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They should also Appendices 711 Injury 6 hours old on the extremities Injury 24 hours old on the face and scalp Tendon, joint, or bony involvement Cartilage involvement Mammalian bite Co-morbid disease (diabetes mellitus, extremes of age, steroid use, morbid obesity) Puncture wound Complex intraoral wound Discharge paperwork for the patient should include explicit instructions on wound care management, as well as specific comments about the possibility of wound infection (Table B. For the wound at higher risk of infection, such as a contaminated laceration of a finger, a human bite of an extremity, or a traumatic wound with devitalized tissue, a scheduled wound check within 48 hours is prudent to look for early signs of infection. Buffered versus plain lidocaine as a local anesthetic for simple laceration repair. Antibiotics to prevent infection of simple wounds: a meta-analysis of randomized studies. Minimizing the pain of local infiltration anesthesia for wounds by injection into the wound edges. Plasma cocaine and tetracaine levels following application of topical anesthesia in children. Wound preparation 712 Appendices Appendix C Laceration repair Laceration repair F. Wound healing and the final cosmetic outcome of a laceration repair depend on many factors, including dynamic and static tension. Static tension is determined by intrinsic skin factors such as collagen concentration. Anatomic determinants such as underlying bone, tendon, muscle and location over a joint space impact the dynamic tension of the repaired laceration. Wounds oriented along these lines are under less stress, and often lead to more favorable cosmetic outcomes. Lacerations that are oriented perpendicular to these lines are under higher tension; therefore, the method selected for closure may require more tensile support. The underlying dermis is one to several millimeters thick depending on its location on the body. In some cases, especially wounds under tension, a separate deep dermal layer of closure may be required. The dermis rests on subcutaneous tissue which contains adipose and other loose connective tissue. Wounds occurring along these lines generally have a more favorable cosmetic outcome. Time from injury to cleansing and closure affects the ability of the wound to be closed primarily Appendices 713 Table C. Allowing a wound to granulate in from the edges with no wound edge re-approximation. Physical re-approximation of wound edges after debridement, packing, and antibiotic prophylaxis for 3­4 days. Patients sometimes sense the presence of a foreign body, and the clinician can often palpate one underneath the skin surface. A comprehensive history may uncover related conditions which can be more important than the laceration. For example, syncope leading to a minor forehead laceration obligates an extensive work-up and likely hospital admission, compared to a mechanical fall leading to a laceration in the same area. Wounds to the face should arouse suspicion for intimate partner violence (Table C. Lacerations on the head and face can generally be closed up to 24 hours after injury, whereas injuries on the hands, feet, and trunk are considered to be at high risk for infection after 12 hours delay. Wounds that occurred more than 24 hours prior to evaluation may be considered for delayed primary closure (Table C. It is important to know medication allergies before giving tetanus prophylaxis, analgesics, wound anesthesia, antibiotics, or using latex products. Crush injuries, puncture wounds, burns, and contaminated wounds (human or animal saliva, feces, soil, organic material) warrant special consideration. Lower threshold for using appropriate antibiotics in wounds that are high risk for infection. Peripheral vascular disease Other Cardiac disease Domestic/child/elder abuse Make sure that the wound resulted from a mechanical and not cardiac etiology. Have a low threshold for suspicion and reporting when the story does not match the injury. This information may help guide decisions whether to use prophylactic antibiotics, and may predict which patients are prone to impaired wound healing (Table C. Physical examination the physical examination should take place in a well-lit area with the patient as comfortable as possible.

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Step 8 - If the student chooses to contest the allegation and/or sanction, the student can appeal to the Provost. An appeal to the Provost can only be based upon irregularities in procedure, new evidence not available for the first hearing, or punishment not consistent with the violation. The Provost will render a decision, in writing, within 10 academic days of receipt of the appeal. Step 9 - If the Provost upholds the decision of the Student Disciplinary Council, and if the student chooses to contest the allegation and/or sanction, the student can appeal to the Board of Regents. An appeal to the Board of Regents can only be based upon irregularities in procedure, new evidence not available at the first hearing, or punishment not consistent with the violation. Grievance Policies Regarding Appeal of Grades Grievance policies regarding appeal of grades can be found online at: studentaffairs. This must be done within three academic days of the occurrence of the situation creating the grievance. The faculty member will investigate and obtain all pertinent information and provide a solution or explanation within three academic days with full explanation of the reasons for the decision. Within five class days after an unfavorable decision by the instructor, the Director will decide one of two options: A. The Director will review the grievance and make a ruling within five academic days. Small problems sometimes tend to become big problems, and are more difficult to resolve when not discussed with an individual who can correct them in a timely fashion. Coupled with this fact, the Athletic Training Education Program believes that both are imperative to succeed in the major, in your career, and in life. The forms must be submitted to the Department of Exercise & Science Secretary weekly to be stamped with date and time received. When a student does not show up or is late for their assigned clinical experience, not only is the efficiency and effectiveness of the healthcare for athletes/patients severely diminished, but more importantly students are missing an opportunity to enhance their clinical education experience. Because of the significance of being punctual and in attendance, the Athletic Training Education Program has established the below policies which will be enforced with no exceptions, regarding tardiness and absenteeism: Clincal Tardy Policies 1. Every student is allowed one time to be tardy if he/she is no more than ten minutes late; you are given the "benefit of the doubt" only one time per semester. With the second unexcused tardiness comes a scheduled conference between the student and the Clinical Coordinator and/or instructor/staff member. At this time, the student will be placed on probation for an undisclosed time and not allowed to participate in certain activities. Probably the most important element of this policy is communication with your clinical instructor/supervisor. We realize there are on occasion, problems that may arise and cause one to miss his/her clinical assignment for that day or to be tardy. Each student that has such a dilemma must make every effort to contact his/her clinical supervisor. Students are encouraged to meet with their academic advisors for more than just course scheduling. The purpose of the conference is to discuss clinical strengths/weakness of each specific student, and satisfactory completion of practicum course competencies and clinical proficiencies. At the end of this conference, students will sign the evaluation that has been completed by their preceptor and to acknowledge that they have reviewed the evaluation form. The student must then submit their evaluation to the instructor of the practicum course in which he/she is enrolled. Additional conferences occur between the student and their assigned academic advisor. Clinical rotations will change from semester to semester and may even vary within a given semester. Clinical education times are inflexible, due to the availability of the preceptors, the practice times of certain athletic teams either on or off campus, and/or the "open" hours of other affiliate clinical settings, thus making part-time employment extremely difficult to impossible. Students must realize their top priority is the educational preparation necessary for the field of Athletic Training.

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The possibility of change of mental competence due to drugs, injury, or physical deterioration is evident. For example, presume that several measurements have been secured in a short time by different examiners and that there are no examinee practice or fatigue effects. They are unavoidable; their presence and magnitude must be recognized in the appropriate employment and interpretations of the results obtained with measuring instruments. For example, perusal of the Stanford-Binet content shows a progressive increase of verbal-type items as one goes from early to later ages. Variations also may be attributed to differences in the standardization norms of different instru- Assessment 57 ments and to changes between different editions of the same scale. As with error of measurement, such variations must be interpreted by appropriately prepared clinicians to avoid literal and absolute use of any obtained score. These agents, which are generally manifest in some form of brain maldevelopment or dysfunction, embrace a very broad range of factors. They include genetic and chromosomal disorders, infectious processes, toxins and chemical agents, nutrition and errors of metabolism, gestational disorders, complications of pregnancy and delivery, and gross brain disease, many of undetermined origin. The number of newly recognized causes of retardation is increasing rapidly because of significant advances in laboratory methodology, sophisticated instrumentation such as mass spectrometry, and increased interest of clinicians and biomedical researchers. With the discovery of new specific genetic syndromes, teratogens, and biochemical abnormalities, the task of classification has become increasingly difficult. What appears to be a separate disease may be one part of another syndrome or causally dependent on the existence of some co-factor. There is little doubt that most of the conditions in the 1983 classification scheme have been both clinically and scientifically validated; however, it is equally certain that no book can keep pace with the proliferation of knowledge from biological research. Organic retardation is far less frequent than "psychosocial disadvantage," as defined here. Individuals in this category are, as a rule, more severely disabled, have associated physical handicaps, and are heavily dependent on adults in their environment for support or survival. Although not perfect, the correlation between intelligence level and biologic retardation is very high. Prenatal and Perinatal Factors Approximately 9 out of 10 cases of biologically based mental retardation are prenatal in origin and manifested at birth or early in infancy. It is not surprising that disturbances in fetal growth sometimes cause central nervous system deficits, for this is a period of rapid brain development. The mature brain can survive the effects of infections, radiation, trauma, and other noxious agents, but they can be devasting to the developing organism. Any factor causing maternal ill-health-physical or, in some instances, even emotional-or an adverse uterine environment can affect the unborn child. The role of maternal infection in the etiology of mental retardation is fairly well defined. Although not a major cause of mental retardation, infectious diseases are, nevertheless, important; furthermore, they can be prevented in many situations. The achievement of this goal in diseases such as syphillis and rubella, for example, has been made possible by a better understanding of the pathogenesis of the infectious process and knowledge of the characteristics of the microorganisms involved and their transmission. Treatment with antibiotics has proved effective for syphillis, and vaccines and mass immunization techniques have prevented rubella and associated tragic fetal outcomes. The nature and extensiveness of damage occurring from infection depends, in part, on whether it is congenital or acquired. Congenital toxoplasmosis, for example, in both its "neurological" and "generalized" forms, has widespread symptomatology, including characteristic abnormal spinal fluid, anemia, and convulsions. Of those who survive, 85 percent are mentally retarded, and most have associated convulsive disorders, spasticity, or impairments in vision. By contrast, acquired forms of toxoplasmosis may result in encephalitis or other symptoms, but with far less severe consequences. When rubella and cytomegalovirus inclusion disease occur during pregnancy, they produce congenital malformations as well as mental retardation. Typology 61 Embryonic tissues are particularly susceptible to damage from disease since the human fetus appears to show no detectable immunological response early in gestation.

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Macrophagesandmonocytes(seeColorPlate7)migrate freely into the tissues from the blood to replenish and reinforce the macrophage population. Thiscommoncommittedprogenitorcellcandifferentiateintothegranulocyteormonocyte-macrophagepathway, depending on the microenvironment and chemical regulators. Circulatingmonocytesmaycontinue to be multipotential and give rise to different types of macrophages. Fixedmacrophageslinetheendotheliumofcapillariesand the sinuses of organs such as the bone marrow, spleen, and lymphnodes. Functionally, the most important step in the maturation ofmacrophagesisthecytokine-drivenconversionofthenormalrestingmacrophagetotheactivatedmacrophage. The terminal stage of development in the mononuclear phagocytecelllineisthemultinucleatedgiantcell,whichcharacterizesgranulomatousinflammatorydiseasessuchastuberculosis. Bothmonocytesandmacrophagescanbeshowninthe lesions in these diseases before the formation of giant cells, thoughttobeprecursorsofthemultinucleatedcells. Host Defense Functions Functionally, monocytes-macrophages have phagocytosis as theirmajorrole,butthesecellsperformatleastthreedistinct but interrelated functions in host defense. The categories of host defense functions of monocytes-macrophages include phagocytosis, antigen presentation and induction of the immune response, and secretion of biologically active molecules. Phagocytosis Theprincipalfunctionsofmononuclearphagocytesinbody defenses result from the changes that take place in these functions when the macrophage is activated (Box 3-1). In addition, macrophages remove and eliminate such extracellular pathogensaspneumococcifromthebloodcirculation. Activation of macrophages or monocytescanresult intherelease of parasiticidalmediators and in receptor-mediate phagocytosis during malaria infection. The most likely location for this innate immune responseiswithinthespleenwhichiscrucialfordevelopmentofimmunitytomalaria. Theyarealsoinvolvedinremoving tissue debris, repairing wounds, and removing debris as embryonictissuesreplaceoneanother. Phagocytic activity increases when there is tissue damage andinflammation,whichreleasessubstancesthatattractmacrophages. Activatedmacrophagesmigratemorevigorouslyin response to chemotactic factors and should enter sites of inflammation. Migrationofmonocytesinto differentbodytissuesappearstobearandomphenomenonin the absence of localized inflammation. Theactivityofmononuclearphagocytesagainstcancercells in humans is less well understood than the phagocytosis of microorganisms. The proteolytic enzymes present on the surface membrane of monocytes also may play a role in tumorrejection. Antigen Presentation and Induction of the Immune Response the phagocytic property of the macrophage is particularly importantintheprocessingofantigensaspartoftheimmune response. Macrophages are believed to process antigens and physicallypresentthisbiochemicallymodifiedandmorereactive form of antigen to lymphocytes (particularly helper T cells)asaninitialstepintheimmuneresponse. Asthe neutrophil becomes activated, it replaces L-selectin with other cell surface adhesion molecules, such as integrins. Secretion of Biologically Active Molecules Monocytes-macrophagesreleasemanyfactorsassociatedwith hostdefenseandinflammation. In addition to their phagocytic properties, monocytesmacrophages are able to synthesize a number of biologically important compounds, including transferrin, complement, interferon, pyrogens, and certain growth factors. Approximately 100 distinct substances have been identified as being secretedbymonocytes-macrophages. This triggers the activation of integrins, which leads to firm leukocyte arrest on the endothelium. In addition, integrin-dependentsignalingeventsinducecytoskeletalrearrangements and cell polarization, modifications necessary to help prepare the attached leukocyte to spread and crawl in searchforawayoutofthevasculatureintotissue. Celsus,apractitionerofGreekmedicinewhowasbornin25 bce,iscreditedwithrecordingthecardinalsignsofinflammation-rubor (redness), calor (heat), dolor (pain), and tumor (swelling). Once inflammation is triggered, it must be appropriately resolvedorpathologictissuedamagewilloccur.

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Analysis of the antibody levels of 439 subjects who had received three or four doses of tetanus toxoid and no revaccination revealed that levels were above 0. The authors concluded that primary immunization in infancy (three doses) gives approximately five years protection and that revaccination within five years of the last dose induces immunity for approximately 20 years. D ata from a cross-sectional study in the Kingdom of the N etherlands (de Melker et al. Each data point represents an indiv idual im m unized with one of the described im m unization schedules (n = 469). Furthermore, booster responses may vary individually and a pronounced dispersion of antibody levels can be expected with time following a primary series of immunizations (Figure 5); hence regular boosters were used to maximize protection for a high proportion of the population. The need for boosters every 10 years has been questioned because of the few numbers of cases and deaths in people who have received a full primary series of three or more doses, and also because of the literature illustrating that the duration of immunity is likely to exceed 10 years - a duration of 20 to 30 years has been suggested (D e Melker et al. It has been widely reported that the higher the pre-booster antibody titre, the lower the relative increase in antitoxin response to immunization (D anilova et al. The clinical relevance of this observation is that boosting an individual with high antitoxin levels does not provide additional short-term or long-term protection. Therefore, immunization schedules need to be appropriately spaced to provide the optimal regime for booster vaccinations. Furthermore, if the schedule of primary or booster immunizations is interrupted, there is no requirement to re-start the primary series as it is likely that the response to the next dose in the series will sufficiently boost the levels of antitoxin. The kinetics of the response to a tetanus booster is of importance, both to predict protection of neonates after administration of boosters to pregnant women, an d b ecau se it is r eco m m en d ed as a p ar t o f m an agem en t o f p at ien t s w it h tetanus-prone wounds. The median period of incubation to onset of tetanus has been reported as seven days [range 0­112 days] (Pascual et al. A measurable increase in antibody titre following a booster dose has been detected after four days (Turner et al. H ence, it is possible that administration of a tetanus booster as part of wound management will not contribute to the prevention of a current tetanus infection in incubation if antitoxin levels are low, but will provide long-term protection against future tetanus episodes. I n su m m ar y, t h r ee D T P d o ses in in fan cy w ill give t h r ee t o five y ear s o f protection and there are limited data suggesting this may persist up to seven years (Volk et al. Booster responses can still be elicited after intervals of 25­30 years, demonstrating the persistence of immunological memory. D ifferences between men and woman are also highlighted, due to either vaccination in the military (mainly males), or countries where tetanus immunization occurs during pregnancy. In general men have higher antibody levels due to immunization during military service; however data from the Republic of India (Misra & Rao, 1988) demonstrated the impact immunization of women during pregnancy has on the antibody profile of females. The difference between males and females is not as apparent, except for the data from the H ellenic Republic of G reece reported in 2003 and the older age groups in the Kingdom of the N etherlands from 1996. The majority of the data comes from developed countries with established immunization programmes, with high coverage during childhood and adolescence and variable booster coverage in adulthood (given with wound care or as part of routine prevention). There is a rise in the antibody levels in fem ales o f ch ild b ear in g age d u e t o the im m u n iz at io n p r o gr am m e in p lace. These data highlight the fact that serosurveys require knowledge of the immunization programme, and coverage for each birth cohort to allow correct interpretation. The serological surveys also illustrate the potential for appropriately scheduled primary ser ies an d b o o st er s t o p r o vid e h igh an t ib o d y levels fo r w o m en t h r o u gh o u t childbearing age. The data shown in Figure 6 and other serological surveys reported in the literature (Maple et al. This does vary by country and immunization schedule, but suggests that a complete primary series of immunizations and subsequent boosters in childhood and ad o lescen ce p r o vid es p r o t ect ive an t ib o d y levels w ell in t o ad u lt h o o d, protecting women (and their newborns) throughout their childbearing years. Tetanus immunity in men and women in different age groups in Kenya 100 90 80 70 % protected 60 50 40 30 20 10 0 1-7 8-11 12-17 18-45 >45 Age (years) Males Protectiv e T hreshold: 0. In many areas where neonatal tetanus is still common, these infections are also widespread. The response of malaria-infected pregnant women to tetanus toxoid immunization is similar to that of non-pregnant healthy adults (Brabin et al. In children, two studies reported a decreased response following one or two doses of tetanus toxoid in children with parasitaemia from an acute attack of malaria compared to n o n - p ar asit aem ic co n t r o ls (E d sall et al. C hemoprophylaxis for malaria can be given without any impairment of the antibody responses to immunization in children (G illes et al. D ietz et al (1997) concluded following a review of available literature, that concurrent malarial infection may decrease the immune response to tetanus toxoid but that complete evaluation of the impact of concurrent malarial infections on the response to tetanus toxoid requires analysis of infected and non-infected individuals; however withholding chemotherapy from the infected group would be unethical.