I have an XML like below
<list id="list01" list-type="roman-upper"><list-item id="item01"><p id="p01"><bold>Intensive care</bold></p>
<list id="list02" list-type="alpha-upper">
<list-item id="item02"><p id="p02"><bold>Definition</bold></p>
<list id="list03" list-type="number"><list-item id="item03"><p id="p03">There is no clear definition of this condition.</p></list-item>
<list-item id="item04"><p id="p04">It is referred to by multiple names, most commonly osteopenia of prematurity, metabolic bone disease of prematurity, or rickets of prematurity.</p></list-item>
<list-item id="item05"><p id="p05">Each of these names implies somewhat different characteristics of the clinical (rickets), laboratory (metabolic bone disease), or radiological (osteopenia and rickets) findings.</p></list-item>
<list-item id="item06"><p id="p06"><bold>In practical terms,</bold> it is the presence of radiological rickets or fractures that determines the clinical symptomatology. However, markedly abnormal laboratory values, including a very high alkaline phosphatase activity are concerning and may require clinical intervention.</p></list-item>
</list></list-item>
<list-item id="item07"><p id="p07"><bold>Incidence</bold></p>
<list id="list04" list-type="number"><list-item id="item08"><p id="p08">As this is not a reportable condition, the incidence is unknown and would depend on which type of definition is used.</p></list-item>
<list-item id="item09"><p id="p09">For example, an elevated alkaline phosphatase, indicative of metabolic bone disease is nearly universal in very low birthweight infants and as such it is not really possible to identify a true upper limit of normal for the serum alkaline phosphatase activity in preterm infants.</p></list-item>
<list-item id="item10"><p id="p10">Clinically apparent fractures are uncommon.</p></list-item>
<list-item id="item11"><p id="p11"><bold>In general,</bold> it has been suggested that low bone mass is present in about half of all VLBW infants, but true rickets is likely much less common in this population except in infants <600 g birthweight, where it may reach 50%. Using modern nutritional methods of providing minerals to infants, the incidence of clinically significant low bone mass is probably about 10% of VLBW infants but this number cannot readily be verified.</p></list-item>
</list></list-item>
<list-item id="item12"><p id="p12"><bold>Pathophysiology</bold></p>
<list id="list05" list-type="number">
<list-item id="item13"><p id="p13">VLBW infants have an extremely high requirement of calcium and phosphorus, the principal components of bone mineral. This need cannot be met using unfortified human milk.</p></list-item>
<list-item id="item14"><p id="p14"><bold>Vitamin D deficiency is not a primary cause of LBM in VLBW infants.</bold></p></list-item>
<list-item id="item15"><p id="p15">However, in full-term infants with malabsorptive problems, such as intestinal failure/short gut and/or cholestatic liver disease, vitamin D deficiency may play an important role in inadequate mineral absorption and bone mass growth.</p></list-item>
<list-item id="item16"><p id="p16">The rare preterm infant with significant renal failure may also present with multiple problems related to bone minerals, including low serum calcium, high serum phosphorus, low vitamin D status, and bone demineralization.</p></list-item>
</list></list-item>
<list-item id="item17"><p id="p17"><bold>Risk factors</bold></p>
<list id="list06" list-type="number"><list-item id="item18"><p id="p18">Clinically important risk factors during hospitalization are those that might decrease mineral intake or absorption or increase mineral excretion.</p></list-item>
<list-item id="item19"><p id="p19">Specifically, these primarily include</p>
<list id="list07" list-type="bullet">
<list-item id="item20"><p id="p20">The use of unfortified or inadequately fortified human milk</p></list-item>
<list-item id="item21"><p id="p21">Frequent use of loop diuretics</p></list-item>
<list-item id="item22"><p id="p22">Use of steroids</p></list-item>
<list-item id="item23"><p id="p23">Fluid restriction</p></list-item>
</list>
<p id="p24">It is impossible in many circumstances to be certain about the most important of these factors, but infants in the NICU frequently encounter more than one of these risks.</p></list-item>
<list-item id="item24"><p id="p25">In many cases, it is lower mineral intake, not bioavailability or even increased renal calcium excretion by loop diuretics (eg, furosemide), which is the principal problem.</p></list-item>
</list></list-item>
<list-item id="item25"><p id="p26"><bold>Clinical presentation</bold></p>
<list id="list08" list-type="number">
<list-item id="item26"><p id="p27"><bold>Signs and symptoms</bold></p>
<list id="list09" list-type="alpha-lower">
<list-item id="item27"><p id="p28">There are often few if any clinical signs in high-risk neonates.</p></list-item>
<list-item id="item28"><p id="p29">Physical signs of rickets or fractures can be present, however, and are similar to those seen in older children. Specifically, bone or joint swelling can occur.</p></list-item>
<list-item id="item29"><p id="p30">Classic signs such as bowing of the legs, frontal bossing, rachitic rosary, and craniotabes are generally difficult to appreciate in the newborn period, especially in preterm infants.</p></list-item>
</list></list-item>
<list-item id="item30"><p id="p31"><bold>Condition variability</bold></p>
<p id="p32">There is considerable variability in the severity and course of neonatal bone demineralization, mostly related to the ability to intervene with additional calcium and phosphorus.</p></list-item>
</list></list-item>
<list-item id="item31"><p id="p33"><bold>Diagnosis</bold></p>
<list id="list10" list-type="number">
<list-item id="item32"><p id="p34"><bold>Biochemical evidence</bold></p>
<p id="p35">Severe bone loss leading to rickets is generally suggested by an extremely high serum alkaline phosphatase, generally >800 IU/L, which is often accompanied by a low serum phosphorus <3.5 to 4.0 mg/dL. These biochemical findings are not diagnostic, however, and the ultimate determination of severe bone demineralization or rickets must be done radiographically.</p></list-item>
<list-item id="item33"><p id="p36"><bold>Radiographic evidence</bold></p>
<list id="list11" list-type="alpha-lower">
<list-item id="item34"><p id="p37">Up to about 40% bone loss may not have any clear signs on radiographic examination.</p></list-item>
<list-item id="item35"><p id="p38">Nonspecific radiological reports using terms such as “washed-out bones” have little if any definitive meaning in patient care.</p></list-item>
<list-item id="item36"><p id="p39"><bold>Radiological rickets</bold> can and should be identified when present using wrist or knee films that demonstrate bone changes compatible with rickets that would also be seen in older children.</p></list-item>
<list-item id="item37"><p id="p40"><bold>Consider performing a wrist or knee x-ray</bold> if the alkaline phosphatase exceeds 1000 IU/L or there are repeated values above 800 IU/L.</p></list-item>
<list-item id="item38"><p id="p41">The use of bone ultrasound or bone mineralization techniques remains experimental at this time for preterm infants and newborns.</p></list-item>
</list></list-item>
<list-item id="item39"><p id="p42"><bold>Consider alternative diagnoses</bold></p>
<list id="list12" list-type="alpha-lower"><list-item id="item40"><p id="p43">Rarely another diagnosis may be considered in very preterm infants that is not the typical low mineral intake form of low bone mass or rickets.</p></list-item>
<list-item id="item41"><p id="p44">Preterm infants can also have osteogenesis imperfecta, hyperparathyroidism, or any of several genetic syndromes associated with low bone mass.</p></list-item>
<list-item id="item42"><p id="p45">These are usually considered when there are multiple fractures or severe rickets without a typical history of low mineral intake.</p></list-item>
<list-item id="item43"><p id="p46">It may occasionally be of value to obtain a screening serum parathyroid level, although these can be difficult to interpret as normal values are not well established in infants.</p></list-item>
</list></list-item>
</list></list-item>
<list-item id="item44"><p id="p47"><bold>Management</bold></p>
<list id="list13" list-type="number">
<list-item id="item45"><p id="p48"><bold>Medical</bold></p>
<p id="p49">Medical management relies on (a) improving nutrient intake relative to key minerals and (b) decreasing losses of key nutrients.</p>
<list id="list14" list-type="alpha-lower">
<list-item id="item46"><p id="p50"><bold>First, consider improving nutrient intake.</bold></p>
<list id="list15" list-type="bullet"><list-item id="item47"><p id="p51">Liberalize TPN and feeding volumes as tolerated to reach nutritional needs.</p></list-item>
<list-item id="item48"><p id="p52">Determine if an infant is receiving maximum calcium and phosphorus in intravenous nutrition (TPN), usually 2 mmol/kg/d of each, and via the diet. In general, this means using specially designed fortifiers for human milk or formulas designed for preterm infants. In some cases, infants with intestinal problems, such as short gut syndrome, may only tolerate formulas not designed for preterm infants. This may need to be directly supplemented with vitamins and minerals. </p></list-item>
<list-item id="item49"><p id="p53"><xref ref-type="tab" rid="t001">Table 21-1a</xref> describes three commonly used formulas designed for preterm infants and two human milk fortifiers designed for preterm infants. The amount of calcium, phosphorus, and vitamin D in these three products is described.</p></list-item>
<list-item id="item50"><p id="p54">As further discussed below, a <bold>vitamin D intake of 400 IU/dshould be provided.</bold> In the presence of cholestasis, up to 1000 IU/d of vitamin D should be given with monitoring of the serum 25-hydroxyvitamin D level every 1 to 2 months. Vitamin D<sub>3</sub> (cholecalciferol) is generally preferredto vitamin D<sub>2</sub> (ergocalciferol), but clinically, little distinction likely exists related to management of preterm infants. </p></list-item>
<list-item id="item51"><p id="p55">There are no currently available forms of vitamin D drops available for use in the United States that only provide vitamin D and iron, a combination often of value in this setting. As such, either a multivitamin with iron or separate vitamin D and iron need to be given. </p></list-item>
</list></list-item>
<list-item id="item52"><p id="p56"><bold>Secondly, consider decreasing nutrient losses or accommodating for them.</bold></p>
<list id="list16" list-type="bullet"><list-item id="item53"><p id="p57">Account for magnesium and zinc losses. This is usually primarily a problem in infants with intestinal diseases including small bowel ostomies and thus may require supplemental minerals in the diet.</p></list-item>
<list-item id="item54"><p id="p58">With regard to preventing mineral losses, careful consideration of the need for loop diuretics, such as furosemide, and the need for steroids. Adding a thiazide diuretic to furosemide may decrease calcium excretion in the urine, but this is unproven in the newborn period. Similarly, there is minimal evidence to support the use of intermittent (such as every other day) furosemide dosing in order to prevent the bone loss.</p></list-item>
</list></list-item>
</list></list-item>
<list-item id="item55"><p id="p59"><bold>Surgical</bold></p>
<p id="p60">There is no role for surgical intervention in the management of bone demineralization or fractures in otherwise healthy preterm or full-term infants. Orthopedic consultation may be obtained for splinting/casting long-bone fractures but these are not treated surgically in this population.</p></list-item>
</list></list-item>
<list-item id="item56"><p id="p61"><bold>Early developmental/therapeutic interventions</bold></p>
<list id="list17" list-type="number">
<list-item id="item57"><p id="p62">The relationship between rickets in any child and developmental outcome is poorly described.</p></list-item>
<list-item id="item58"><p id="p63">In preterm or other high-risk neonates, low bone mass is usually associated with other better-defined causes of delayed development and it is relatively unlikely that the bone health issues are a significant independent factor. However, infants who have poor bone health often have had substantial problems with other aspects of their nutrition and this may serve as a marker of a need for close follow-up.</p></list-item>
<list-item id="item59"><p id="p64">Additionally, care should be provided regarding the handling of babies with severe bone demineralization to limit trauma that might lead to increased fractures. Physical therapy may be undertaken in at-risk infants but should be done cautiously, especially if mineral intake is limited (eg, long-term TPN, fluid restriction).</p></list-item>
</list></list-item>
<list-item id="item60"><p id="p65"><bold>Prognosis</bold></p>
<list id="list18" list-type="number">
<list-item id="item61"><p id="p66"><bold>Early predictors and outcomes</bold></p>
<list id="list19" list-type="alpha-lower">
<list-item id="item62"><p id="p67">Even in the presence of significant rickets and fractures, the overall prognosis for neonatal bone loss is excellent.</p></list-item>
<list-item id="item63"><p id="p68">Recovery of full bone mass and healing of fractures is universal when the etiology is nutritional and a more optimal mineral intake is achieved.</p></list-item>
</list></list-item>
</list>
<p id="p151">(This section does not include a description of very rare endocrine-related causes of bone demineralization or genetic disorders such as osteogenesis imperfecta. The prognosis for bone health in these disorders is much more variable.)</p></list-item>
</list></list-item>
<list-item id="item64"><p id="p69"><bold>Convalescent care</bold></p>
<list id="list20" list-type="alpha-upper">
<list-item id="item65"><p id="p70"><bold>Definition</bold></p>
<list id="list21" list-type="number">
<list-item id="item66"><p id="p71">The definitions of the bone loss disorders are consistent whether they occur in the acute phase of management or later in the course of care of a high-risk infant.</p></list-item>
<list-item id="item67"><p id="p72">For the purposes of this section, the care of infants who are past the initial weeks of life and are preparing for hospital discharge will be discussed.</p></list-item>
</list></list-item>
<list-item id="item68"><p id="p73"><bold>Risk factors</bold></p>
<list id="list22" list-type="number"><list-item id="item69"><p id="p74"><bold>Therapeutic interventions</bold></p>
<p id="p75">Some VLBW infants may be receiving therapies that would decrease their retention of calcium and phosphorus. These wouldmost commonly be fluid restriction and loop diuretic use (furosemide).</p></list-item>
<list-item id="item70"><p id="p76"><bold>Exclusive human milk feedings</bold></p>
<p id="p77">An additional risk factor would be infants who were discharged with elevations in alkaline phosphatase activity and/or radiological rickets and are receiving only human milk after discharge.</p></list-item>
</list></list-item>
<list-item id="item71"><p id="p78"><bold>Diagnosis</bold></p>
<p id="p79"><bold>Monitoring of bone health</bold></p>
<list id="list23" list-type="number"><list-item id="item72"><p id="p80">A key issue in the convalescent phase for VLBW infants is whether it is necessary to continue to monitor alkaline phosphatase activity.</p>
<list id="list24" list-type="alpha-lower"><list-item id="item73"><p id="p81"><bold>Begin monitoring (Ca, phos, alk phos) at about 4 to 5 weeksof age</bold> in very preterm or VLBW infants and continuing monitoring every 2 weeks until full feeds are achieved and the infant has demonstrated a serum alkaline phosphatase <500 IU/L and not on the rise.</p></list-item>
<list-item id="item74"><p id="p82">It is important to identify that the infant is tolerating an appropriate mineral intake and does not have any ongoing conditions making it likely that bone minerals will be substantially lost.</p></list-item>
</list></list-item>
<list-item id="item75"><p id="p83">The measurement of any values of alkaline phosphatase activity in otherwise healthy preterm infants who are over 1500 g birthweight is controversial. There are no data to suggest such monitoring is needed.</p></list-item>
<list-item id="item76"><p id="p84">There are no data to support the routine monitoring of vitamin D [25(OH)D] levels in healthy preterm infants of any birthweight.</p></list-item>
<list-item id="item77"><p id="p85">Infants with very poor long-term nutrition, known malabsorptive disorders, or cholestasis may benefit from monitoring vitamin D levels.</p></list-item>
</list></list-item>
<list-item id="item78"><p id="p86"><bold>Management</bold></p>
<list id="list25" list-type="number">
<list-item id="item79"><p id="p87"><bold>Medical</bold></p>
<list id="list26" list-type="alpha-lower">
<list-item id="item80"><p id="p88"><bold>Formula fed</bold></p>
<list id="list27" list-type="bullet">
<list-item id="item81"><p id="p89">Several infant formulas are available designed specifically for discharge use. These formulas are usually called transitional formulas and contain 22 kcal/oz, when mixed according to label.</p></list-item>
<list-item id="item82"><p id="p90">The current amount of minerals provided by these transitional formulas for a 2.0-kg infant is shown in the accompanying <xref ref-type="tab" rid="t002">Table 21-1b</xref>. Values for a 4.0-kg infant are shown in <xref ref-type="tab" rid="t003">Table 21-1c</xref>. These products represent an approximate midcontent of routine and preterm formulas for most nutrients. </p></list-item>
<list-item id="item83"><p id="p91">Formula-fed infants who are <1500 g are routinely discharged using one of these products, although many will discharge all infants <1800 to 2000 g with one of these products. </p></list-item>
</list></list-item>
<list-item id="item84"><p id="p92"><bold>Breast fed</bold></p>
<list id="list28" list-type="bullet">
<list-item id="item85"><p id="p93">For those receiving only human milk at discharge, careful monitoring of growth and serum alkaline phosphatase after discharge is essential. </p></list-item>
<list-item id="item86"><p id="p94">It may be of some benefit to provide additional vitamin D to the infant or mother, or direct calcium and phosphorus supplementation to the infant. These options are considered in <xref ref-type="tab" rid="tb2">Table 21-2</xref>.</p></list-item>
<list-item id="item87"><p id="p95">In most cases, however, provision of five to six breast-feedings/day and two to three feedings of a transitional formula until the infant is growing well and achieves at least the 25% of weight and length on the World Health Organization growth curves is recommended.</p></list-item>
</list></list-item>
</list></list-item>
</list></list-item>
</list></list-item>
</list>
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Required Output I need is
D. Risk factors 1. Clinically important risk factors during hospitalization are those that might decrease mineral intake or absorption or increase mineral excretion. 2. Specifically, these primarily include 1. The use of unfortified or inadequately fortified human milk 2. Frequent use of loop diuretics 3. Use of steroids 4. Fluid restriction It is impossible in many circumstances to be certain about the most important of these factors, but infants in the NICU frequently encounter more than one of these risks. 3. In many cases, it is lower mineral intake, not bioavailability or even increased renal calcium excretion by loop diuretics (eg, furosemide), which is the principal problem.
And the lower-alpha list is also not coming properly instead of which number list is coming. Please suggest.
Current output is
D.
Risk factors 1.
Clinically important risk factors during hospitalization are those that might decrease mineral intake or absorption or increase mineral excretion. 2.
Specifically, these primarily include 1.
The use of unfortified or inadequately fortified human milk 2.
Frequent use of loop diuretics 3.
Use of steroids 4.
Fluid restriction It is impossible in many circumstances to be certain about the most important of these factors, but infants in the NICU frequently encounter more than one of these risks. 3.
In many cases, it is lower mineral intake, not bioavailability or even increased renal calcium excretion by loop diuretics (eg, furosemide), which is the principal problem.
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