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The movement to create a new Census category for mixed race persons in the United States seems to follow this rst option in conceptualizing the mixed race person as having a new identity with substantive attributes of its own treatment plan goals and objectives buy cheap isoniazid on line. By not specifying anything other than the fact of being mixed itself medications diabetic neuropathy isoniazid 300mg low price, this option encompasses Asian/ white symptoms wisdom teeth purchase isoniazid 300 mg without prescription, African American/Latino medications while breastfeeding isoniazid 300mg fast delivery, Native American/African American treatment episode data set discount isoniazid 300 mg mastercard, and so on without speci cation or differentiation medicine lodge kansas isoniazid 300mg generic. But because of the immense variety of possible combinations, and the variable way such persons will be publicly inter pellated and treated, it seems to make little sense to create a social category based on simply being bi or multiracial. There are probably some experiences such persons have in common, but the variability seems too great to warrant a single category for all. Imagine a group of people brought together because they are all mixed race of one sort or another. Each may potentially have experienced some challenges in life due to this feature of their identity, but the speci c challenges that they faced would probably have much to do with the speci c communities to which they were attached. In providing such a box the Census would not have been able to count how many of such persons are part black, part Latino, part Native, part Arab, or part Asian American, thus skewing the statistical tabulations of these communities. Thus, the rst option for characterizing mixed identity is too metaphysically and phenomenologically thin to provide much information and has political disadvantages for minority communities as a system of counting. The second characterization follows the Latin American concept of mestizo more accurately, which is not simply a way to note mixing of any and every type but is an acknowledgment of a very speci c mix: in this case Spanish and Indian. On this understanding, the mixed race person manifests an identity of a new type, with its own substantive features, its own phenomenological being in the world and hermeneutic horizon. For Vasconcelos, the mestizo combines elements of its di verse forebears but creates something new, a new identity with new and different political values and possibilities. The question here is whether mixed race persons in the United States have created something new, an identity, a political orien tation, a way of thinking about themselves in the world, all of which have come out of being positioned in a certain way in the society. Mestizo peoples in much of Latin American have existed for several centuries, have held a unique political and social status, have been recognized by the state as mestizos, and thus arguably have developed an identity (or features that contribute toward their identity). This is not obviously the case in North America, where mixed race persons have generally been identi ed by only one of their multiple identities, where there has been almost no official or even social recognition, and where there is little community and historical experience from which a horizon might emerge. The third option for understanding mixed race identity is the model of hy phenation, in which the person is understood as both or all of what they are, in combination. That is, rather than interpellated by an entirely new category, the person is interpellated by combining his or her actual genealogy, such as Latino/ white, African American/Asian American, and so on. Moreover, by pre serving the particular identities that the mixed person has connections with, the capacity for moving between such groups might be acknowledged. It seems to me that this is the most accurate characterization for many mixed race persons in the North today: they are often capable of negotiating elements of more than one identity, perhaps experiencing the double consciousness Du Bois describes in a new way. So their social or public recognition needs to acknowledge not simply that they are mixed, but what the mix is in particular to understand that person. First, some will argue, rightly, that for some mixed race persons their phenome nological experience of embodiment is tantamount to having a single racial identity. In the context of the United States, this is most often true of persons with a black parent, who are then simply assimilated to blackness by the dominant culture because of the one-drop rule. Phenomenologically, white people are much more used to accepting that black people come in a huge array of shades than they are to the idea that white people could come in just as many shades. This is a historical 284 Latino/a Particularity fact, and it is changing, but slowly. In the account I developed in chapter 4, identity includes lived experience, the horizon of meanings to which a person has access, in other words, their own subjectivity. If person A is viewed as an X by whites, that will be a signi cant aspect of their existence without doubt, but it is not all-determining over their life experience, what his torical narratives they experience a connection with, what cultural resources they have access to , how various nonwhite groups will categorize them, and so on. Thus, I would argue that the hyphenated model might still make intelligible sense as an accurate description of an identity that is part black. A second argument against the hyphenated model comes from those who are concerned that any mixed conception retains the essentialist and homogeneous understanding of the identities that the mixed race person combines. Thus, on this third option, a hyphenated identity simply marks a person as having a connection to more than one historically changeable, dynamic, and complex social identity. The three options as I de scribed them are meant simply to help us begin a conversation about representing mixed race identities. I never reach shore: I never wholly occupy either the Anglo or the Latina identity. Paradoxically but predictably, in white society I feel my latinidad, and in Latin society I feel my whiteness, as that which is left out: an invisible present, sometimes as intrusive as an elephant in the room and sometimes more as a pulled thread that subtly alters the design of my fabricated self. What I seek now is no longer a home, but perhaps a lighthouse that might illuminate this place in which I live, for myself as much as for others. C onclusion n the West, the principal social struggles of the modern era can be characterized Ias, rst, struggles of social status, then, of social class, and only then of social identity. From the beginning of the Conquest, Europeans justi ed genocide and enslavement via claims about the cultural identity and in herent characteristics of indigenous groups, and their opponents, such as Bartolomede Las Casas, developed counterarguments that claimed the Indiansright to cul tural self-determination, a right Las Casas made strong enough to dismiss even the missionariesrhetoric of eternal salvation. The great Mexican rev olution at the start of the twentieth century itself articulated its demands in the name of not simply the abstractions workers and peasants, or trabajadores y cam pesinos, but in the name of los Indios y mestizos, that is, the founding categories of Mexican national identity itself. Social identities were understood to be both the crux of the oppression and the nodal point of the imperialist project. Thus, the focal point of the resistance was a contestation over the meanings, limitations, signi cance, and future possibilities of those very identities. We have yet to formulate a theory that can incorporate with explanatory adequacy the struggles regarding social status, social class, and social identity into 285 286 Conclusion one overarching account. Liberalism, Marxism, and even feminism and critical race theories tend to focus on, or highlight, one type of struggle at a time. One of the most serious obstacles facing any attempt to formulate an overarching theory is, as I have argued, that the ontological basis of the focal point is very different if we are talking about status, about class, or about social identity. The Marxist critique of liberalism, for example, argued that the individualist ontology liberalism used to critique the aristocratic view did not work for class; it could only justify negative liberty, and more than this was needed to understand the ways in which people became constituted as workers and the ways in which the relations of production affected interests and choices. Liberalism could effectively liberate the bourgeois class against the strictures put on their capital accumulation by the aristocratic system of noble inheritance, but it could not effectively liberate the working class from being forced to engage in alienated labor. For that, one needed to understand the ontology of class identity in a different way, as a social and historical construction that required radical structural transformation in society from the ground up. Similarly today, many of us are urging that the ontologies of liberalism and Marxism not be misapplied to social identity. The ontology of status and class calls for a dissolution of the constitutive conditions in which these categories are formed, but this does not follow in a simple analogy for social identities. Liberation comes, in other words, when the very categories of class and status are deconstructed, when we dismantle the social structures that create a class whose only option is to sell its labor power. But the social ontology of these forms of oppression are not explanatory of social identities such as sex/gender or race/eth nicity. Race may be a modern phenomenon (this is still under debate), but racial eliminativists are generally concerned about group identity of any sort, which they see as scripts that compromise moral commitments and constrain individual choice. The discourse of antisexist and antiracist identity-based liberation movements has by and large not demanded a dissolution of the categories, but has demanded instead a radical transformation of the ways they are interpreted and valued, how their relation to other categories is understood, and how their relation to historical events and social systems is accounted for. It is quite clear that equality and human dignity cannot be maximized in societies organized through permanent hierarchies of status and class, but it is far from clear that equality and human dignity require the elimination of the rich differences of life interpretation that are developed via the social identities based on ethnicity, gender, sexuality, and other such group cate gories. Neither the ontology nor the social genealogy of all of these diverse kinds of categories are identical, nor are they even similar in some important respects. In short, there are excellent reasons to eliminate class and status differences, but these reasons do not apply to all other identity groups per se. Some theorists have been too quick to assume that the theoretical analysis of one type of op pression can be applied to all. The contribution of this book has been to provide a critique of that over generalization of identity categories and also a multitude of arguments about the Conclusion 287 speci c salience of race and gender to an account of the self. I have given an explanation and account of the epistemic and political salience of social identities, and addressed speci c issues of debate regarding the grounds for these identities, for example, in embodiment and visible difference. My overall aim has been to strengthen the case for taking social identities into account as deep features of the self, even while I have argued against the idea that identities have ready-made political orientations or xed meanings. Social identities are not simply foisted on people from the outside, as it were, but are more properly understood as sites from which we perceive, act, and engage with others. These sites are not simply social locations or positions, but also hermeneutic horizons comprised of experiences, basic beliefs, and communal values, all of which in uence our orientation toward and responses to future experiences. It should be clear, then, that identities are not analogous to scripts that we are consigned to play out. To say that we have identities, histories, social locations, experiences, cultures, and so on is simply to say that we exist. Identities are best understood as ways in which we and others around us represent our material ties to historical events and social structures. Those events may be traumatic and those structures may be oppressive, but this indicates that the events need to be carefully understood and analyzed and that the structures need to be transformed, not that the identities themselves need to be left behind. We will always have a material tie to historical events and structures, even under the best of circumstances. The implication of this argument is that we need a different understanding of the relationship between identity and oppression. The view I have criticized holds that identities just are oppressive, under any conditions, although perhaps some are more oppressive than others. But even in this latter case, to say that they have been created is to say that they truly exist; thus they are not simply mistakes in reference, or mistaken ways to characterize human experience. The question is not how to overcome identity, but how to transform our current interpretations and understandings of them. How might we imagine them differently within a less violent and strati ed social context The more speci c question of this book has been whether social identities of race and gender are necessary, or are necessarily problematic. That is, does that material tie to historical events and social structures need to be represented in the way that race and gender categories represents it, to categorize and group humans 288 Conclusion into these particular kinds I have raised this question about race and gender in this book because of the commonality between raced and gendered identities. I have wanted to emphasize the material, visible, and physical character of race and gender, but I have also argued that the meanings and implications of even these visible identities will be determined largely by how the historical events and social structures that demarcate identities are interpreted and understood. This is an ongoing, active process involving both individual and collective agency. Indi viduals cannot transform the public meanings, effects, and implications of their identities by a sheer act of will, but collective acts of creative expression and resistance constantly contest and transform the meanings, implications, and po litical effects of such identity markers as skin color, body shape, language use, and role in reproduction. Identities are embodied horizons from which we each must confront and negotiate our shared world and speci c life condition. They are largely unchosen (just as our bodies are unchosen), but just as in the case of bodies, our identities can be reshaped, and they absolutely require interpretation. As I argued in the last chapter, the situation of mixed race persons today most obviously requires inter pretation and involves a range of choice; it is becoming increasingly clear to many people that the identity of a mixed race person is not simply one thing, but a combination that involves both their public interpellations depending on their appearance and their context, as well as their personal history, experience, political values, beliefs, and community commitments. Mixed race individuals cannot in dividually create meaningfully effective identity options for themselves; their in terpretations will be misunderstood and misread if there are no available and accessible social meanings through which they can exert the new and different self presentation that they may wish to put forward. Yet every individual presentation can in uence the possibilities for new con gurations of identity. This dialectic between the individual and the collective interpretation and self-formation is true for every type of social identity. Gendered identity is both more fundamental than sometimes supposed and less determinate than it has historically been portrayed. But this is only one feature within a constellation of elements that go to make up gender identity in any given culture and society, all of which involve interpretive practices. The cultural revolution that is called feminism is precisely a collective contestation over the formation of that identity in the large and meaningful sense, not restricted simply to the meaning and organization of reproductive capacities and activities.

Surgical arthrotomy for large joints is the rule; however this clinical intervention is not always indicated for involvement of smaller joints medicine vicodin purchase genuine isoniazid on-line. The purpose of surgery is to produce an environment with minimal inflammatory products so that antimicrobial therapy is maximized medicine zocor buy 300mg isoniazid free shipping. After surgical intervention medications not to take during pregnancy purchase 300 mg isoniazid fast delivery, empiric parenteral antibiotic coverage for Staphylococcus aureus should be initiated treatment broken toe purchase 300 mg isoniazid free shipping. The antibiotic regimen can then be narrowed once the cultures and sensitivities are received treatment tinea versicolor best buy for isoniazid. This can be done because antibiotic concentrations in the synovium are often higher than that of the serum due to slow reabsorption of the drugs (from the synovium) symptoms 16 dpo order isoniazid with visa. However, all of the following criteria must be met: organism identified and sensitivity to oral antibiotics is documented, the patient is able to take and keep down oral antibiotics, a clear response to parenteral treatment is demonstrated, and routine compliance is assured (2). In conclusion, for straight forward cases of septic arthritis, the overall prognosis is good. Differentiating infectious from non infectious etiologies of joint pain can be a clinical dilemma. The clinician must utilize a broad range of clinical tools to expeditiously diagnose and treat this condition so that outcomes are favorable. True/False: Septic arthritis is a disease most commonly found in adolescent males. True/False: In septic arthritis, the hips and knees are the most commonly affected joints. True/False: In a child with septic arthritis of the hip, redness, swelling, and warmth are often detectable on physical exam. True/False: the most common bacterial etiology of septic arthritis is Staph aureus. True/False: Haemophilus influenzae type B used to be a common cause of septic arthritis in young children, but this is very uncommon today. True/False: Surgical arthrotomy is always warranted for cases of septic arthritis. Septic Arthritis Versus Transient Synovitis of the Hip: the Value of Screening Laboratory Tests. It is a condition that usually affects younger children early in the first decade of life. The hip joint is deep and has a significant amount of surrounding tissue, thus inflammation may not be easily detected on physical exam. Decreased and painful range of motion is the best way to detect an effusion by physical exam. This is why differentiating between toxic synovitis and septic arthritis can be a difficult clinical problem. However in cases of septic arthritis of smaller joints, medical management can be carried out with good results. Orthopedic surgical consult should always be obtained expeditiously whenever the diagnosis is considered. He has difficulty standing with both feet together and prefers to externally rotate his left foot. Although his chief complaint relates to pain near his knee, your examination suggests that his problem is in his hip. The pediatric orthopedist admits him to the hospital for insertion of a screw to secure the unstable growth plate. Activity restrictions include no running or jumping (no sports) until the growth plate has closed radiographically. Due to the deformity, mild arthritis may occur in the fifth to sixth decade of life. Pain is not a specific complaint, but may help the examiner to localize the area of interest to a specific joint or limb. Absence of pain does not narrow the list of causes as infection and neoplasia can present with a painless limp. Broad overlap can occur so one should not ignore a possible diagnosis just because it is not typical in a certain age group. Leg length discrepancy and neuromuscular conditions such as cerebral palsy can affect the gait pattern of a child at any age. In the toddler (age 1 to 4 years), primary consideration should be given to infectious causes such as septic joint or osteomyelitis. In the child/juvenile (age 4 to 10 years), infection and transient synovitis must be excluded. It should be noted that hip pathology may deceptively present with thigh or knee pain. Thus, the hips must be thoroughly examined in patients presenting with thigh or knee pain. In the ambulatory child, the dislocated or dysplastic hip will be evident by a limp, waddle, or leg-length difference on examination. Early recognition of the dysplastic or unstable hip is important so that treatment can be instituted before significant deformity occurs and at a time when sufficient growth remains to enhance hip development (1). If the diagnosis is missed, patients may present in late childhood or in their teen or adult years with severe degenerative damage to the hip. A cleft forms at the 7th week of development and the gross structure of the joint is formed by the 11th week. The development of the acetabulum and the femoral head is dependent upon concentric reduction of the round ball in the cup. Dislocation of the femoral head from the acetabulum will cause deformity of both parts of the hip. Growth of the depth and width of the cup is determined genetically by the acetabular cartilage and the triradiate cartilages (2). Risk factors include female gender, first born child, and breech lie in pregnancy (1). Although the etiology is unknown, idiopathic, capsular laxity, hormonal, genetic, crowding, and syndromic causes have been proposed. Evidence for the crowding phenomenon is noted by the relationship of torticollis, hip dysplasia, oligohydramnios, and metatarsus adductus (8). The palpable clunk associated with the relocation of the femoral head is often called the Ortolani sign. This Ortolani finding disappears as the soft-tissues around the dislocated hip become contracted in the first two-weeks of life. Similarly, the Barlow sign is likely present in the first few weeks of life, but this sign gradually disappears soon thereafter, making it imperative that a thorough examination of the hips be performed and documented several times during the newborn period. In addition, the dislocated hip effectively shortens the thigh length giving the appearance of limb length discrepancy or the Galeazzi sign. The apparent thigh shortening often leads to dramatic asymmetry of the Page 625 gluteal skin folds. With regards to prognosis, hip stability (stable/unstable) and the resting position of the hip (dislocated/reduced) are important concepts to recognize. A newborn with an unstable but reduced hip requires treatment directed at maintenance of stability. More active intervention such as surgery is needed for the ambulatory child with a fixed dislocation (2). Treatment must be directed in achieving a concentric reduction of the femoral head in the acetabulum, stability of the hip joint, and proper remodeling of the growth cartilages throughout childhood. Treatment algorithms are age dependent: birth to six months, six months to 18 months, and greater than 18 months. The risk of complications such as deformity, avascular necrosis, and arthritis increases directly with the complexity of the treatment regimen. In the infant (birth to six months), a flexible harness designed to hold the hips in a reduced position and allow some movement is the primary form of treatment. The Pavlik harness is the simplest and most commonly used harness in the United States. Pavlik failures are associated with bilateral dislocations, Ortolani negative hip, application of the harness after 7 weeks of age, and noncompliance (10,11). Although early success with the Pavlik harness can be expected to result in development of a normal hip in the majority of cases, late dysplasia can be found in 10-20% of adolescents or adults (12,13). For the child (six months to 18 months), closed manipulation and application of a body cast are often employed to reduce the dislocated hip. In the older child or juvenile, open surgical reduction of the hip with reconstruction of bone deformity of either side of the hip joint is often required. The decision for reconstruction will depend on the magnitude of arthritis already present at the time of diagnosis. The condition is characterized by limp, loss of hip internal rotation and abduction, and progressive deformity of the femoral head. The shape of the head, congruency of the hip joint, and range of motion of the hip at maturity determine long term prognosis. The disease is more common in certain geographical locations especially urban centers. Affected children are thought to manifest a specific psychological profile such as hyperactivity. Ethnic variations show a higher risk in Japanese, Eskimos, and central Europeans while American Indians, Polynesians, and African Americans have a lower risk. Growth abnormalities may represent alterations of growth hormone dependent somatomedin activity (14-16). Although the etiology is unknown, most current theories involve vascular compromise to the femoral epiphysis. Increased blood viscosity, thrombophilia, and intraosseous venous hypertension have been proposed as mechanisms for vascular compromise (17-19). The syndrome is typified by certain classic radiographic stages: initial, fragmentation, reossification, and residual phases (20). Synovitis and restricted hip motion lead to deforming forces that compress the femoral head. Potential for remodeling of the deformity is related to the age of onset as a younger child has more years of growth remaining to reshape the head. Therefore, age of disease onset is the second most important factor related to outcome, preceded only by residual deformity. In general, affected children younger than 8 years of age at onset have a better prognosis. Physical examination is marked by limited abduction and internal rotation of the hip. The patient is then asked to stand on one leg which should result in gluteus medius muscle contraction on the weight bearing side and the contralateral pelvis should elevate on the unsupported side, indicating that the gluteus medius muscle on the weight bearing side is working properly (negative Trendelenburg sign). A positive Trendelenburg sign is recognized if the pelvis on the unsupported side does not elevate. Limb length should be measured as any significant discrepancy may predict a poor prognosis if due to head collapse. Early in the disease course, the x-rays will show increased density of the femoral head. With reossification of the femoral head, the deformity will become fixed in the new bone (25). Arthrography is often used to document true head deformity in the younger child especially in early phases of the disease (26). The differential diagnosis may be broad and careful selection of laboratory and radiographic studies should make the diagnosis clear. The primary goals in the treatment are to prevent deformity, to minimize growth disturbance, and to prevent degenerative joint disease. The critical concept is the containment of the femoral head in the acetabulum through the period of risk of deformity (19). Non operative treatment requires maintenance of sufficient range of motion through therapy and bracing protocols. Surgical treatment is oriented toward redirecting the softened femoral head into the acetabulum to cover the vulnerable regions and to provide a mold for femoral head remodeling (25,32). For the hip that cannot be contained in the socket, sophisticated surgical techniques are used to treat pain, length discrepancy, and restricted motion. Well controlled studies with uniform treatment protocols in patients matched for age, gender, degree of head involvement, and other factors are needed to determine direct management of this complex disease in the future. This condition is characterized by a displacement of the femoral head through the physeal plate. Since the femoral head is held securely in the acetabulum, the femoral neck displaces anteriorly causing an apparent varus deformity of the proximal femur. Weakening of the perichondral ring associated with puberty leads to a separation of the physis through the widened zone of hypertrophy. Boys are commonly affected between ages 9-16 years and girls are affected between 8-15 years of age. An antalgic gait or painful limp (Trendelenburg gait) with the foot turned outward is commonly seen. Whenever knee or thigh pain is the chief complaint, the hip must be thoroughly evaluated since the pathology may be originating from the hip. Due to the deformity of the femoral head, the hip will turn in external rotation to prevent impingement of the femoral neck on the acetabulum with hip flexion (obligate hip external rotation with flexion). The differential diagnosis includes trauma, infection, neoplasia, rheumatoid disease, avascular necrosis, congenital hip dysplasia or dislocation. The child should be restricted in his/her activity immediately after recognition of the problem.

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Peripheral anemia medicine 44291 buy 300 mg isoniazid, caused by the disease medications via peg tube safe 300 mg isoniazid, sends signals to the bone marrow to increase production of erythrocytes 8h9 treatment order 300 mg isoniazid free shipping. With time symptoms 2 months pregnant 300mg isoniazid overnight delivery, the marrow cavities (skull bones treatment ear infection discount 300mg isoniazid mastercard, facial bones symptoms 1974 order 300mg isoniazid otc, and ribs) expand, leading to the classical facial features and skull X-ray findings ("hair on end" in untreated patients due to excessive extramedullary hematopoiesis). Erythrocytes that do enter the circulation are noted to be abnormal by the reticuloendothelial system (spleen and liver), and are taken up by these organs with ensuing enormous hepatosplenomegaly. In untreated patients, death usually occurs by the end of the second decade of life from anemia and congestive heart failure. Currently, part of the standard treatment for beta thalassemia major is lifelong transfusions given every 2-4 weeks. The intent of these transfusions is to keep their hemoglobin trough above 9 or 10 gm/dl. With each milliliter of transfused packed red blood cells, the patient receives one milligram of elemental iron. Iron, in addition to being relatively difficult to absorb, is also not easily excreted. Regularly transfused patients need to be on lifelong chelation therapy to help their bodies excrete the excess iron. Currently, most regularly transfused thalassemia patients receive their chelation as a subcutaneous infusion of deferoxamine over 10 hours each night (lifelong). With the combination of transfusion and chelation therapy, life expectancy can to be normal. A form of alpha thalassemia occurs when any number of the four genes that control alpha globin production are missing, thereby causing an excess of non-alpha globin chains. The various forms of alpha thalassemia with their genetic correlate are listed below: A. Those with alpha thalassemia trait are clinically normal, but their hemoglobin is slightly low and their hemogram demonstrates microcytic indices. Their hemoglobin electrophoresis is normal unless it is done in the newborn period at which time Hemoglobin Barts is present (recall this finding in the case example at the beginning of the chapter). Traditionally, people with alpha thalassemia trait are taught that they have a benign condition and no further education is provided. There is suspected sustained morbidity in persons with thalassemia trait, who are on repeated, or continued iron supplementation. Additionally, such iron supplementation is generally useless, even in menstruating females, as their stores are readily replenished by a greater degree of absorption of dietary iron from the gut. Additionally, parents with this, so called, "benign" alpha thalassemia trait, can produce offspring with fatal hydrops fetalis if both parents pass on alleles with two defective alpha genes. In developed countries with otherwise good medical care, it is not a disease, but rather a condition. There are some rare variants, such as Hemoglobin H Constant Springs, (the Constant Springs is an abnormal gene, rather than a deletion, named after a U. These people are missing 2 genes from one allele, and have the severely dysfunctional Constant Springs gene on the other allele. People with Hemoglobin H need to avoid all forms of supplemental iron, and pregnant women need very close prenatal care for their own health matters. Since the bone marrow of thalassemia patients requires excess folic acid (due to erythroid hyperplasia), most clinicians advise Page 413 lifelong supplementation of 1 milligram daily of folic acid to avoid relative folate deficiency. During times of severe illness, or in pregnancy, the hemoglobin may drop significantly below baseline in Hemoglobin H disease, and a transfusion may be recommended. Again, iron is generally not deficient and, thus iron supplementation is not helpful, nor is it appropriate. In infants, gamma chains predominate over beta chains, and Hemoglobin Barts (four gamma chains) is formed. Hemoglobin H and Hemoglobin Barts are both useless, with no effective oxygen carrying capacity. There has been a lot of confusion between this abnormal Hemoglobin H (4 beta chains clumped together) and the clinical condition in which 3 alpha genes are missing, called "Hemoglobin H disease or condition". The abnormal Hemoglobin H exists (in varying amounts) in all 4 clinical alpha thalassemia categories. Similarly in newborns, Hemoglobin Barts exists in varying amounts in all alpha thalassemia categories. Hemoglobin H and Hemoglobin Barts do not cause the degree of ineffective erythropoiesis seen in beta thalassemia. Therefore, the classical "thal facies", "hair on end" skull X-rays, and enormous hepatosplenomegaly, all typical of beta thalassemia, are not seen to such degree in severe alpha thalassemia. Hemoglobin E results from a single amino acid substitution on the beta globin chains. However, when combined with beta thalassemia minor, significant anemia develops over time. Such people usually become transfusion dependent later in the first decade of life, and if treatment is not sought or maintained, early death is most likely. Homozygous Hemoglobin E usually causes mild microcytic hypochromic anemia, which resembles alpha thalassemia trait. In reference to the case presentation at the beginning of the chapter, what is the best approach to an otherwise healthy, asymptomatic 12 month old female with the hemoglobin of 9. Indicate whether iron supplementation is indicated or contraindicated in each of the following clinical situations. Beta thalassemia patient who just lost a modest amount of blood from a scalp laceration. Healthy alpha thalassemia trait male who wants to build up his hemoglobin to run a marathon. Menstruating female with alpha thalassemia trait who has had heavy and prolonged periods for the past year. Some ethnic groups with alpha thalassemia trait have a small risk of hydrops fetalis, but other groups have no risk. Liver injury to iron overload in thalassemia: histopatholoultrsstructural studies. Since the child had Hemoglobin Barts on the newborn screen, a form of alpha thalassemia is present. There is no need to do a hemoglobin electrophoresis, since the type of thalassemia (alpha) is already known. Additionally, Hemoglobin H is so fast moving that it is typically missed on routine hemoglobin electrophoresis, thereby giving "normal" results. In general, therefore, hemoglobin electrophoresis is typically useless in evaluating for alpha thalassemia. This patient and her family should be provided with genetic counseling and education. She should be counseled to avoid supplemental iron, as a true iron deficiency is extremely rare in Hemoglobin H thalassemia. If iron deficiency is ever suspected, iron studies should be done to clearly document a true deficiency before iron supplementation is started. The two most likely etiologies of the anemia in this young lady are iron deficiency or a form of thalassemia. In this case, the mild anemia would indicate a heterozygous beta thalassemia (beta thalassemia minor). If the hemoglobin electrophoresis is normal, or near normal, then alpha thalassemia is the most likely cause. Fe is contraindicated since it will not improve the hemoglobin and it will add to the potential for iron toxicity. Fe is contraindicated, since it will not improve his hemoglobin and it will add to the potential for iron toxicity. Despite the presence of thalassemia, iron deficiency is documented by laboratory studies, so iron supplementation is indicated until iron deficiency resolves. Once iron deficiency is no longer present, iron supplements become contraindicated. Her spleen in not palpated below the left costal margin, and her liver is palpated 2 cm below the right coastal margin. Her primary care physician is contacted to discuss the case and to determine whether she should be hospitalized. There are over 100 known hemoglobinopathies, but sickle cell disease remains the best described and is the prototype for all hemoglobinopathies. Sickle cell disease is a clinically significant condition which involves the sickle cell gene. However, it is important for these individuals to be aware of their trait status for purposes of genetic counseling. Historically, 10% of children with sickle cell diseases died before their 10th birthday, most often due to overwhelming infection. Survival and morbidity have been unpredictable, largely due to problems with disease recognition and availability of medical care. Therefore, sickle cell diseases are now identified on the newborn screen in almost all states. This permits a proactive approach to the health maintenance of these patients, resulting in less morbidity and mortality. The gene mutations for both sickle cell and hemoglobin C disease result in a single amino acid substitution on the beta globin chain. A valine substitution here results in hemoglobin S, while a lysine substitution in the same position results in hemoglobin C. A single sickle cell gene is carried by about 10% of African Americans and the gene for Hemoglobin C is carried by about 2% of African Americans. The normal hemoglobin electrophoresis in a person greater than 6 months of age shows about 92. Since the sickle cell gene produces an abnormal beta globin chain, hemoglobin S is comprised of 2 alpha globin chains and 2 abnormal beta globin chains. In the heterozygous state, the normal beta globin gene produces sufficient beta globin chains to produce enough normal hemoglobin A (asymptomatic heterozygous state). Likewise, hemoglobin C Page 415 consists of 2 alpha globin chains and 2 abnormal beta globin chains. Both hemoglobin S and hemoglobin C are also easily picked up on the newborn screen, which utilizes methods that separate out and identify various hemoglobins, abnormal and normal alike. Hemoglobin F (fetal hemoglobin) predominates in the normal newborn, and is completely replaced with hemoglobin A by 6 months of age. Since hemoglobin F has no beta globin chains, it is not affected by the sickle cell gene. On the newborn screen, hemoglobin S is identified quantitatively at birth in its relation to hemoglobin F. If more hemoglobin S than F is present, the child most likely has sickle cell disease. If more hemoglobin F than S is identified, the child likely has sickle cell trait. Sickle cell anemia occurs when both alleles of the beta globin gene on chromosome 11 are affected by a single amino acid substitution of valine for glutamic acid (resulting in hemoglobin S). The presence of hemoglobin S within the red blood cells causes an unnatural stiff folding, or sickling of the red blood cell, especially under conditions of oxidative stress. These sickled cells have a tendency to stack up on one another, and thus causes intravascular clogging in the microvasculature. This in turn leads to a vascular occlusion crisis with infarction of local tissue, and severe pain (vaso-occlusive crisis). The presence of sickle hemoglobin alone, decreases erythrocyte survival leading to chronic hemolytic anemia. The clinical syndromes as a result of this sickling vary depending on whether one is seeing a pediatric or adult patient. Sickle cell anemia does not present clinically before 6 months of age because of the protective effect from the uninvolved Hemoglobin F. But after 6 months of age, the usual clinical manifestations include infection (usually respiratory), failure to thrive, unexplained fever, and irritability. Before routine newborn screening for sickle cell disease, young children often presented with dactylitis (hand-foot syndrome), which is a swelling of the dorsum of the hands or feet, associated with pallor and fever. Since appropriate and prompt attention is given to symptoms such as fevers, pain, and swelling without a delay in diagnosis, children presenting with dactylitis from sickle cell anemia has become mostly a thing of the past. The pediatrician is most often confronted with infectious complications of sickle cell anemia. These children are especially prone to bacterial infections such as pneumococcus, Haemophilus influenzae B and Salmonella. Historically, infections have been the primary cause of death during early childhood. One reason for the high rate of infections in children with sickle cell disease is that they are functionally asplenic. Because the spleen acts as a sponge for these abnormal sickled cells, subclinical intermittent episodes of intrasplenic vaso-occlusion occur causing local splenic infarcts. Therefore, by the age of 8 years, sickle cell patients are completely functionally asplenic (due to infarction). All sickle cell patients are given prophylactic penicillin, especially during childhood. Additionally, by now identifying children with sickle cell disease at birth, prophylactic pneumococcal vaccine, plus strict attention to the routine childhood vaccinations have been shown to dramatically decrease childhood morbidity and mortality from infection. Rarely, infants have massive splenic congestion of red blood cells called the splenic sequestration crisis. When this occurs, it is frequently fatal, since it rapidly removes enormous amounts of red blood cells from the circulation, which can lead to circulatory collapse. A pain crisis is one of the most common reasons for hospitalizing an older child with sickle cell anemia. In a pain crisis, a specific limb or other body part is affected by the vaso-occlusive effects of the sickling cells in the microvasculature.

A quick and easy method that I have devised to calculate how many "cc/kg" of any dextrose solution to draw up in order to administer 0 medicine remix order genuine isoniazid. The answers to these questions will provide valuable information about: a) the severity of the ingestion treatment atrial fibrillation buy cheap isoniazid 300mg on-line. If at all possible have a family member bring the bottle medications covered by medicare order isoniazid 300mg on line, box or container of the suspected toxin to the emergency department so that you yourself can verify the specific product and active ingredients medicine 834 buy isoniazid in united states online. Local poison Page 501 control centers have computerized data bases of over a million substances medicine 2020 300mg isoniazid sale, which can be accessed via a specific product name or via the individual active ingredients symptoms 2 dpo isoniazid 300 mg online. If the suspected ingestion involved a plant, have a family member bring in as much of the actual plant for identification. If the time from the ingestion to the time of arrival to the emergency department is within 1-2 hours, gastric lavage may be beneficial. In general, gastric lavage is not very effective if performed more than two hours post-ingestion. Knowing the time of the ingestion is also necessary when attempting to interpret specific drug levels. For example, an acetaminophen level of 100 mcg/ml cannot be interpreted and plotted on the nomogram unless the time of ingestion as well as the time of the blood draw are known. The level of 100 mcg/ml may not be toxic if it was obtained two hours post-ingestion, whereas the very same level would be considered toxic if it was obtained 20 hours post-ingestion. Often, the most difficult aspect of the toxicologic history for the parents to answer is regarding the exact amount of the toxin or drug that may have been ingested. When confronted with this dilemma, the physician should always assume the worst case scenario rather than minimizing the amount that may have been potentially ingested. The physician must be a medical detective in some aspects when attempting to estimate how much the child may have ingested. For example, if a child presents to the emergency department after potentially ingesting some tablets, questions which could be asked include the following (3): a) Was the medication just recently purchased, and if so was the bottle completely full prior to the child getting to the pills Once the total milligrams of the potential ingestion has been determined, then one must calculate how much was ingested in mg/kg to determine severity potential. Although the majority of the substances that are typically ingested by children are either nontoxic or mildly toxic, there are a few substances that can potentially be fatal even when ingested in very small amounts. Some of these highly toxic substances with the corresponding amounts which could potentially be lethal for a 10 kg child are: amanita phalloides (one mushroom), amphetamines, antimalarials (one chloroquine tablet), calcium channel blockers (one nifedipine tablet), camphor (one teaspoon), clonidine (one 0. Toxic ingestions in children typically present to an emergency department in one of two scenarios. The first is that of a child who presents with a witnessed or suspected ingestion. The second scenario is that of a child who presents with a constellation of signs and symptoms which may include the possibility of a toxic ingestion within the working differential diagnosis. The following is my quick and easy to remember method of simplified pediatric vital signs (5). Heart rate Respiratory rate Newborn to 1 year old 140 40 1 year old to 4 years old 120 30 4 years old to 12 years old 100 20 > 12 years old 80 15 the key elements of a toxicologic physical examination include the following elements (3): a) Eyes: pupillary size, symmetry and response to light presence of nystagmus (vertical or horizontal). Toxidromes refer to a specific constellation of signs and symptoms which one may expect to see with a specific class or type of toxic substance. The five distinct toxidromes and the common toxins of each of the toxidromal classes are listed below (3): 1. Page 502 In 1985 ipecac administration was recommended in 15% of the poisoning cases handled throughout the country by the American Association of Poison Control Centers. However the recommended use of ipecac in the home has continually declined over the past several years to only 0. Because of this, the American Academy of Pediatrics Committee on Injury and Poison Prevention is currently recommending that syrup of ipecac no longer be used as a poison treatment intervention in the home setting. Gastric lavage provides a quicker, more controlled and safer route of gastric emptying than ipecac. The typical method of performing gastric lavage is to perform lavage with saline until the retrieved gastric contents are clear, then activated charcoal with sorbitol is instilled down the lavage tube. Gastric lavage by itself is only effective at removing toxins that are still within the stomach. Lavage is not capable of removing any toxins that have already passed into the small intestines. Thus, because large orogastric lavage tubes cannot always be safely placed in children, the option of gastric lavage may not be feasible and/or effective in smaller children. However, when the ingested substance is a liquid preparation, then a smaller sized tube would be sufficient, although it must be performed much sooner in order to be effective since liquid preparations are more quickly absorbed than pills or tablets. Activated charcoal is very effective at adsorbing many ingested toxins and thereby prevents systemic toxicity. The majority of activated charcoal preparations currently available have adsorptive surface areas of 1,000 square meters per gram of charcoal. Some of the newer "super" adsorptive activated charcoal preparations reportedly have up to 2,000 square meters of adsorptive surface area per gram of charcoal. Because activated charcoal is able to prevent systemic toxicity by effectively binding so many different ingested toxins, many poison control centers have been recently recommending the administration of activated charcoal alone (without first performing gastric lavage) for ingestion cases of mild to moderate severity. Although activated charcoal has been sometimes referred to as the "universal antidote" because it adsorbs so many different toxins, there are nine scenarios in which activated charcoal may not be clinically effective. Even though charcoal has a very low affinity for cyanide, it may still be effective in preventing systemic cyanide toxicity if the amount of cyanide ingested is within the 100-500 mg range. Although charcoal is not necessary for ingestions of plain hydrocarbons, it should be considered if the ingested hydrocarbon contains systemic toxins. If the ingested hydrocarbon does not pose any risk in terms of systemic toxic effects, charcoal administration should be avoided because the charcoal may predispose the patient to vomiting, which will definitely worsen the aspiration toxicity of the hydrocarbon. Although charcoal is very effective at adsorbing camphor, the administered charcoal may not be very effective depending on the time that the child presents to the emergency department. Because the majority of camphor containing products are typically found in liquid preparations, by the time the child presents to the emergency department, most of the liquid camphor has already been completely absorbed from the stomach and therefore there will be nothing left for the activated charcoal to adsorb. However if the child presents to the emergency department with 30 minutes after ingesting a potentially toxic amount of camphor, gastric lavage should probably be attempted in order to prevent systemic toxicity. Multiple doses of activated charcoal (without cathartics) are sometimes used as a method of "gastrointestinal dialysis" for certain drugs that undergo enterohepatic circulation. Cathartic agents by themselves are not a very effective method of gastrointestinal decontamination. The main role of cathartics is to more quickly eliminate the charcoal bound toxin complex from the intestines before the toxins have the opportunity to dissociate from the activated charcoal. Sorbitol is the most commonly used of the cathartics because of its rapid gastrointestinal transit time. Sorbitol also comes premixed with activated charcoal ranging from 27-48 grams of sorbitol per 120 milliliter bottle of activated charcoal. Sorbitol can be safely used in children as long as it is administered only once per 24 hours and the stool output and the cardiovascular and hydration status are closely monitored. Adults and teenagers can be given 1-2 liters of GoLytely per hour via a nasogastric tube until the ingested toxin is completely eliminated per rectum and the rectal effluent is clear in color. Although there are multiple methods available to enhance the elimination of specific toxins from the body, the majority of pediatric poisoning cases can be treated with one or more of the decontamination methods mentioned above. The urinary pH can be manipulated in order to enhance the urinary excretion of certain drugs and toxins. Other more complex methods of enhanced elimination techniques include peritoneal dialysis, hemodialysis and hemoperfusion. The exact laboratory tests which one would obtain in a poisoning case will depend upon the specifics of each individual case as well as the overall severity of the case. Although blood and urine toxicologic screens and specific drug levels may be obtained, the results of these studies typically are not available for several hours. Once the results Page 503 of the electrolyte panel are known, one can also calculate the anion gap, which may provide helpful clues to the potential toxin in cases of the unknown or suspected ingestion. Another very useful laboratory study is the measured serum osmolality and the serum osmolar gap. Substances that classically elevate the measured serum osmolality (which are not part of the calculated osmolality) include the alcohols. Thus a patient who has ingested one of the alcohols will typically exhibit an elevated measured serum osmolality despite a normal calculated serum osmolality. The serum osmolar gap (measured serum osmolarity minus the calculated serum osmolarity) should be <5-10 mosm/Liter. This factor will differ if the alcohol involved is something else such as ethylene glycol or methanol. Although the majority of poisoning cases do not require any specific antidotes, some of the common toxins with antidotes are: acetaminophen (N-acetylcysteine), benzodiazepines (flumazenil), calcium channel blockers (calcium chloride), carbon monoxide (oxygen), cholinergics (atropine +/ pralidoxime), cyanide (cyanide antidote kit), cyclic antidepressants (sodium bicarbonate), digoxin (digoxin immune Fab antibodies), ethylene glycol or methanol (fomepizole), iron (deferoxamine), methemoglobinemia (methylene blue), opiates (naloxone), phenothiazine induced dystonic reactions (diphenhydramine), salicylates (sodium bicarbonate). Because the majority of pediatric nonintentional ingestions typically do not involve highly toxic substances and/or large amounts, the majority of children who present to the emergency department with an accidental overdose can be safely discharged after a thorough assessment and an adequate period of observation. Hospitalization should be considered for the following situations: a) Severe signs and symptoms upon presentation to the emergency department. Since prevention is the best method of reducing accidental poisoning in children, physicians should routinely incorporate poison prevention guidelines/tips into their healthcare maintenance discussions with their parents. Some of these points are listed below: a) Keep the phone number of your local poison control center near the telephone. The majority of accidental ingestions in the pediatric population occur in which age group Immediately give the child eight ounces of water or milk to dilute the concentration of pills in his stomach. Advise no interventions at the present time, but also advise her that if the child should begin to develop any symptoms to go to the emergency department for further treatment. The gastrointestinal decontamination method of choice for a child who presents to the emergency department with multiple episodes of vomiting two hours after ingesting a toxic amount of iron is: a. A child with a suspected ingestion presents to the emergency department with delirium, tachycardia, mydriasis, dry mucus membranes and warm/dry skin. A parent suspects that her 18 month old son may have accidentally ingested a few pellets of rat poison. Not panic and simply wait to see if her son develops any signs and symptoms of toxicity before calling her pediatrician. Call her local poison control center immediately for advice, rather than waiting to see if her son will develop signs and symptoms of toxicity. Rush her son to the nearest emergency department for immediate gastric lavage and activated charcoal. Clinical pearls in pediatric toxicology: A systematic approach to the poisoned child. Abstract from the American Academy of Pediatrics Committee on Injury and Poison Prevention, July 2001. Her mother reports that she (the patient) had an argument with her boyfriend last night. There are 8 tablets remaining in the bottle (maximum 11 grams of acetaminophen ingested). Her abdomen is soft, with normoactive bowel sounds, minimal epigastric tenderness, no rebound, and no guarding. Because acetaminophen is an ingredient found in many over-the-counter cold medications, it should be considered in intentional overdoses, as the patient may not realize that it is one of the components in the combination product taken. Acetaminophen is metabolized in the liver via glucuronidation, sulfation, and through the cytochrome P-450 pathway. The majority of acetaminophen is metabolized via the sulfation and glucuronidation pathways into nontoxic products which are then excreted via the urine. In children 1 to 5 years, severe liver toxicity is rare with a single ingestion of acetaminophen, for reasons which are unclear. In stage I (first 24 hours), the patient may have symptoms of anorexia, nausea, and vomiting. The patient may have vomiting, jaundice, abdominal pain, bleeding, confusion, lethargy, or even be in a coma. The patient may have coagulation defects, such as disseminated intravascular coagulopathy. In the management of acetaminophen ingestions the, basic principals of toxicology are followed. If it was an intentional ingestion, acetaminophen and aspirin levels should be obtained. Patients may present stating that they took "aspirin" when in fact they took acetaminophen. Blood and urine toxicologic screens should be done as well as a pregnancy test if the patient is a menstruating female. If the patient presents with altered level of consciousness, a co-ingestion must be suspected because acetaminophen does not produce any changes in mental status. Syrup of ipecac is not used as a form of gastrointestinal decontamination in the emergency department setting. Gastric lavage in a patient who presents to the emergency department is controversial. There are some toxicologists who feel that gastric lavage has not been proven to be helpful and should be used only if the ingestion is potentially rapidly fatal and the patient presents to the emergency department within 1 hour of the ingestion. Another controversial area in the management of acetaminophen ingestion is activated charcoal administration. With intentional overdoses, there may be other occult co-ingestants that may be inactivated by the charcoal. For single acetaminophen ingestions a Rumack-Matthew nomogram is used to estimate the severity of the poisoning. The serum acetaminophen concentration is plotted against the time (hours) post-ingestion.