, are responsible for rapid shallow breathing and they 1. Metastatic lesions of the lung except in secondaries are stimulated by pulmonary congestion, oedema due to choriocarcinoma and renal cell carcinoma. The chemoreceptors in the carotid arteries, aorta and reticular substance of medulla which respond to Dyspnoea oxygen lack, carbon dioxide excess and decrease in It is defined as the undue awareness of respiratory effort pH or of the need to increase the effort. Receptors in the respiratory muscle which are immediate cause of appreciation of dyspnoea. Minutes Increased demand of breathing is present in conditions Pneumothorax like: Pulmonary oedema due to cardiac arrhythmias 1. Hours Increased respiratory effort is needed in: Asthma (but can also be acute) 1. Grading of Dyspnoea Days Pneumonia Medical Research Council Classification Adult respiratory distress syndrome Left heart failure Grade I Shortness of breath when hurrying on a level Repeated pulmonary embolism ground or walking up a small hill. Cyanosis (Mode of onset of respiratory disorder Muscle weakness Chronic obstructive pulmonary disease determines the presence or absence of cyanosis. In chronic lung disorder, unless bilateral Chest Pain extensive involvement is present, cyanosis may be absent) Pleural Pain 5. Anaemia may occur when there is It is caused by stretching of the inflamed parietal pleura. Excessive sputum production and protein loss catchy pain occurring with deep inspiration or coughing c. Loss of appetite leading to malnutrition and relieved by shallow breathing or lying on the 6. Pancoast Syndrome Pancoast syndrome is caused by either a superior sulcus Clubbing (Fig. It is a selective bulbous enlargement of the distal portion of the digit due to increased subungual soft tissue. The components of this syndrome are: the normal angle between the nail and the nail-bed a. Compression of C8, T1, T2 nerve roots resulting in is 160 and is known as the Lovibond angle. Clubbing first appears in the stellate ganglion, producing Horners syndrome index finger. Upper Retrosternal Pain It is a momentary pain which increases in intensity on coughing and subsides when the cough becomes productive. Mid or Lower Retrosternal Pain It is constrictive in character and may be present in: 1. Hypoxia: Persistent hypoxia causes opening of deep A-V fistulae of the terminal phalanx 5. Platelet derived growth factor: this factor which is released secondary to infection anywhere in the body, also causes vasodilatation and this is the latest and most acceptable theory for clubbing. Causes of Clubbing Congenital/Familial* Note: *Congenital hypertrophic pulmonary osteoarthropathyPachydermoperiostosis. Grade I Obliteration of the angle between the nail and the nail-bed and positive fluctuation test Unidigital clubbing: It is seen in: (Fig. Aneurysmal dilatation of aorta, subclavian or Schamroths Sign innominate arteries When the dorsum of the distal phalanges of the fingers ii. Bronchogenic carcinoma (rare in adenocarciHorners syndrome Pancoast tumour noma) Iridocyclitis Tuberculosis and collagen b. Longstanding pulmonary tuberculosis Colour blindness Ethambutol (Red-green colour f. Scalene Lymph Node It is a group of nodes in a pad of fat on the surface of scalenus anterior muscle just in front of its insertion Cardiovascular Causes into the scalene tubercle of the lst rib. Large and fixed in secondary involvement from a primary lung malignancy Gastrointestinal Causes 2. Hard and craggy, matted, with or without sinus formation in healed and calcified tuberculous a. Whole of right lung and left lower lobe to right supraclavicular lymph node It may be seen in: c. Genito-urinary system and gastrointestinal the chemical system malignancies also involve the left c. Leukaemia due to tissue infiltration supraclavicular lymph node due to retrograde d. Scrofuloderma (caused by atypical mycobacteria, In superior vena caval syndrome look for presence of M. External markers of cor pulmonale vein, collateral venous circulation on the anterior sur1. Raised jugular venous pressure face of chest wall is less prominent as the intercostal 2. Inspection of Lower Respiratory Tract Non-malignant Causes All the findings in the clinical examination should be compared on both sides in the following areas: 1. Position of Trachea Trails sign: It is the undue prominence of the clavicular head of sternomastoid on the side to which the trachea is deviated. The pretracheal fascia encloses the clavicular head of sternomastoids on both sides. When the trachea is shifted to one side, the pretracheal fascia covering the sternomastoid on that side relaxes, making the clavicular head more prominent on the side of tracheal deviation. Barrel chest: the anteroposterior to transverse Symmetry of Chest diameter ratio is 1 : 1. Seen in physiological states Normal chest is symmetrical and elliptical in cross like infancy and old age and in pathological states section. Hollowness or fullness in the supraclavicular and It is the exaggeration of the normal hollowness over infraclavicular fossae the lower end of the sternum. If the convexity of the spine and the lung lesion are on the same side, it is most likely that the scoliosis is congenital. If the convexity of the spine is on one side and the lung lesion is on the opposite side, it indicates an acquired scoliosis. Empyema necessitans in which there is an intercostal swelling close to the sternum. Harrisons sulcus: It is due to the indrawing of ribs to form symmetrical horizontal grooves above the costal margin, along the line of attachment of diaphragm due to hyperinflation of the lungs and repeated strong contraction of the diaphragm as occurs in chronic respiratory disease in childhood, childhood asthma, rickets and blocked nasopharynx due to adenoid enlargement 6. Scorbutic rosary: It is the sharp angulation, with or without beading or rosary formation, of the ribs, arising as a result of backward displacement or pushing in of the sternum. It reduces the ventilatory capacity of the Rate lung and increases the work of breathing. Tachypnoea: It is an increase in respiratory rate more Movement of the Chest than 20 per minute. Conditions causing tachypnoea It is described in terms of rate, rhythm, equality and are: type of breathing. Biots breathing: It is characterised by apnoea between several shallow or few deep inspirations. Apneustic breathing: It is characterised by pause at full inspiration, alternating with a pause in expiInspiration: It is an active process brought about by the ration, lasting for 2 to 3 seconds. It occurs in pontine contraction of the external intercostal muscles and the lesions diaphragm (Fig. Cogwheel breathing: It is an interrupted type of Expiration: It is a passive process and it depends upon breathing pattern, seen in nervous individuals elastic recoil of the lungs. Pursed lip breathing: this form of breathing is seen in Accessory muscles of inspiration (Fig. Abnormal Breathing Patterns Palpation Abnormal breathing patterns may be regular or irregular (Fig. The position of the trachea is confirmed by slightly flexing the neck so that the chin remains in the midline. Regular abnormal breathing patterns the index finger is then inserted in the suprasternal a. Cheyne-Stokes breathing: It is characterised by notch and the tracheal ring is felt. Kussmauls breathing: It is characterised by increase in rate and depth of breathing. External mass lesions like thyroid, thymus, lymph nodes causing displacement of trachea must be kept in mind while ascertaining tracheal position. Scoliosis (scoliosis with right sided convexity will displace the cardiac impulse further to the left) b. In the absence of the above conditions, the shift of trachea and apical impulse is due to disease of the lung altering the position of the mediastinum. The trachea may be shifted to the same side in the presence of pleural effusion in the following conditions: a. The normal circumference of the chest and its expansion with deep inspiration is measured. In males, the measurement is done at the level of the nipple and in the females the measurement is done below the breasts. The sign is said to be positive when a downward tug is felt by the fingers during cardiac Assessing Symmetry of Chest Expansion systole. Equality of expansion of the upper part of thorax is done False-positive sign: In mediastinal tumour attached to by facing the patients back and placing both hands over aortic arch. The extent of upward movement of the hands, during quite False-negative sign: In non-pulsatile aortic aneurysm respiration, is compared on both sides (Fig. After a Minimal difference in chest expansion of the two deep breath, the degree of expansion is compared on hemithoraces can be assessed in a cooperative patient, both sides by movement of the thumb away from the without dyspnoea in the following way. The difference in expansion A similar procedure is carried out over the posterior of each hemithorax can then be assessed. The difference in chest expansion can be assessed by Tenderness over the Chest Wall holding a loose fold of skin in between the thumbs, approximated in the midline, whereby even a slight It may be due to: difference in chest expansion can be assessed easily. Infiltration with tumour the alteration of the percussion note by the underlying 4. Anterior percussion: the patient sits erect with the Detection of Subcutaneous Emphysema hands by his side Spongy crepitant feeling on palpation suggests subcutab. Tactile Fremitus these are palpable added sounds (rhonchi are better Objectives of Percussion felt than crackles). It is done to find out the degree of resonance over the Friction Fremitus symmetrical areas of the two sides of the chest and to map out areas in which percussion note is abnormal. The pleximeter: the middle finger of the examiners It is a vibration felt by the hand when the patient is left hand should be opposed tightly over the chest asked to repeat ninety-nine or one-one-one, by putting wall, over the intercostal spaces.

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The etiology of liver cirrhosis is varied blood pressure chart diastolic micardis 40mg with visa, but alcohol abuse and hepatitis viruses B and C are the most frequently incriminated heart attack 2o13 purchase micardis with amex. Thus heart attack film buy micardis 20 mg lowest price, in a study carried out for 3 years in the Department of Gastroenterology Timisoara regarding the etiology of liver cirrhosis blood pressure chart kaiser buy micardis 40 mg otc, hepatitis C virus was the most frequent (33 hypertension 1 order micardis in india. It goes without saying that in some situations the etiology is multifactorial blood pressure 3060 cheap 20mg micardis overnight delivery, the combination of a viral infection with alcohol abuse being extremely common. In addition to the major etiologies of liver cirrhosis (alcohol or hepatitis viruses), 5-10% of cases have rare causes, being secondary to: autoimmune cirrhosis, Wilson cirrhosis (ceruloplasmin deficiency), hemochromatosis, alpha-1-antitrypsin deficiency cirrhosis, primary biliary cirrhosis, drug-induced cirrhosis, and cryptogenic cirrhosis (a rare condition). Thus, in a group of 1200 liver transplants performed in Dallas, almost 10% were performed for cryptogenic cirrhosis. In our group (in an endemic hepatitis virus area), the frequency of cryptogenic cirrhosis is much lower, but this might be due to the fact that cirrhosis is too easily labeled as alcoholic when no other etiological factor can be determined (without taking into account the need for alcohol consumption in a toxic dose for a long enough time). The inspection of the abdomen and chest can reveal collateral abdominal circulation (not a very specific sign) or the presence of spider angiomas (spider naevi) on the chest. Applying pressure makes them disappear, while if the pressure stops they will subsequently reappear, this being a criterion for differentiation of various vascular angiectasis. The patient in dorsal decubitus, with the knees slightly bent for the relaxation of the abdominal muscles, will be asked to perform deep inspiration-expiration movements, which will allow for an accurate liver palpation in order to assess the consistency of the liver. During deep inspiration, the liver will descend (pushed by the diaphragm) and will be easily accessible. Palpation will continue during expiration, when the clinicians hand will follow the margin of the withdrawing liver. After several inspiration/expiration movements, based on palpation, a doctor with good clinical experience will be able to assess if hepatomegaly is present or not, as well as the liver consistency (clinical elastography). We insist on the adequate and correct palpation of the liver, for this method is superior to certain imaging methods used in order to evaluate liver size. Ultrasound examination in liver cirrhosis may reveal multiple changes, but in some cases it can be normal (in up to 20% of cases). Caudate lobe hypertrophy the caudate lobe or the first hepatic segment suffers from hypertrophy in the evolution of liver cirrhosis; therefore it will be frequently enlarged in patients suffering from this condition. Several ways of evaluating the caudate lobe have been described; for example, the calculation of its volume or its relation with the size of the right hepatic lobe. In current practice, the easiest method is to measure the anteroposterior diameter of the caudate lobe by means of ultrasound. In order to differentiate the anteroposterior diameter of the caudate lobe in healthy and cirrhotic subjects, we performed a prospective study which included 200 healthy subjects (126 women and 74 men). Enlarged caudate lobe By comparing these results with a group of 24 cases of known liver cirrhosis, we found that the mean diameter of the caudate lobe in cirrhosis was 47 mm (p<0. These data led us to use the 19 caudate lobe hypertrophy as a sign of liver cirrhosis (Fig. Based on a long ultrasound experience and personal studies, we consider the upper normal limit for the anteroposterior diameter of the caudate lobe to be 35 mm. However, there is an overlapping of normal and cirrhosis cases, so that we generally consider a size of the caudate lobe greater than 40 mm as relevant for cirrhosis (Figs. In current ultrasound practice, approximately 2/3 of cirrhosis cases have a hypertrophic caudate lobe; sometimes with a typical ultrasound appearance (a large, globulous appearance being particularly useful for diagnosis). The caudate lobe size will be used for the diagnosis of liver cirrhosis only in a well known clinical context. Subsequently, the maximum anteroposterior diameter of the caudate lobe should be measured. Measurement of the caudate lobe can be difficult in cases of marked steatosis (ultrasounds are strongly absorbed by fatty tissue) or, more rarely, in the case of ascites. Heterogeneous liver echotexture Liver echotexture changes, particularly hepatic heterogeneity occur in approximately half of cirrhotic cases (Fig. Hepatic heterogeneity is the consequence of fibrous changes that lead to the formation of regenerative nodules. However, there are liver cirrhosis cases without imaging changes of the hepatic echotexture. Liver micronodulation is a histological reality in cirrhosis, but ultrasound cannot evidence these small nodules. The way to accurately diagnose hepatic nodules by ultrasound is to evaluate the liver surface in cases with ascites (Figs. The anterior and, to a smaller extent, the posterior liver surface are easy to examine if ascites is present. Thus, nodules with a size of less than 5 mm in micronodular cirrhosis and more than 5 mm in macronodular cirrhosis can be seen. In ascites-free cirrhosis, it is almost impossible to notice liver surface changes. If a change in the liver architecture (heterogeneity) is found, a possible cirrhogenic liver disease should be suspected. Clinical, biological, and endoscopic examination, as well as elastography (FibroScan) can diagnose cirrhosis that was completely unknown before the ultrasound examination. Studies have shown that these methods are sensitive and specific for diagnosing chronic hepatitis with significant fibrosis (Ffl2) or cirrhosis. Splenomegaly An enlargement of the spleen (over 12 cm long) is frequent in cases of liver cirrhosis (Figs. The spleen of a cirrhotic patient is larger than in chronic hepatitis, so that approximately 80% of cirrhosis cases are accompanied by splenomegaly, which frequently exceeds 15 cm. Sometimes, splenomegaly larger than 18 or even 20 cm can be found, which is often accompanied by hematological hypersplenism (thrombocytopenia < 100,000/mm3 and/or leukopenia < 3000/mm3 and/or anemia). In other situations, the increase in the long axis of the spleen is not necessarily very important, but the spleen has a globulous appearance, through the increase of its width and thickness. We must emphasize the importance of a correct measurement of the spleen along the long axis, especially for beginners in ultrasound. Thus, splenomegaly is diagnosed if the long axis of the spleen is larger than 12 cm. Considering the statistical frequency of diseases with splenomegaly, the following clinico-biological approach to hepatic pathology should be initiated. One should search for a history of liver disease followed by clinical examination where liver palpation is essential (it will possibly demonstrate hepatomegaly and will assess liver consistency). Then, the patient will be evaluated using FibroScan, a method with a sensitivity of more than 90% for the diagnosis of cirrhosis. If clinical hepatomegaly is absent, the aminotransferases are normal, the viral markers are normal, and the FibroScan values are less than 7 kPa, the hepatic etiology of splenomegaly can almost be excluded. In this case, hemolytic anemia, lymphoma, chronic myeloid leukemia and other hematologic causes of splenomegaly should be suspected and investigated. Considering that in Romania ultrasound is an inexpensive and repetitive method available to the clinician, it should always be used for assessing the presence and volume of ascites. The palpation and percussion of the abdomen for the evaluation of ascites is already of historical value, because we probably all had cases in which ascites was suspected following the clinical exam, but abdominal ultrasound showed no ascites (severe obesity, tumors or abdominal cysts). Ascites should be investigated using ultrasound in the pouch of Douglas, in Morrisons pouch (inter-hepato-renal space), in the perihepatic (Figs. The latter can signify old ascites, protein-rich ascites, superinfected ascites, chylous or hemorrhagic ascites. It can assess the macroscopic aspect of the fluid (hemorrhagic or chylous), also allowing the evaluation of proteins concentration, and particularly of the number of leukocytes and polymorphonuclear cells/ml. It is considered that more than 500 leukocytes/ml or more than 250 polymorphonuclear cells/ml in the ascites fluid are signs of infected ascites (spontaneous bacterial peritonitis), even if the culture of the ascites fluid is sterile. Exploratory paracentesis should be performed on the first evaluation of a patient with vascular decompensated cirrhosis or if the patients general condition worsens. It can be performed in the classical manner, without ultrasound control, or, in the case of small ascites, with a thick abdominal wall, under ultrasound guidance. Protein content (exudate or transudate) and other pathological biological elements should be analyzed from the fluid extracted. In unexplained worsening of the clinical status of a patient with vascular decompensated cirrhosis, paracentesis is mandatory to diagnose a possible spontaneous bacterial peritonitis. In cases of cirrhosis with ascites, the subjective ultrasound evaluation of the ascites volume (minimal, small, moderate and large) is performed based on the amount of fluid in the Douglas pouch and in the perihepatic area. This evaluation, even if subjective, is useful from a therapeutic point of view, in order to establish the diuretic treatment doses and the general therapeutic approach. We consider that in minimal ascites, the amount of peritoneal fluid is approximately 1-2 l, in small ascites 3-4 l, in moderate ascites 7-8 l, and in large ascites more than 10-15 l. The consequences of portal hypertension include collateral abdominal circulation, the opening of vascular shunts and the formation of varices most frequently located in the esophagus. If liver cirrhosis is suspected based on clinical signs, the abdomen should be inspected for collateral circulation (special attention should be paid to the possible confusion between collateral circulation and abdominal blood vessels that might be visible through the transparency of the skin). It starts with the assessment of the portal vein, by measuring its size in the hilum, considered to be normal up to a diameter of 13 mm. A diameter of the portal vein greater than 13 mm is a sign of portal hypertension. However, based on a long ultrasound experience and personal studies, we demonstrated that there is always a correlation between the diameter of the portal vein and the severity of portal hypertension. Thus, in a group of liver cirrhosis cases without esophageal varices (the easiest way to assess portal hypertension), the mean diameter of the portal vein was 12. In patients with grade I esophageal varices, the mean diameter of the portal vein in the hilum was 13. This study showed that in the initial phases of portal hypertension, there is a linear correlation between the diameter of portal vein 25 and the endoscopic size of esophageal varices, but later, as portal hypertension worsens and the collateral esophageal veins (esophageal varices) open, the diameter of the portal vein decreases. There is a small number of patients, particularly taller and heavier men, who may have normal anatomical portal vein variants with a diameter of up to 15 or even 16 mm. Its assessment is somewhat subjective, as there are no normal limits for its size. Thus, splenic vein preaortic diameter greater than 10 mm and a hilum diameter greater than 8 mm are both signs of portal hypertension. The detection of collateral epigastric circulation (dilatation of the gastric coronary vein) (Fig. Thus, the evaluation of the flow direction in the splenic and portal veins proved to be useful for prognosis. Using pulsed Doppler, Bolondi demonstrated that in approximately 8% of cirrhosis cases, a reversed flow occurs in the portal and splenic veins due to opening of spontaneous venous shunts. At the same time, Bolondi has proven that flow reversals have a protective role, decreasing the risk of variceal bleeding. Regarding the value of pulsed Doppler in the evaluation of portal pressures and flows, the results were disappointing (due to non-reproducibility of results). After years of studies in search of the best parameters to evaluate, current clinical practice no longer uses Doppler parameters for the evaluation of portal hypertension or of the risk of variceal bleeding. Color Doppler or power Doppler are also useful for demonstrating the vascular character of some anechoic structures. Combining power Doppler with pulsed Doppler will allow differentiating between a dilated tortuous hepatic artery (as is frequently the case in liver cirrhosis) and the portal vein or the common bile duct. Power Doppler is also useful for the evaluation of the portal system in order to detect potential portal thrombosis (Fig. Thus, liver stiffness values lower than 20 kPa are rarely associated with esophageal varices, while values higher than 40 kPa suggest an increased risk of variceal rupture. Changes in the gallbladder wall Assessment of the gallbladder wall by ultrasound is part of the diagnosis in cases suspected to have liver cirrhosis. The normal size of the gallbladder wall is less than or equal to 4 mm, measured at the level of the anterior wall. There are two major situations in which the thickening and most frequently also doubling of the gallbladder wall occur: acute cholecystitis and liver cirrhosis. Acute cholecystitis is most frequently calculous and is accompanied by sonographic Murphys sign (intense pain caused by pressing the ultrasound probe over the visualized gallbladder). In liver cirrhosis, the gallbladder wall can be thickened, reaching 6-8 or even 10 mm (Figs. Doubled gallbladder wall in cirrhosis is caused mainly by hypoalbuminemia (which is why it can also occur in nephrotic syndrome), and also by portal hypertension and lymphatic stasis. In one of our studies that included 62 patients with known liver cirrhosis who were compared to 12 patients with peritoneal carcinomatosis, we found that 52/62 (83. In the 12 cases with peritoneal carcinomatosis (diagnosed by laparoscopy and morphology), the mean diameter of the gallbladder wall was 3. Based on this study and on published data, we may consider that the aspect and thickness of the gallbladder wall are the first ultrasonographic signs suggestive of etiology in ascites of unknown etiology. Another practical aspect that should be known is the association of liver cirrhosis with gallstones in approximately 1/3 of cases. They have a complex etiology, but their main cause is the impairment of conjugation of indirect bilirubin, which precipitates excessively. Detection of gallstones in cirrhosis is frequent, but most times they are asymptomatic, without requiring surgery. The clinical decision is complicated in cases of gallstones in patients with cirrhosis and thickened gallbladder wall. The answer is given by the clinical signs with intense colicky pain and possibly fever, and particularly by the positive ultrasound Murphys sign (the pressure of the ultrasound probe on the gallbladder will cause intense pain), which all support the diagnosis of acute cholecystitis. Another practical aspect related to the gallbladder and liver cirrhosis is the possibility to detect biliary sludge by ultrasound (Figs. Biliary sludge appears as a solid structure in the gallbladder, changing its position and shape with the patients position. The causes, the ultrasound appearance, the evolution of biliary sludge will be discussed in the chapter on the Ultrasound of the gallbladder of this book.

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