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A physical or occupational therapist can offer adaptive devices or techniques to help the child accomplish these tasks. Furthermore, radial deficiency- incomplete formation of the radius-is associated with numerous syndromes, further emphasizing the need for a thorough investigation (Table 1). This mild deficiency may go unrecognized, and many individuals with this type of deficiency are not diagnosed until later in life when everyday activities such as buttoning a shirt or tying shoes have become more difficult. This deficiency is more involved and is characterized by a narrowing of the web space between the thumb and index finger, 102 Chapter 5: Hand and Arm Abnormalities absence of the thenar (thumb) muscle at the base of the thumb, and instability of the metacarpophalangeal joint in the middle of the thumb (Figures 1A and B). A) Absent thenar muscles; B) Narrowed thumb-index web space with instability of the metacarpophalangeal joint. These abnormalities usually involve tendons that arise within the forearm and travel into the thumb. This type of deficiency, known as a pouce flottant (floating thumb) or residual digit, lacks bones and muscles and is mainly comprised of skin and soft tissue (Figure 2). Figure 2 (see Figure legend on next page) 103 Fanconi Anemia: Guidelines for Diagnosis and Management Figure 2. The thumb classifications listed above can guide treatment recommendations, as shown in Table 2 (3,4, 5). Tendon transfer improves the active motion and function of the thumb and has a negligible effect on the donor finger (Figure 4B). A) Z-plasty of the narrowed thumb-index web space; B) tendon transfer to overcome the deficient thenar muscles; C) ligament reconstruction to stabilize the metacarpophalangeal joint instability. In cases with severe instability, fusion of the joint may be the best option to provide a stable thumb for firm grasps. The main distinction between a thumb that can be surgically reconstructed and a thumb that requires amputation is the presence or absence of a stable base. The decision to remove a hypoplastic thumb without a stable base is often a difficult process for parents and caregivers. Discussions with the surgeon and conversations with families who have made similar decisions are often helpful to parents tasked with making this decision for their child (Video 1 in online supplementary information). An X-ray of a 2-year-old child reveals a thumb metacarpal that tapers to a point, indicative of an unstable carpometacarpal joint. The right index-long web space has widened and the index has rotated out of the palm. Because an opposable thumb is critical for manipulating many objects, a functional replacement can be constructed by surgically moving the index 106 Chapter 5: Hand and Arm Abnormalities finger and its nerves, arteries, tendons, and muscles to the thumb position. This age range remains controversial, however, and there has been a trend toward surgery between 6 months to 1 year of age, which is prior to the normal development of oppositional or fine pinch at about 15 months of age. Surgery can be safely performed in patients who have platelet counts greater than 80,000. In reality, parents should not feel pressured to make an immediate decision about surgery for their child; some children undergo successful surgery during adolescence. Pollicization requires meticulous surgical technique because the index finger must be shortened, rotated, and reconstructed with the index muscles to give the appearance and function of a thumb (Figure 7). Pollicization of the index finger requires careful surgical technique to give the appearance and function of a thumb. The differentiation is further complicated by the delayed maturation of the bones at the base of the thumb; these bones (the trapezium and trapezoid) do not finish developing until 4 to 6 years of age. Ultrasound imaging shows promise as a tool for defining the anatomy without the need for anesthesia. A thumb metacarpal (the bone that connects the thumb to the wrist) that tapers to a point at the base of the metacarpal is also indicative of an unstable carpometacarpal joint (Figure 6). The outcome of pollicization is directly related to the status of the index finger prior to surgery: A mobile index finger can provide stability for grasp and mobility for fine pinch, whereas a stiff index finger will provide a stable thumb for coarse grasping, but fine pinching will be unlikely (Figure 8; Video 2 in online supplementary material). Good results shortly after pollicization have been shown to persist into adulthood (6,7). Figure 8A Figure 8B (see Figure legend on next page) 108 Chapter 5: Hand and Arm Abnormalities Figure 8. A) Thumb used for grasping large objects; B) mobile thumb incorporated into fine pinch.

Other approaches are linked to the revealed behavior of either individuals or governments. The magnitude of the higher wage relative to the decrease in life expectancy provides an estimate of how the employee values the risk. An alternative the economics of adressing nutritional anemia 21 approach to valuing reduced mortality is based on the behavior of governments. In particular, the resources actually used in a society to avert a death provide an estimate of the average value that the public places on averting a death (4). These two approaches generally result in estimates that are far apart, but as they measure different things they cannot be directly compared. Other studies report sensitivity estimates and details on the underlying assumptions, so that it is possible to see if the economic rationale for an investment changes over a reasonable range of presumed values for deferred mortality (5). As with any analysis of causality, it is necessary to distinguish the specific consequences of anemia from its correlates when determining the expected benefits from a specific intervention. This is less of an issue with respect to contemporaneous impacts of anemia on productivity, since there are experimental approaches that have been used to directly assess changes in productivity. In such cases, however, it is still important to determine the incentive structure a beneficiary faces; a capacity for increased work does not necessarily translate into increased effort unless there are incentives for the worker to increase performance. Still, it is comparatively straightforward to assign a value to the output from increased effort, controlling for economic context. The impact of improved iron status during childhood on subsequent adult productivity, however, is seldom obtained directly from experimental evidence. In the absence of longitudinal studies that track experimental interventions over decades, in order to estimate the economic impact of increased cognitive development due to supplementation or fortification in childhood, it is necessary to draw upon the general literature on productivity enhancement. Using the same data set, but a different measure of ability, another study shows that the net impact of ability is both the direct impact on wages as well as the impact that works through schooling choices (9). This study found that a half standard deviation decline in this measure leads 1 Non cognitive skills may have as much, or more, impact on earnings. However, while these may be influenced by developmental programs, it is less clear that they are malleable to micronutrient interventions. The point estimate drops by two thirds in estimates that include both years of schooling as well as achievement in school, both of which are indirectly affected by ability. Since improvements are the result of intervention in childhood, for any comparison of the program costs of such benefits, it is necessary to account for the time lag between the intervention and the stream of benefits. Benefits incurred at different times have to be given different economic values, due to the fact that monetary intervention carries a greater long-term impact if it takes effect early in life rather than later. This is also because the sooner it is obtained, then economic benefits can be reinvested and further productive returns gained. Unfortunately, although the rationale for discounting future benefits is not in dispute, there is no unambiguous way to determine this discount rate. All discount rates reduce the present value of future benefits relative to current costs; the larger the discount rate, the greater the importance given to immediate returns. A final consideration before discussing the potential economic benefits as well as the cost of interventions in addressing iron deficiency anemia is whether low income countries can expect that robust income growth will address the need for interventions at all. Even though it is currently widespread, if anemia were to decline rapidly in concurrence with progress in providing equitable growth, it might be a moot point to prioritize programs which tackle iron deficiency. For example, for every 10% increase in income per capita, the percentage of underweight children declines by 5%; a similar estimate undertaken for this paper using data from Mason, Rivers and Helwig (13) shows that a 10% increase in income per capita is associated with a decline of only 2. This estimate also reveals a slight trend in lower rates of anemia over time, after controlling for national incomes. As indicated, the share of children in the upper income quintile that are underweight is less that half the share in the lower income group.

Although their erythrocytes were more sensitive to peroxide-induced hemolysis, overt anemia did not develop. It was not until the mid1960s that vitamin E deficiency was described in children with fat malabsorption syndromes, principally abetalipoproteinemia and cholestatic liver disease (99). By the mid-1980s, it was clear that the major vitamin E deficiency symptom in humans was a peripheral neuropathy characterized by the degeneration of the large caliber axons in the sensory neurons (99). This neurodegeneration is apparent as a cause of the ataxia that is observed in these subjects. Deficiency symptoms Vitamin E deficiency was first described in rats in 1922 by Evans and Bishop (95). Deficiency symptoms in various animal species were described by Machlin in his comprehensive book on vitamin E 164 M. Similarly, peripheral neuropathy likely occurs due to free radical damage to the nerves (74). Chronic under consumption of vitamin E will lead to overt vitamin E deficiency symptoms if the -tocopherol levels in target tissues. Thus, children historically have been the susceptible population in which vitamin E deficiency has been observed. Elderly have been suggested to suffer vitamin E inadequacy, causing immune dysfunction (102). It should be emphasized that subjects with peripheral neuropathies, especially those with ataxia or retinitis pigmentosa, should be evaluated to assess if they are vitamin E deficient because these are recognized symptoms that occur with vitamin E deficiency. The symptoms are characterized by a progressive peripheral neuropathy with a specific "dying back" of the large caliber axons of the sensory neurons, which results in ataxia (105). Importantly, vitamin E supplementation stops or slows the progression of retinitis pigmentosa caused by vitamin E deficiency (108). Vitamin E deficiency caused by genetic defects in lipoprotein synthesis Vitamin E deficiency is also caused by genetic defects in lipoprotein synthesis that result in fat malabsorption. These patients have steatorrhea from birth because of the impaired ability to absorb dietary fat, which also contributes to their poor vitamin E status. Clinical features also include retarded growth, acanthocytosis, retinitis pigmentosa and a chronic progressive neurological disorder with ataxia. The acanthocytosis is a spicular shape to the erythrocytes, likely due to abnormal cholesterol distribution in the membrane. Nonetheless, it is important to note that this disorder, which is associated with poor vitamin E status, is also associated with abnormalities in erythrocyte function. Clinically, both hypobetalipoproteinemic or abetalipoproteinemic subjects become vitamin E deficient and develop a characteristic neurologic syndrome, a progressive peripheral neuropathy, if they are not given large vitamin E supplements (approximately 10 g per day) (109, 110). Despite low plasma concentrations, adipose tissue -tocopherol concentrations reach normal levels in patients given large (10 g/day) vitamin E doses (110). Vitamin E deficiency caused by fat malabsorption Vitamin E deficiency also occurs secondary to fat malabsorption because vitamin E absorption requires biliary and pancreatic secretions. Failure of micellar solubilization and malabsorption of dietary lipids leads to vitamin E deficiency in children with chronic cholestatic hepatobiliary disorders, including disease of the liver and Oxidative stress and vitamin E in anemia 165 anomalies of intrahepatic and extrahepatic bile ducts (73). Children with cholestatic liver disease, who have impaired secretion of bile into the small intestine, have severe fat malabsorption. Neurologic abnormalities, which appear as early as the second year of life, become irreversible if the vitamin E deficiency is uncorrected (30, 73, 111). Children with cystic fibrosis can also become vitamin E deficient because the impaired secretion of pancreatic digestive enzymes causes steatorrhea and vitamin E malabsorption, even when pancreatic enzyme supplements are administered orally (73). It should be emphasized that any disorder that causes chronic fat malabsorption can lead to vitamin E deficiency. Thus, generally poor intake of nutrients in combination with chronic diarrhea in children could lead to vitamin E deficiency, if the fat malabsorption is sufficiently severe and the child has low -tocopherol body stores. However, fat malabsorption has been reported as a confounding clinical observation during recovery from extreme malnutrition (127). Therefore, Vitamin E status in humans can be compromised during anemia as a result of the oxidative stress caused by erythrocyte hemolysis. Antioxidant molecules and enzymes mentioned vide supra critically maintain the redox balance in the erythrocytes that contain high hemoglobin-bound iron concentrations. Anemia, especially during release of free iron in hemolytic anemia, increases the oxidative stress and iron toxicity (116).

As a result, the adequacy of complementary foods to provide some or all of these nutrients may have important effects on child development. Atopic diseases, including food allergy and allergic skin disease, are relatively common in the United States, with an estimated 5 to 8 percent of children experiencing confirmed food allergies11 and approximately 30 percent of the U. Finally, it is important to recognize that how infants and toddlers are fed, not just what they are fed, can influence health outcomes. What is the relationship between complementary feeding and growth, size, and body composition? What is the relationship between complementary feeding and food allergies and atopic allergic diseases? What is the relationship between types of dietary fats consumed during infancy and toddlerhood and risk of cardiovascular disease? What is the relationship between seafood consumption during infancy and toddlerhood and risk of cardiovascular disease and neurocognitive development? The conclusion statements that answer these questions were taken directly from the existing systematic reviews and the wording reflects the findings of those reviews, which included articles published between 1980 and 2016 or 2017 depending on the review. A description of the process the Committee used to determine that these existing systematic reviews were relevant to their questions and timely enough to not require updating is provided in Part C. In addition, detailed information about the methodology used to complete these systematic reviews can be found at the following website: nesr. Chapter 5: Foods and Beverages Consumed During Infancy and Toddlerhood Methodology specific to Question 6 is in Part D. Chapter 12: Added Sugars and methodology specific to Questions 7 and 8 is in Part D. These questions intended to examine the consumption of added sugars, dietary fats, and seafood in infants and toddlers as well as other age groups. Grade: Moderate Limited evidence suggests that introducing complementary foods or beverages before age 4 months of age may be associated with higher odds of overweight or obesity. Grade: Limited There is not enough evidence to determine the relationship between introduction of complementary foods or beverages at 7 months of age or older on growth, size, or body composition. Grade: Grade Not Assignable Conclusion Statements and Grade Types and Amounts of Complementary Foods or Beverages Moderate evidence indicates that higher vs lower meat intake or meat vs iron-fortified cereal intake over a short duration (about 3 months) during the complementary feeding period does not favorably or unfavorably influence growth, size, and/or body composition [Grade: Moderate]. There is insufficient evidence to determine a relationship between meat intake and prevalence/incidence of overweight or obesity. Chapter 5: Foods and Beverages Consumed During Infancy and Toddlerhood Limited evidence suggests that type or amount of cereal given does not favorably or unfavorably influence growth, size, body composition, and/or prevalence/incidence of overweight or obesity. Grade: Grade Not Assignable 1 Moderate evidence suggests that consumption of complementary foods with different fats and/or fatty acid composition does not favorably or unfavorably influence growth, size, or body composition [Grade: Moderate]. There is not enough evidence to determine a relationship between consumption of complementary foods with different fats and/or fatty acid composition and prevalence/incidence of overweight or obesity. Limited evidence suggests that sugar-sweetened beverage consumption during the complementary feeding period is associated with increased risk of obesity in childhood, but is not associated with other measures of growth, size, and body composition. Grade: Limited Limited evidence showed a positive association between juice intake and infant weight-forlength and child body mass index z-scores. Grade: Limited No conclusion could be made about the relationship between other complementary foods (vegetables, fruit, dairy products and/or cow milk, cereal-based products, milk-cereal drink, and/or categories such as "ready-made foods") and growth, size, body composition, and/or prevalence/incidence of overweight or obesity. Grade: Grade Not Assignable No conclusion could be made about the relationship between distinct dietary patterns during the complementary feeding period and growth, size, body composition, and/or prevalence/incidence of malnutrition, overweight or obesity. Chapter 5: Foods and Beverages Consumed During Infancy and Toddlerhood Question 2. What is the relationship between complementary feeding and developmental milestones, including neurocognitive development? Grade: Grade Not Assignable Conclusion Statements and Grade Types and Amounts of Complementary Foods or Beverages There was insufficient evidence to draw a conclusion about the relationships between types and amounts of complementary foods and beverages consumed and developmental milestones. However, a conclusion could not be drawn due to low generalizability and heterogeneity in exposures, observed effects, and potential confounding.