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Talal I Dahhan, MD
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Clinical Issues Committee of the American Society for Bariatric and Metabolic Surgery blood pressure chart uk nhs purchase moduretic online. Adolescent bariatric surgery: treatment delayed blood pressure jnc 8 cheap 50 mg moduretic visa, treatment denied pulse pressure calculator cheap moduretic 50mg fast delivery, a crisis invited blood pressure reader buy moduretic now. Pediatricians hypertension abbreviation buy generic moduretic 50 mg, parents heart attack xanax order moduretic overnight, and others who take care of children are recognizing disordered eating attitudes and behaviors in children as young as 2 years, and these occur well into the geriatric years. Earlier editions also did not recognize that very young children as well as adolescent boys might develop eating disorders. Specific changes include the elimination of amenorrhea as a criterion, as it does not necessarily predict medical risk or treatment outcome. Furthermore, it does not apply to premenarchal girls or males, or postmenopausal women. The lowered frequency stemmed from the lack of difference in psychopathology or treatment outcomes between patients with once a week cycles of binges and purges versus more binge-purge episodes. Binge eating disorder is defined by binges without inappropriate compensatory behaviors. They were also more likely than obese patients without eating disorders to progress to metabolic syndrome. These children, adolescents, and adults fail to meet nutritional needs for reasons other than weight control. They may begin to avoid food after a choking or gagging incident, with fear of repeating that sensation. Abdominal pain, dislike of sensory characteristics of food, and other factors may keep a child from needed intake for growth. Unlike the child with anorexia nervosa, these children do not state that they fear weight gain or do not want to grow; rather, they fear the consequences of eating (abdominal pain, eating a food the picky eater would rather avoid, or other challenge). Restriction of energy intake relative to requirements leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal, or, for children and adolescents, less than that minimally expected. Intense fear of gaining weight or becoming fat or persistent behavior that interferes with weight gain, even though at a significantly low weight. Specify current type: Restricting Type: during the last 3 months, the person has not engaged in recurrent episodes of binge eating or purging behavior. Binge-Eating/Purging Type: during the last 3 months, the person has engaged in recurrent episodes of binge eating or purging behavior. Recurrent episodes of binge eating, characterized by both: (1) Eating, in a discrete period of time (for example, within any 2-hour period), an amount of food larger than most people would eat during a similar period of time and under similar circumstances. Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise. The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months. No evidence of lack of available food or an associated culturally sanctioned practice. Furthermore, this study had more pronounced findings than those found in a community sample of adolescents8 or in adults. Pediatricians need to take seriously any concern from a parent or other caring adult that a child or adolescent may be developing an eating disorder; many of these patients either already have or are in the process of hardwiring maladaptive eating attitudes and behaviors that could be prevented or treated with earlier intervention. Disordered eating and the female athlete triad are not just contained to the "visual sports" such as ballet, figure skating, and gymnastics; individuals can develop the triad who are C students, do P90X or find their favorite gym over exuberantly. Children and adolescents have been found to run in place or in school bathrooms to the point of developing blistering heels and toes, stress fractures, and other physical findings. Diane Neumark-Sztainer suggests avoiding "weighty conversations," or having home or dinner table talk centered around dieting or weight problems. Neumark-Sztainer states, if a child is a poor reader, calling them stupid will not help them read better and in fact may delay the process. Similarly, chiding a child for being overweight or creating derogatory weightrelated nicknames will not help them better manage their weight, exercise, or meal planning. In adolescent medicine, we prefer to treat "diet" as a four-letter word; adolescents who "diet" are more likely to end up at a higher weight, with short losses replaced by sustained weight gain. For the adolescent with disordered eating attitudes and behaviors, the clinician can use epigenetics as an explanation; "if you fast or have insufficient energy intake, your body thinks it has to store up nuts for the winter, or have enough energy in the form of fat or other tissues in order to last through the next perceived famine, or fasting period. This rationale makes sense to many patients and families and can help them start to break a cycle of abnormal eating attitudes and behaviors. Similarly, in patients with anorexia nervosa who state that they are just "fine," yet who have significant medical findings such as bradycardia, orthostatic hypotension, and amenorrhea, epigenetics can serve as a rational explanation of why these changes happen. If a child falls off the growth curve or crosses percentiles, the astute clinician should assess immediately for disordered eating attitudes and behaviors, while simultaneously doing a review of systems that could tease out newly manifesting celiac disease, inflammatory bowel disease, or other systemic process. Child abuse-physical, emotional, or sexual-may manifest as inappropriate weight gain or loss. Clinicians can start with parent(s) and child together, asking the child or adolescent why they are seeing you today. The clinician may need to referee, or curtail the intrusive parent who will not let the teen get a word in edgewise, or, for the quiet child or teen who will not say a word, ask their permission to elicit information from the parent, by stating, "Is it okay if the peanut gallery (your parent) answers this one Assess quantity and quality for breakfast, snack, lunch, snack, dinner, and snack. Are there any foods you used to eat that no longer feel "safe" or taste right to you If heterosexual and has had sex, what do you use for your two methods of contraception Children with underlying anxiety disorder may fear a perceived risk, such as vomiting unintentionally or other aversive conditioning. Asking about diet history and exercise can be particularly useful with both parent and child together, as "the peanut gallery" may use body language or words that can be queried to clarify whether the child is eating just bites of cereal or half a box. Near holidays, asking about what happens at the family dinner and how stressful or easy it is for the child can be revealing. Many patients laud the new interest a child or adolescent may have in eating healthy, especially if weight has been a family concern or a parent/family member has had a heart attack, diabetes, or other complication of obesity. Parents faced with a new vegetarian or vegan may not understand how to feed their child appropriately yet may be trying to be respectful of their desire not to eat meat after viewing content about animal rights in the classroom, or other scenario. It is useful to obtain a family history with child and parents present, educating about risk for the adolescent, in particular. Helping to open the lines of communication can also diminish the negative power of "family secrets. The clinician needs to state clearly the rules of confidentiality and its exceptions, for instance, "Everything we talk about without your parent in the room is private or confidential, meaning I am not going to share your private concerns with your parent unless you tell me something life-threatening or dangerous. Similarly, everything I talk about privately with your parent will be kept confidential, meaning I will not share with you their private thoughts or concerns, unless they tell me something life-threatening or dangerous. The child or adolescent with an eating disorder may be avoiding situations where food is involved, isolating themselves socially from family or friends. Obsessivecompulsive behaviors may have been missed; asking if the child is a perfectionist can be illuminating. Eating disorder questions may need to be asked privately, as some patients go to great lengths to cover or hide their behaviors. Use of motivational interviewing can elicit history while also helping to manage change and reducing morbidity. For instance, in discussing vomiting habits, the clinician can ask how often they purge, and in what situations. If it is always after school at home alone, is there a place the teen could go at that time that he or she could keep from vomiting. Teaching the purging adolescent to gargle with mouthwash, water with baking soda, or even just plain water is safer than brushing, and the teen can be taught that the latter helps acid reach surfaces it may otherwise not have reached. Most teens will begin behavior modifications such as these, in simple steps, if given the opportunity. Signs of chronic disease such as inflammatory bowel disease, thyroid symptoms, or other process can be useful. Blinded weights can be useful for the child or adolescent who is numbers obsessed or to help refocus on health rather than the scale. Some patients do better knowing the numbers, while others fall to pieces and escalate their behaviors before and after visits to manipulate the scale. Until you know how your patient will react, proceed with caution on sharing numbers rather than trends. Nursing staff can help orient the patient to the process, with words such as, "It is our policy to weigh patients backward on the scale after voiding, and screen for diabetes, protein in the urine, or other problems, and we will save all discussion of findings for you and your doctor. In the face of extreme dehydration and/or use of caffeine/stimulants, patients who should be bradycardic from starvation may actually have a normal heart rate or relative tachycardia. Gastrointestinal: early satiety, bloating, fullness, abdominal pain, reflux, constipation, diarrhea Russell sign in an adolescent girl who uses her finger to induce vomiting to control weight. Adolescents should be warned about this phenomenon when working on quitting purging behaviors. It is important to warn them that while quitting, each purge may cause a flare of parotitis-and that it is not just their face getting fatter, as many fear. Dental erosions on the lingual and occlusal surfaces can also be found with vomiting. Hair thinning, lack of shine or fullness, can occur with insufficient protein and fat intake. Lanugo hair may be found on the trunk and extremities when starvation has occurred of sufficient duration for the body to sense the need for an extra-induced layer of warmth. Carotinemia can occur in those patients eating more orange vegetables than anything else. Telltale effects of purging can also include subconjunctival hemorrhages (red spots in the white of the eye) as well as unexplained nosebleeds without associated nasal pathology. Orthostatics should be checked in that order, lying then standing; if abnormal when done immediately with standing, the patients should stand for 2 minutes and have the standing vital signs rechecked, as a percentage of normal individuals may take up to 2 minutes for values to normalize when shifting position from horizontal to vertical. Orthostatic findings can be explained to the patient and family as the body having blood and the oxygen it carries rushing away from the head with standing, and the heart trying to beat faster to get it back up to the head again. A mitral valve click may be heard, as approximately one-third of patients with anorexia nervosa lose cardiac mass and develop a floppy mitral valve. Tanner staging of breasts and pubic hair for girls, and pubic hair and genitals for boys, should be performed. Girls may have atrophy of breasts with starvation, and when an eating disorder occurs early or in mid-puberty, a patient may be Tanner 4 or 5 for a prolonged period without experiencing menarche. Asking an amenorrheic patient when they started noticing pubic hair and breast buds, and when there were too many pubic hairs to count (indicating Tanner 4) can help determine whether puberty has been delayed or has been progressing. Abdominal masses may include palpable loops of stool from constipation; hepatosplenomegaly can occur in the context of refeeding syndrome with congestive heart failure. Any significant neurologic findings such as blurred optic disc margins warrant neuroimaging of brain, as a brain tumor may mimic an eating disorder. All cardiac changes are fully reversible, with the exception of the irreversible direct myocardial damage that occurs with chronic emetine use, the active ingredient in ipecac. Although ipecac is no longer available in the United States, it still may be found in other countries, with risks of misuse and fatalities. Chapter 15 - Eating Disorders in Children and Adolescents 175 Effects on the Brain: Starvation can cause reductions in gray and white matter, a change that can occur within months. Although cortical volumes may increase with weight gain, gray matter volume changes may not be completely reversible. What is seen clinically with prolonged starvation is psychomotor retardation, or a slowing of thought, speech, and movement, all reversible relatively quickly (over a period of days to weeks) with refeeding. Because 40% to 60% of bone density is deposited in early adolescence (ages 11 to 14 years) in girls and late adolescence in boys (ages 15 to 17 years), disordered eating during those crucial times can pose substantial risk for osteopenia. Even a 5% to 10% decrease in bone deposition during these crucial times can result in significant fracture risk in the third decade of life. Hematologic Effects of Starvation: Children and adolescents who restrict intake long enough will first show neutropenia, followed usually by a normochromic or hypochromic anemia, and finally pancytopenia (platelet formation is initially preserved). Of interest, the bone marrow in anorexia nervosa appears to be replaced by a fatty marrow. Higher fat in the marrow may lead to diminished structural bone integrity, with diminished bone mass and lowered skeletal strength. Thus, lower red marrow and higher yellow marrow may lead to the observed increased fracture risk. Other endocrine changes include a euthyroid sick syndrome picture, with hypothermia, slowed metabolism, and perception of always being cold. Delayed puberty is defined as no secondary sexual characteristics by age 14 years or menarche that has not occurred within 3 years of onset of thelarche/ adrenarche. In fact, most girls achieve menarche within 2 years of occurrence of both thelarche and adrenarche, with 3 years representing more than 2 standard deviations from normal. Secondary amenorrhea means the absence of menstruation after cycles have been previously established, usually defined as no periods in at least 3 months. Amenorrhea can precede weight loss in 50% to 75% of patients with eating disorders. In children and adolescents with eating disorders, failure to deposit bone at age appropriate times as well as increased resorption set the stage for osteopenia. For girls, a critical time of bone deposition should occur between ages 11 and 14 years, with 40% to 60% of peak bone mass deposited in healthy girls at that time; for boys, peak growth spurt with increased bone deposition occurs slightly later (Box 15-5). An additional 5% accrues in the third decade, with even that low amount accounting for a significant decrease in fracture risk. Excess glucocorticoids decrease calcium absorption from the gut and inhibit bone formation through direct, receptor-mediated osteoblast effects. Exercise that is not excessive may offer some protection against bone loss in anorexia nervosa,64 but there is a fine line between exercise balance and "too much of a good thing," as occurs with hyperexercising. Eumenorrhea, without hormonal help, can be a useful marker for balanced levels of exercise.
Cytokine gene polymorphisms are associated with irritable bowel syndrome: a systematic review and meta-analysis heart attack wiki purchase 50 mg moduretic otc. Intestinal serotonin release blood pressure smoothie 50mg moduretic visa, sensory neuron activation heart attack move me stranger cheap moduretic online mastercard, and abdominal pain in irritable bowel syndrome arrhythmia ablation is a treatment for purchase cheap moduretic online. Impaired uptake of serotonin by platelets from patients with irritable bowel syndrome correlates with duodenal immune activation blood pressure chart during the day buy moduretic 50mg free shipping. Genetic risk factors for post-infectious irritable bowel syndrome following a waterborne outbreak of gastroenteritis prehypertension due to anxiety moduretic 50mg on line. G-protein beta3 subunit C825T Polymorphism in patients with overlap syndrome of functional dyspepsia and irritable bowel syndrome. Recurrent abdominal pain in children: evidence from a population-based study that social and familial factors play a major role but not Helicobacter pylori infection. Early parental and child predictors of recurrent abdominal pain at school age: results of a large population-based study. Relationship between the decision to take a child to the clinic for abdominal pain and maternal psychological distress. Parental reinforcement of recurrent pain: the moderating impact of child depression and anxiety on functional disability. Family reinforcement of illness behavior: a comparison of adolescents with chronic fatigue syndrome, juvenile arthritis, and healthy controls. Anxiety and somatic complaints in children with recurrent abdominal pain and anxiety disorders. Recurrent abdominal pain in children: psychiatric diagnoses and parental psychopathology. Abdominal pain in Dutch schoolchildren: relations with physical and psychological comorbid complaints in children and their parents. Children with recurrent abdominal pain and their parents: more somatic complaints, anxiety, and depression than other patient families Psychological comorbidity and stress reactivity in children and adolescents with recurrent abdominal pain and anxiety disorders. Quality of life predictors of outcome in pediatric abdominal pain patients: findings at initial assessment and 5-year follow-up. In: Measuring health-related quality of life in children and adolescents: implications for research and practice. Functional abdominal pain in childhood and long-term vulnerability to anxiety disorders. Functional abdominal pain patient subtypes in childhood predict functional gastrointestinal disorders with chronic pain and psychiatric comorbidities in adolescence and adulthood. Health-related quality of life in children with abdominal pain due to functional or organic gastrointestinal disorders. Models of anxiety, depression, somatization, and coping as predictors of abdominal pain in a community sample of school-age children. Are child anxiety and somatization associated with pain in pain-related functional gastrointestinal disorders Recurrent abdominal pain in primary and tertiary care: differences and similarities. Autonomic testing in functional gastrointestinal disorders: implications of reproducible gastrointestinal complaints during tilt table testing. Manometric abnormalities in the postural orthostatic tachycardia syndrome: a case series. Comorbidities in pediatric patients with postural orthostatic tachycardia syndrome. The functional development of descending inhibitory pathways in the dorsolateral funiculus of the newborn rat spinal cord. Long-term alteration of pain sensitivity in school-aged children with early pain experiences. A rat model of chronic gastric sensorimotor dysfunction resulting from transient neonatal gastric irritation. Neonatal gastric suctioning results in chronic visceral and somatic hyperalgesia: role of corticotropin releasing factor. A rat model of chronic postinflammatory visceral pain induced by deoxycholic acid. A new model of chronic visceral hypersensitivity in adult rats induced by colon irritation during postnatal development. Long-term sensitization of primary afferents in adult rats exposed to neonatal colon pain. Early life events: infants with pyloric stenosis have a higher risk of developing chronic abdominal pain in childhood. Long-term effect of surgery on the risk of childhood functional gastrointestinal disorders. Abdominal sensitivity in the first year of life: comparison of infants with and without prenatally diagnosed unilateral hydronephrosis. Early life events predispose the onset of childhood functional gastrointestinal disorders. Abdominal pain and functional gastrointestinal disorders in children with celiac disease. A prospective communitybased study of gastroenterological symptoms in school-age children. Urinary tract infection in infancy is a risk factor for chronic abdominal pain in childhood. Neonatal maternal separation alters stress-induced responses to viscerosomatic nociceptive stimuli in rat. Early life stress alters behavior, immunity, and microbiota in rats: implications for irritable bowel syndrome and psychiatric illnesses. Effects of neonatal maternal separation on neurochemical and sensory response to colonic distension in a rat model of irritable bowel syndrome. Neonatal maternal separation enhances central sensitivity to noxious colorectal distention in rat. Neonatal maternal separation elevates thalamic corticotrophin releasing factor type 1 receptor expression response to colonic distension in rat. Chronic peripheral administration of corticotropin-releasing factor causes colonic barrier dysfunction similar to psychological stress. Estimating the contribution of acute gastroenteritis to the overall prevalence of irritable bowel syndrome. An outbreak of acute bacterial gastroenteritis is associated with an increased incidence of irritable bowel syndrome in children. Postinfectious irritable bowel syndrome after a food-borne outbreak of acute gastroenteritis attributed to a viral pathogen. Enhanced perception of physiological intestinal motility in the irritable bowel syndrome. Selective dysfunction of mechanosensitive intestinal afferents in irritable bowel syndrome. Patients with irritable bowel syndrome have greater pain tolerance than normal subjects. Effect of acute physical and psychological stress on gut autonomic innervation in irritable bowel syndrome. Rectal distention testing in patients with irritable bowel syndrome: sensitivity, specificity, and predictive values of pain sensory thresholds. Altered rectal perception is a biological marker of patients with irritable bowel syndrome. Alterations in rectal sensitivity and motility in childhood irritable bowel syndrome. Somatic referral of visceral sensations and rectal sensory threshold for pain in children with functional gastrointestinal disorders. Evidence for the hypersensitivity of lumbar splanchnic afferents in irritable bowel syndrome. Repetitive sigmoid stimulation induces rectal hyperalgesia in patients with irritable bowel syndrome. Lower functional gastrointestinal disorders: evidence of abnormal colonic transit in a 287 patient cohort. The expression and the cellular distribution of the tight junction proteins Chapter 6 - Chronic Abdominal Pain of Childhood and Adolescence 73. Associations among gut permeability, inflammatory markers, and symptoms in patients with irritable bowel syndrome. Abnormal intestinal permeability in subgroups of diarrhea-predominant irritable bowel syndromes. Leaky gut in patients with diarrheapredominant irritable bowel syndrome and inactive ulcerative colitis. Intestinal permeability in patients with irritable bowel syndrome after a waterborne outbreak of acute gastroenteritis in Walkerton, Ontario. Urine sugars for in vivo gut permeability: validation and comparisons in irritable bowel syndrome-diarrhea and controls. Increased gastrointestinal permeability and gut inflammation in children with functional abdominal pain and irritable bowel syndrome. Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in postdysenteric irritable bowel syndrome. Impaired intestinal barrier integrity in the colon of patients with irritable bowel syndrome: involvement of soluble mediators. The role of gut microbiota (commensal bacteria) and the mucosal barrier in the pathogenesis of inflammatory and autoimmune diseases and cancer: contribution of germ-free and gnotobiotic animal models of human diseases. Short-chain fatty acids and the irritable bowel syndrome: the effect of wheat bran. Increase in fecal primary bile acids and dysbiosis in patients with diarrhea-predominant irritable bowel syndrome. Molecular analysis of the luminal- and mucosal-associated intestinal microbiota in diarrhea-predominant irritable bowel syndrome. Alterations in composition and diversity of the intestinal microbiota in patients with diarrhea-predominant irritable bowel syndrome. The fecal microbiota of irritable bowel syndrome patients differs significantly from that of healthy subjects. Global and deep molecular analysis of microbiota signatures in fecal samples from patients with irritable bowel syndrome. Gastrointestinal microbiome signatures of pediatric patients with irritable bowel syndrome. Specific probiotic therapy attenuates antibiotic induced visceral hypersensitivity in mice. Regulation of tight junction permeability by intestinal bacteria and dietary components. Small intestine bacterial overgrowth in irritable bowel syndrome: a retrospective study with rifaximin. Do interventions which reduce colonic bacterial fermentation improve symptoms of irritable bowel syndrome Breath test for differential diagnosis between small intestinal bacterial overgrowth and irritable bowel disease: an observation on non-absorbable antibiotics. Results of small intestinal bacterial overgrowth testing in irritable bowel syndrome patients: clinical profiles and effects of antibiotic trial. Small intestine bacterial overgrowth and irritable bowel syndrome-related symptoms: experience with Rifaximin. Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome. Normalization of lactulose breath testing correlates with symptom improvement in irritable bowel syndrome. Prevalence of small intestinal bacterial overgrowth in children with irritable bowel syndrome: a case-control study. Lactulose breath testing does not discriminate patients with irritable bowel syndrome from healthy controls. Double-blind, placebo-controlled antibiotic treatment study of small intestinal bacterial overgrowth in children with chronic abdominal pain. A randomized doubleblind placebo-controlled trial of rifaximin in patients with abdominal bloating and flatulence. Review article: Associations between immune activation, intestinal permeability and the irritable bowel syndrome. Activated mast cells in proximity to colonic nerves correlate with abdominal pain in irritable bowel syndrome. Mast cell-dependent excitation of visceral-nociceptive sensory neurons in irritable bowel syndrome. Activation of human enteric neurons by supernatants of colonic biopsy specimens from patients with irritable bowel syndrome. Hypothalamic-pituitarygut axis dysregulation in irritable bowel syndrome: plasma cytokines as a potential biomarker Mucosal immune cell numbers and visceral sensitivity in patients with irritable bowel syndrome: is there any relationship Immunomodulatory mast cells: negative, as well as positive, regulators of immunity. Mucosal mast cell counts correlate with visceral hypersensitivity in patients with diarrhea predominant irritable bowel syndrome. Differential expression of toll-like receptors in patients with irritable bowel syndrome. Role of toll like receptors in irritable bowel syndrome: differential mucosal immune activation according to the disease subtype.
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With this in mind prehypertension early pregnancy order moduretic in united states online, the method is valuable for guiding biopsy blood pressure goals purchase moduretic line, leading to more accurate pathology reports arteria coronaria dextra purchase moduretic no prescription. Clinical Point of View Cholangiocarcinoma is a silent malignancy that is nonresectable in 45% of patients at the time of diagnosis blood pressure medication side effects moduretic 50mg low cost. Nonetheless hypertension icd 9 purchase cheap moduretic line, in another 45% of cases hypertension home remedies purchase moduretic paypal, the tumor is completely resectable, with no residual malignancy left behind after surgery. However, a very high incidence of local recurrence (up to 100%) is reported in this cancer. Therefore, imaging modalities have an important role in the diagnosis and localization of recurrent tumors. They are particularly beneficial for the optimization of therapy approach after surgical procedures. Female gender, obesity, high-fat and high-calorie diet, porcelain gallbladder, chronic typhoid, and increased parity are other risk factors. T2: Tumor invades the perimuscular connective tissue; there is no extension beyond the serosa or into the liver. T3: Tumor perforates the serosa (visceral peritoneum) and/or directly invades the liver and/or one other adjacent organ or structure, such as the stomach, duodenum, colon, pancreas, omentum, or extrahepatic bile ducts. T4: Tumor invades the main portal vein or hepatic artery or invades two or more extrahepatic organs or structures. Clinical Point of View Gallbladder cancer is a rare malignancy with a relatively high chance of hepatic and regional lymph node metastases at the time of diagnosis. Hepatic arterial infusion of chemotherapy agents may be beneficial in highly selected patients. For the assessment of recurrent disease, functional imaging may provide superior information compared with conventional imaging modalities. Discussion Gallbladder carcinoma is the most common cancer of the biliary system with a high mortality rate. It also introduced the method as accurate for the diagnosis of gallbladder cancer. Low-grade-to-moderate uptake was present in the pituitary, choroid plexus, pharynx, soft palate, lungs, myocardium, mediastinal blood pool, testicles, and muscles. It may also provide additional prognostic data, because opposite to less aggressive tumors and inflammatory lesions, more aggressive cancers show increased uptake on delayed scan. Systematic review: outcome of compensated cirrhosis due to chronic hepatitis C infection. Management of hepatocellular carcinoma in Asia: consensus statement from the Asian Oncology Summit 2009. Meta-analysis: surveillance with ultrasound for early-stage hepatocellular carcinoma in patients with cirrhosis. Diagnosis of hepatic nodules 20 mm or smaller in cirrhosis: prospective validation of the noninvasive diagnostic criteria for hepatocellular carcinoma. The role of positron emission tomography using carbon-11 and fluorine-18 choline in tumors other than prostate cancer: a systematic review. Partial hepatectomy or orthotopic liver transplantation for the treatment of respectable hepatocellular carcinoma Comparison of 11C-acetate positron emission tomography and 67Gallium citrate scintigraphy in patients with hepatocellular carcinoma. Liver International: Official Journal of the International Association for the Study of the Liver. Diagnostic accuracy of 18F-methylcholine positron emission tomography/computed tomography for intra- and extrahepatic hepatocellular carcinoma. Imaging lipid synthesis in hepatocellular carcinoma with [methyl-11C]choline: correlation with in vivo metabolic studies. Evaluation of benign vs malignant hepatic lesions with positron emission tomography. Positron emission tomography scanning in the evaluation of hepatocellular carcinoma. The role of [18F] fluorodeoxyglucose positron emission tomography imaging in the evaluation of hepatocellular carcinoma. Fluorine-18 fluorodeoxyglucose positron emission tomography predicts tumor differentiation, P-glycoprotein expression, and outcome after resection in hepatocellular carcinoma. Prognostic value of 18Ffluorodeoxyglucose positron emission tomography/ computed tomography in patients with Barcelona Clinic Liver Cancer stages 0 and a hepatocellular carcinomas: a multicenter retrospective cohort study. Update on inflammatory bowel disease in patients with primary sclerosing cholangitis. Metastatic colon cancer from extrahepatic cholangiocarcinoma presenting as painless jaundice: case report and literature review. Guidelines for the diagnosis and treatment of cholangiocarcinoma: consensus document. Prognostic factors in patients with advanced cholangiocarcinoma: role of surgery, chemotherapy and body mass index. Prognostic nomogram for intrahepatic cholangiocarcinoma after partial hepatectomy. Diagnostic accuracy of fluorine-18-fluorodeoxyglucose positron emission tomography in the evaluation of the primary tumor in patients with cholangiocarcinoma: a meta-analysis. Prognostic factors in patients with gallbladder cancer after surgical resection: analysis of 279 operated patients. Diagnostic accuracy of fluorine18-fluorodeoxyglucose positron emission tomography in gallbladder cancer: a meta-analysis. Positron tomography with 18F-fluorodeoxyglucose in the preoperative evaluation of gall bladder lesions suspicious of malignancy. Positron emission tomography with [18F]fluoro-2-deoxy-D-glucose for diagnosis and staging of bile duct cancer. Impact of integrated positron emission tomography and computed tomography on staging and management of gallbladder cancer and cholangiocarcinoma. Primary tumor maximum standardized uptake value measured on 18F-fluorodeoxyglucose positron emission tomography-computed tomography is a prognostic value for survival in bile duct and gallbladder cancer. Prognostic Factors3,4 For the different subtypes of lymphomas, various prognostic scores, including the International Prognostic Index (see later discussion as an example), Follicular Lymphoma International Prognostic Index (versions 1 and 2), Mantle Cell International Prognostic Index, and Cumulative Illness Rating Scale score, have been defined. Most of these prognostic indices include simple clinical parameters for pretherapeutic stratification of patients. Five-Year Survival1 Survival differs according to the subtype and stage of the disease. However, it is closely related to the histopathology of the lymphoma, which could be different for the various subtypes. Hodgkin lymphoma: Initial staging (including noninvasive assessment of bone marrow involvement) is imperative for the choice of therapy. However, as the stage is an integral part of prognostic scoring systems, correct staging is still of importance to the clinicians. In addition, data revealed that bone marrow biopsy can be skipped if there are negative findings on functional imaging modalities. Teaching points this modality is also capable of differentiating posttherapeutic fibrotic scar tissue from residual malignancy. However, lack of metabolically active bilateral hilar lymph nodes is not typical for sarcoidosis in this patient. Interim study after three cycles of chemotherapy (B) shows partial metabolic response to therapy. A focal uptake in the left distal ureter is accumulation of radioactive urine (A, green arrow). Correlation with tissue diagnosis is strongly recommended to prevent unnecessary surgeries in the case of lymphoma. Comparison of tracer intensity with the primary tumor is crucial for clarification. A low uptake in the residual left inguinal lymph node is less than that in the liver. A metabolically active tumor within the right iliac bone with infiltration to the adjacent abdominal wall is also malignant in nature. A follow-up scan demonstrates a favorable metabolic response to therapy (B,D, and F). Case 9: Staging and Restaging Burkitt Lymphoma Findings A 23-year-old male with Burkitt lymphoma. The pattern of uptake is homogeneous for reactive and heterogeneous for bone marrow infiltration. A focal uptake in the dorsal right hand is the site of tracer injection (arrowhead). A follow-up scan demonstrates a favorable complete metabolic response to chemotherapy (B). History of recent chemotherapy and favorable metabolic response in primary lesions on surveillance scan are the key points for correct interpretation. These patients and those with liver or splenic involvement have poor prognosis compared with those with isolated nodal malignancy. Cost-effectiveness of Fluorine-18-Fluorodeoxyglucose positron emission tomography in tumours other than lung cancer: a systematic review. Giant Cell Tumor of the Tendon Sheath With Discordant Metabolism as a False Positive on Staging of Mantle Cell Lymphoma. Nodular fasciitis mimicking recurrent lymphoma on positron emission tomography-computed tomography. Fluorine18-fluorodeoxyglucose Positron Emission Tomography in Diffuse Large B-cell Lymphoma. Clinical Point of View Cervical cancer is currently the third most common cancer in women and presents in advanced stages in a vast majority of cases, particularly in developing countries. All other cases need more aggressive surgery and if risk factors such as G3 histology or positive margins are detected, further adjuvant treatments are necessary. However, because surgical lymph node assessment may not be available in all centers in developing countries, it is not per se mandatory. Currently, in these cases, palliative care with platinumbased chemotherapy is the standard strategy. Moreover, the metabolic activity of metastatic lymph nodes can predict response to therapy as well as risk of recurrence in the pelvis. However, for the detection of lymph node metastasis, the sensitivity, specificity, and accuracy were comparable in both techniques (92%, 88%, and 90%, respectively). Antihormonal treatment such as tamoxifen or aromatase inhibitors may be used for the former, whereas platinum-based chemotherapy, combined with taxanes, is the standard regimen for the latter. In contrast to cervical cancer, endometrial carcinomas are diagnosed in lower stages due to the postmenopausal vaginal bleeding as the first symptom. Since the symptoms such as pain, constipation, loose stools, or bleeding develop late in the course of disease, it is still the fourth common cause of cancer related to females. Ascites and pleural effusion are more common in patients with advanced malignancy. Abdominal ultrasonography could be the first step to assess suspected cases, supplemented with the transvaginal method to identify malignant phenotypes. However, the surgical approach is favored in operable cases because the suspected imaging findings need histologic verification, and the treatment plan commonly relies on surgical and histologic rather than imaging findings. Overall, surgery plays an essential role in primary ovarian cancer, and a complete cytoreduction is an important parameter to provide better prognosis in these patients. Second-line options are either a repeat of carboplatin/paclitaxel if patients are platinum sensitive (>12 months duration of response) or administration of gemcitabine/pegylated doxorubicin or topotecan. However, it is not established as a standard procedure in routine clinical practice yet. Case 4: Staging and Restaging Cervical Cancer Findings A 68-year-old female with cervical cancer.
Alcoholic hepatitis is acute damage; cirrhosis blood pressure medication exercise buy 50 mg moduretic with amex, steatosis blood pressure how to take purchase moduretic 50mg on-line, steatohepatitis arteria bologna 23 novembre cheap 50mg moduretic free shipping, or fibrosis contributes to chronic liver damage blood pressure chart pdf uk purchase moduretic 50 mg on-line. Damage to the liver is a serious concern because of the many specialized functions performed by the hepatocytes heart attack calculator cheap 50 mg moduretic free shipping. Alcohol is especially damaging to the hepatocytes and contributes to progressive deterioration of the liver cells hypertension 120 80 buy genuine moduretic, starting with a condition known as fatty liver. The first enzyme, alcohol dehydrogenase, converts small amounts of alcohol to a toxic substance called acetaldehyde. Once alcohol has been broken down, the liver uses these enzymes to make fatty acids that accumulate in the liver as fat. A fatty liver will heal if the person stops drinking at this stage; it will progress to fibrosis or cirrhosis if the drinking continues, damaging the hepatocytes. In this system, different enzymes are typically used for metabolizing drugs and foreign substances. No matter the method of alcohol metabolism, the end result is triglycerides or fat deposits in the liver. Treatment options are discussed with the Birklands, and they agree with the decision to use imageguided ablation. His jaundice, pruritus, and ascites improve over the next several months, and his laboratory values 43. Cirrhosis is more serious than fatty liver because the hepatocytes are replaced as scar tissue, causing metabolic functions in the liver to be impaired. This constriction forces blood out of the liver in vessels that have a lower pressure, thus contributing to portal hypertension. The increased abdominal fluid puts pressure on the diaphragm, making it difficult for the person to breathe, even at rest. Congestive heart failure, nephrosis, peritonitis, and neoplastic cancer are other causes of ascites. Factors include the pattern of drinking, the amount of alcohol consumed, and how many years the person has been drinking alcohol. Someone who consumes alcohol on a regular basis has a higher risk of liver cirrhosis than does someone who drinks alcohol intermittently. The patient with metabolic syndrome and obesity has an increased risk of damage because the liver is aggravated by the higher caloric intake, which naturally leads to the fat deposits. If drinking continues, inflammation of the liver cells causes fibrosis and further damage of the liver tissue and to the cell membranes and organelles, including the mitochondria. Clinical Manifestations the vascular and regenerative abilities of the liver, as well as its deep location in the abdominal cavity, tend to delay diagnosis of liver damage. Palpation to the abdomen reveals an enlarged liver (often found by chance during a routine examination). Bile duct Branch of the portal vein Branch of the hepatic artery Fatty liver Ingested alcohol is primarily metabolized in the liver. Acetaldehyde, formed when alcohol is metabolized, damages hepatocytes and impairs the oxidation of fatty acids. Other alcohol metabolism by-products, including oxygen free radicals, promote in~amma tion and may stimulate autoantibody production. Autoantibodies Free radicals Alcoholic hepatitis With continued alcohol intake, liver cells degenerate and spotty cellular necrosis occurs. Weblike bands of connective tissue develop around the portal triads and central vein, eventually connecting with one another. Pressure in the portal venous system, which drains the gastrointestinal tract, pancreas, and spleen, increases. Male newborns often have breast tissue that is palpable as a result of the estrogen from the mother that crosses the placenta, causing the male breast tissue to swell. Changes in estrogen-to-testosterone levels also cause breast tissue enlargement in males during puberty and as part of the aging process after age 50. Asterixis is a muscle tremor that causes the downward flap of the hand when the arm is extended and dorsiflexed at the wrist. This can also be noted in the feet or tongue of the patient with portal hypertension. The dilated arteriole is seen as a small red dot with tiny, fragile veins surrounding it, giving it a spiderweb appearance. The abdomen has bluish veins just under the skin that radiate out across the umbilicus as a result of ascites and increased abdominal pressure. Esophageal varices, another abnormal finding, is swollen esophageal veins that are the result of increased pressure in the vessels due to portal hypertension from liver scarring. The lack of vitamin K metabolism and storage in the liver contributes to the clotting problems, making bleeding esophageal varices a very serious condition. Portal hypertension causes the shifting of fluids within body compartments, such as ascites and generalized edema. Hypoalbuminemia contributes to ascites of the abdomen because of the loss of colloid osmotic pressure of plasma. Normally, proteins such as albumin keep the fluid in the intravascular spaces instead of allowing this plasma-rich fluid to leak into the extravascular spaces. Hyperaldosteronism also encourages excess body fluid resulting from the retention of sodium and water. Restlessness is a vague, early symptom of systemic toxicity for the nurse to note. The patient may also initially manifest with agitation or impaired judgment, progressing to confusion, disorientation, and decreased cognition with increased cerebral edema. The pressure inside the cranium continues to increase, causing cerebral hypoxia that will manifest in changes to cognitive status. Without the conversion to urea in the liver, ammonia remains in the blood as a toxin. Medications can also accumulate to toxic levels without the liver to metabolize them. Liver biopsy, still considered the gold standard for diagnosis, can help to determine whether the patient has simple steatosis or a more serious condition, such as cirrhosis. Abstinence improves the prognosis in any stage of the disease, as long as the abstinence is sustained. Malnutrition is considered to indicate a rather poor prognosis for patients with liver disease. Changes in diet include the addition of lean protein as well as polyunsaturated fatty acids and phytochemicals. Resveratrol is one such phytochemical that is being researched because it has the ability to neutralize free radicals and inflammatory cytokines, thus reducing oxidative stress. Treatment includes band ligation, medications to slow blood flow, or placement of a shunt to divert blood away from the portal vein. A shunt can also be implanted to help remove the fluid but retain the albumin in the body. Similar symptoms and physical changes in the liver from liver cancer were discussed previously. Cholelithiasis, or stone formation, is the most common disorder of the gallbladder. Etiology and Pathogenesis the presence of fatty chyme in the duodenum causes smooth muscular contraction to release bile. The hormone cholecystokinin from the duodenal mucosa is the stimulus for the gallbladder and pancreas to contract, releasing their digestive juices bile and pancreatic juices, as well as the relaxation of the hepatopancreatic sphincter of Oddi. Disorders of the gallbladder most often result from gallstone formation and blockage of bile, causing inflammation and tissue damage. Although much less common, gallbladder cancer can be caused from the damage caused by gallstones in the gallbladder and biliary tract. Most stones form in the gallbladder and then migrate to the bile ducts, causing an obstruction and inflammation. Stones in the gallbladder obstructing flow are formed from cholesterol or pigment, 80% of the stones being formed from cholesterol. Precipitating factors in the formation of gallstones include changes in metabolism, biliary stasis, obstruction, hypertriglyceridemia, and infection. Forty Other risk factors include a sedentary lifestyle, diabetes mellitus, regional enteritis, and having family members who have had cholelithiasis. In liver damage, liver inflammation, or liver obstruction pathologies, what diagnostic tests on the liver panel will show an elevation What pathologic process increases the risk of liver cancer in patients infected with hepatitis B virus or hepatitis C virus The results confirm the presence of several gallstones in both the gallbladder and the biliary tract. Rowe the options for treatment, which include either surgery of modification of her diet. A referral to a dietitian at the Neighborhood Patient Education Center is arranged. Martin about eating low-fat and low-calorie foods to promote weight loss and manage her symptoms. If this approach does not prove successful in eliminating her gallstones, what are some of the factors that are likely to contribute to the lack of success Why might patients think they are having a heart attack instead of a gallbladder attack In addition to ultrasound, what imaging studies are available to help make a definitive diagnosis of Mrs. Linking Pathophysiology to Diagnosis and Treatment the gallbladder concentrates the bile by absorbing some of the water and ions. From the time when the bile enters the gallbladder until its release, the bile becomes 10 times more concentrated. Obstruction of the common bile duct causes bile to reflux back into the liver, causing damage to the hepatocytes. The pancreas can also be damaged by this obstruction in the common bile duct from enzymes that cause autodigestion. Lab values for amylase and lipase are elevated, demonstrating involvement of the pancreas. Diagnostic tests may include an abdominal x-ray, ultrasound, oral cholecystogram, or a gallbladder scan. Treatment is conservative if the patient is asymptomatic and has a low risk of complications from the presence of stones. Medications such as ursodiol and chenodiol can be used to decrease cholesterol production in the liver and dissolve the stone. This form of treatment can take up to 2 years to dissolve the stone, and the stones can reoccur once the medication has been discontinued. Symptomatic patients require surgical intervention with either a laparoscopic cholecystectomy or an open cholecystostomy not only to remove the gallbladder, but also to explore the common bile duct with possible placement of a T-tube to maintain patency of the common bile duct as a result of inflammation. If the bile is able to reflux into the liver, jaundice, pain, and damage to the hepatocytes can occur. If the obstruction is located in the common bile duct, the pancreas can also be involved. When increased bilirubin is eliminated by the kidneys, the urine is a dark tea color. Steatorrhea (greasy, foulsmelling feces containing undigested fats) is often reported and results from the lack of bile to digest the fat in the duodenum. Bile salts that accumulate in the blood are finally eliminated via the integumentary system, causing pruritus. She has a stressful family life and is also experiencing perimenopause with hot flashes and weight gain. Her Choledocholithiasis and Cholangitis Choledocholithiasis is a gallstone in the common bile duct. Obesity and symptomatic cholelithiasis in childhood: Epidemiologic and case-control evidence for a strong relationship. A stone located in the common bile duct can also cause complications for the liver and pancreas. Etiology and Pathogenesis Stones found in the common bile duct most often originate in the gallbladder, but a stone can also form in the common bile duct. Cholangitis is a serious condition in which the gallstone becomes impacted in the bile duct with resulting inflammation. Untreated, this impacted stone can cause bacteremia and septicemia and is associated with a higher mortality rate when diagnosis and treatment are delayed. The patient with advanced cholangitis will have clinical signs consistent with sepsis, such as hypotension and changes in mental status. Several diagnostic tests can be completed by using contrast dye to visualize the obstruction. An intravenous cholangiogram visualizes the blood through the liver and is excreted with bile to the gallbladder. When the dye is injected directly into the biliary tree through the abdominal wall, this test is percutaneous transhepatic cholangiography. When the dye is ingested in the form Clinical Manifestations Patients with choledocholithiasis and cholangitis present with symptoms similar to those of cholelithiasis and acute cholecystitis, which is covered below.
Decreased colonic transit time after transcutaneous interferential electrical stimulation in children with slow transit constipation blood pressure medication to treat acne purchase moduretic 50 mg on line. Improvement of quality of life in children with slow transit constipation after treatment with transcutaneous electrical stimulation blood pressure chart cholesterol buy 50mg moduretic. Long-term effects of transabdominal electrical stimulation in treating children with slow-transit constipation artaria string quartet order moduretic american express. Lack of benefit of laxatives as adjunctive therapy for functional nonretentive fecal soiling in children hypertension treatment guidelines jnc 7 buy discount moduretic on line. Loperamide suppositories in an adolescent with childhood-onset functional nonretentive fecal soiling high blood pressure medication new zealand discount moduretic 50 mg with mastercard. Longitudinal follow-up of children with functional nonretentive fecal incontinence heart attack proove my heart radio cut moduretic 50 mg without prescription. When a child does not grow well, or "fails to thrive," it can be an important sign of an underlying health or psychosocial problem. Failure to thrive is not a disease itself, but medical professionals are obliged to recognize and evaluate it with the goal of identifying and treating any underlying problems, as well as of restoring the child to normal growth and development. Most broadly, it is used to describe a patient of any age with poor weight gain, particularly after a stable growth pattern has been previously established. Another factor that makes prevalence data difficult to interpret is the inconsistent inclusion of infants with low birth weight in published studies. Ideally, malnutrition is assessed via a Subjective Global Nutritional Assessment, although this evaluation will require more time and more application of professional judgment than does anthropometry alone. Kwashiorkor is protein-energy malnutrition, the result of protein deficiency relatively greater than caloric deficiency. It is preferable to obtain serial measurements on the same scale, to avoid equipment-related variability, and to have the same provider obtain serial measurements of length/height. Length/height is more difficult than weight to measure accurately, as it can be easily confounded by squirming, posture, nonstandardized techniques, and inconsistently trained personnel. One center found that on standardized re-measurement of infant length, "true" length was an average of 2. Starting at the age of 24 months, children who can stand unsupported should be measured on a stadiometer. They describe the growth of children in the United States during a span of approximately 30 years (1963-1994), using data from multiple studies. The weight of children born preterm should be corrected for gestational age until they have reached 24 months of postnatal age, and length should be corrected until 40 months of postnatal age. Although some normal infants may have low weight or slow growth from the start, it is also possible for normal, healthy infants to experience "catch-down" growth. This phenomenon occurs when a child who may have been born large for gestational age or who had very rapid early weight gain then experiences a deceleration in weight gain, ultimately arriving at his or her "correct" weight. In other words, the pediatrician "must be an advocate for the child without becoming an adversary of the parents. Neither did they have poorer outcomes in educational attainment after correcting for factors such as socioeconomic status. Early iron deficiency is well known to cause irreversible developmental deficits that carry into adulthood, including decreased likelihood of completing secondary school or marrying, and an increased likelihood of poor emotional health. Almost any severe or chronic childhood illness may cause poor growth, whether directly or indirectly. Factors include inadequate nutritional intake, inadequate absorption, or increased metabolic needs. Even children who may be at risk for obesity later in life, such as those with Prader-Willi syndrome, may have poor weight gain in infancy and require special nutritional attention to achieve appropriate early growth. However, more than 80% of children with inadequate growth do not have any underlying medical disorder. In addition, involvement of a lactation consultant, occupational or speech therapist, and a variety of medical specialists may be necessary to properly address common maternal and infant factors in early breast-feeding that can lead to inadequate milk production and/or poor latch, and for coordination of breathe-suck-swallow patterns in term or preterm infants with oral motor delay. Abdominal bloating or ascites with muscle wasting and edematous hands and feet is particularly suggestive of kwashiorkor, a condition that is rare in the United States. On occasion, the evaluation of a child with poor growth leads to a suspicion of child maltreatment. In this situation, the local agency for child protective services should be called. Diagnosis and treatment of these feeding disorders requires a multidisciplinary team that may include nutrition, occupational therapy, hearing and speech, psychology, and psychiatry, in addition to medical subspecialists. Children with this disorder are at increased risk for future developmental difficulties. Home visiting by trained lay visitors may be helpful for some of these infants,30 although an initial inpatient admission is necessary in severe cases or when the safety of the child is in question. The child may be distractible while feeding, even during the first few months of life, although this condition often develops somewhat later at the time of transition to spoon-feeding or self-feeding. It is characterized by the acute onset of severe and consistent refusal of solids, liquids, or all textures. Children with this disorder show distress in anticipation of feeding and may refuse to swallow food placed in the mouth. Preterm infants and those with suck-swallow incoordination may be at particular risk for a posttraumatic feeding disorder. However, hospital admission may be warranted if neglect is suspected, when a patient is at risk for refeeding syndrome, or when outpatient management fails. The pressuring or coaxing tactics that parents may use to encourage their children to eat can be counterproductive, and are associated with increased food refusal even in the absence of sensory food aversion. This situation may occur when families are overly concerned about obesity and cardiovascular disease,33 or are fearful about food allergies or gluten sensitivity. On the other hand, nonspecific abnormalities may also lead to unnecessary anxiety and further workup. For instance, a finding of low serum bicarbonate may lead to further testing for renal tubular acidosis, leading to frequent "overcalls" of acidosis and potentially unwarranted subspecialist referrals. Zinc deficiency may itself contribute to poor growth, by causing anorexia, immune dysfunction, and poor deposition of muscle. Zinc supplementation trials have had an overall positive effect on both weight and height. However, supplementation of these particular micronutrients has not proven to improve growth in the absence of anemia or severe vitamin A deficiency. Diarrhea may become more apparent to parents after weaning or after introduction of solid foods to the diet. Among infants, the presence of gross blood in the stool or positive stool guaiac testing is frequently indicative of milk protein intolerance and should prompt consideration of a dairy-free diet. At any age, a decrease in stool pH or the presence of reducing substances is suggestive of carbohydrate malabsorption, although may also indicate other gastrointestinal conditions such as small intestine bacterial overgrowth. A marked elevation in spot fecal fat is suggestive of pancreatic insufficiency, such as in cystic fibrosis versus intestinal malabsorption, and may warrant testing of fecal elastase. Generally, neutral fat in the stool is more consistent with pancreatic insufficiency, whereas split fat is more consistent with intestinal fat malabsorption. The presence of a large number of small drops of split fat in the stool frequently indicates concomitant lactose maldigestion associated with mucosal injury. Malnutrition can itself cause small bowel atrophy and villous blunting, and in addition can directly suppress lactase expression by enterocytes. In those cases, it is generally preferable to use a ready-to-feed nutrient-dense formula if it is available. Otherwise, one can use an "energy supplemented" formula such as a powdered infant formula mixed to high concentration or with added fats or carbohydrates. Energy supplemented formulas may have inappropriate solute load or inadequate nutrient density, and are prone to contamination and errors in mixing. In a study comparing the use of nutrient-dense to energy-supplemented formulas in infants with poor growth, caloric intake and weight gain were the same, but the nutrient-dense formula group received 42% more protein and 15% to 40% more vitamins and minerals, and maintained a normal mean blood urea concentration. However, the group receiving energysupplemented formula had a 50% decrease in blood urea concentration, suggesting inadequate protein intake, and a decline in length z-score was observed. In general, caloric density should not exceed 26 kcal/oz for infants and 45 kcal/oz for toddlers. The recommendation to offer supplemental formula to a breast-fed infant should be made with care and sensitivity. Most infants and toddlers will gain weight effectively when a greater volume of food or food of higher caloric density is offered. However, some malnourished children are unable to take in adequate calories by these means because of anorexia. In children who have had chronic and substantial caloric deprivation, there is risk of refeeding syndrome with initiation of adequate nutrition, with possible hypokalemia, hypophosphatemia, and hypomagnesemia. Careful monitoring is required in these patients and a gradual increase of calories toward the eventual goal should take place over several days. The duration of supplemental tube feeds can range from a few days to months or years, as in the case of children with oral aversion or oral motor dysfunction, and ultimately a more permanent solution such as gastrostomy tube may be more practical and comfortable for the child and family. For preterm infants, continuous feeds require less energy expenditure than do bolus feeds. In cases where there is mucosal damage or atrophy, or if there is mucosal edema secondary to hypoalbuminemia, nutrient uptake may be limited, and slow continuous feeds are most appropriate. In the setting of short bowel syndrome, continuous feeds are recommended to maximize caloric absorption as well as intestinal adaptation. Gastroesophageal reflux episodes are not completely eliminated by transpyloric feeds, however. Regardless of the type of tube feeding, plans should be made for frequent nursing support in the home and/or clinic during the early weeks of feeding tube use. Parents should be educated in advance about the appropriate measures to take for equipment malfunction, tube dislodgment, feeding intolerance, leaking at the G-tube stoma, or other concerns. Parents may also derive support from the Oley Foundation as well as local groups of families dealing with the need for tube feeds. The caloric intake needed for "catch up" growth exceeds that needed for normal weight. For infants, it is often appropriate for an initial goal to be intake of 150% of caloric requirement for age, with the objective of achieving two to three times the average weight gain for corrected age. It is possible to calculate the anticipated caloric needs over baseline more precisely based on the desired composition of new tissue (fat vs. Regardless of the method used to select goal caloric intake, frequent weight checks are necessary, as calculations of resting energy expenditure, and therefore of caloric requirements, are frequently inaccurate. Whenever there is a concern for potential refeeding syndrome, initial feedings should be limited to 10% to 20% above the resting metabolic rate and slowly advanced. Children with kwashiorkor, with severe depletion of lean body mass, or with conditions of high metabolic need, such as cystic fibrosis or a postoperative state, may require higher protein intakes. Prompt and effective intervention to restore normal growth may also mitigate associated developmental concerns, particularly in more resource-poor areas. Diagnosis and treatment of feeding disorders in infants, toddlers, and young children. A 16-month-old child is admitted to the hospital with fever, cough, and volume depletion. Her physical examination and chest radiographs are consistent with pneumonia, with laboratory results typical of acute bacterial infection and iron deficiency anemia. During an observed meal, she takes only a few sips of milk and two bites of a chicken nugget. Have a multidisciplinary feeding team evaluate her oral intake in the outpatient setting B. Request that a nurse feed the child, and continue to offer her typical home diet C. At the age of 2 months, a full-term infant weighs only 600 g more than his 3600 g birth weight. He is exclusively breast-fed and is the first child of his parents, with a normal state newborn screen. He has at least six to eight wet diapers throughout the day, but is now passing a soft stool only every 2 days, decreased from the first weeks of life. Rectal examination is normal, but the stool obtained on digital exam is guaiac positive. Supplement breast-feeding with a standard infant formula offered after each nursing session B. Start lactulose, 5 mL daily, and reassure parents that the child has a normal growth pattern E. An 18-month international adoptee from Haiti has just arrived in the United States. Begin fat-soluble vitamin supplementation in addition to an oral hypoallergenic formula with medium-chain triglycerides C. Admit to the hospital for multidisciplinary evaluation and initiation of continuous nasogastric tube feedings with a standard toddler formula D. The child has been admitted for an acute respiratory illness, but her physical examination is also consistent with a chronic state of undernutrition. A multidisciplinary feeding evaluation may be indicated but should not delay the initiation of nutritional supplementation. Because the child has malnutrition and anemia, nutritional rehabilitation is indicated, but should be initiated carefully due to the risk of refeeding syndrome. Caloric intake 150% over estimated requirement might ultimately be needed, but would not be an appropriate initial regimen.
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