Diarrhoea and Malnutrition in Childhood
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Prenatal malnutrition and early life growth patterns can alter metabolism and physiological patterns and have lifelong effects on the risk of cardiovascular disease. Inadequate food intake, infections, psychosocial deprivation, the environment lack of sanitation and hygiene , social inequality and perhaps genetics contribute to childhood malnutrition. Inadequate food intake such as a lack of proteins can lead to Kwashiorkor , Marasmus and other forms of Protein—energy malnutrition.
The World Health Organization estimated in that globally, half of all cases of undernutrition in children under five were caused by unsafe water, inadequate sanitation or insufficient hygiene. In almost all countries, the poorest quintile of children has the highest rate of malnutrition. Diarrhea and other infections can cause malnutrition through decreased nutrient absorption, decreased intake of food, increased metabolic requirements, and direct nutrient loss.
Other diseases that cause chronic intestinal inflammation may lead to malnutrition, such as some cases of untreated celiac disease and inflammatory bowel disease. Children with chronic diseases like HIV have a higher risk of malnutrition, since their bodies cannot absorb nutrients as well. The nutrition of children 5 years and younger depends strongly on the nutrition level of their mothers during pregnancy and breastfeeding.
Infants born to young mothers who are not fully developed are found to have low birth weights. Short stature of the mother and poor maternal nutrition stores increase the risk of intrauterine growth retardation IUGR. A study in Bangladesh in reported that rates of malnutrition were higher in female children than male children.
Measures have been taken to reduce child malnutrition. Studies for the World Bank found that, from to , the number of malnourished children decreased by 20 percent in developing countries. The Progresa program in Mexico combined conditional cash transfers with nutritional education and micronutrient-fortified food supplements; this resulted in a 10 percent reduction the prevalence of stunting in children 12—36 months old.
In Nigeria, the use of imported Ready to Use Therapeutic Food RUTF has been used to combat malnutrition in the North, However, a research has shown that Soy Kunu , a locally sourced and prepared blend consisting of peanut, millet and soya beans contains the components of the Ready to Use Therapeutic Food RUTF and this has been used massively to reduce malnutrition in the north. Breastfeeding can reduce rates of malnutrition and dehydration caused by diarrhea, but mothers are sometimes wrongly advised to not breastfeed their children. Treatment with antibiotics such as amoxicillin or cefdinir improve the response and survival rate of severely malnourished children to an outpatient treatment plan which provided therapeutic food.
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As underweight children are more vulnerable to almost all infectious diseases, the indirect disease burden of malnutrition is estimated to be an order of magnitude higher than the disease burden of the direct effects of malnutrition. From Wikipedia, the free encyclopedia.
A condition in children from eating a diet in which some nutrients are either not enough or are too much. Main article: Breastfeeding. Goldbach, Lacey N. LaGrone, Guthrie J.
This topic provides information about Childhood diarrhoeal diseases and its management.
Meuli, Richard J. Wang, and Kenneth M. Maleta January 31, The New England Journal of Medicine. The addition of antibiotics to therapeutic regimens for uncomplicated severe acute malnutrition was associated with a significant improvement in recovery and mortality rates.
Watkins, W. Allan Nutrition in pediatrics: basic science, clinical application. Hamilton: BC Decker. Safer water, better health — Costs, benefits and sustainability of interventions to protect and promote health. Food and development. Abingdon, Oxon: Routledge.
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- Relationship between diarrhea and malnutrition.
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The establishment of a day cutoff value to distinguish acute from persistent diarrhea was justified by the fact that mortality rates were found to be roughly 0. At birth, the bowel is usually sterile; colonization by the maternal vaginal and fecal microbial flora begins in the first days of life. This first colonization is one of the most important immune exposures of neonatal life. Humans are constantly challenged by pathogenic organisms viruses, bacteria, and protozoa. The frequency with which a given enteropathogen is isolated from stool samples can differ between developed and developing nations; within geographic regions; according to age, immunocompetence, and presence or absence of breastfeeding; and depending on the season.
The enteropathogenic agents isolated during PD are not always the same found in the acute stage of the diarrheal episode, which suggests that secondary infection may play a major role in the um persistence of diarrhea. The following list provides an overview of the main enteropathogenic microorganisms isolated from stool cultures of children with PD, as reported by various centers worldwide. The epidemiological features of PD patients do not differ significantly depending on causative agent.
In most cases, children with PD were not breastfed or were weaned at an excessively early age. Diarrhea is similar to that of acute episodes, but is associated with a malabsorption syndrome. This phenomenon is made even more serious when nutritional support remains inadequate during the convalescent stage, which is usually the case due to anorexia and improper refeeding practices.
PD is the end result of a variety of insults sustained by children who are exposed to frequent, severe diarrheal episodes due to a combination of host-dependent factors and highly prevalent environmental contaminants. These episodes generally occur in children under the age of 3.
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Bhutta et al. Furthermore, there are other host-related indicators, including young age, worsening nutritional status, and immune deficiency. They also note that errors in nutritional and pharmacological management of acute diarrheal episodes can also lead to persistence of the disease process. Recurring intestinal infection causes mucosal injury of the small bowel, and, as such, may lead to villous atrophy.
This reduces the absorptive surface area of the small intestine, increases inflammatory infiltration of the lamina propria, and encourages breakdown of the epithelial permeability barrier, facilitating penetration of potentially allergenic foreign proteins and thus increasing the likelihood of persistent diarrheal disease due to development of intolerance to multiple foodstuffs. Progression from acute to persistent diarrhea is due to an interaction between several complex pathophysiological mechanisms that affect the patient's nutritional status.
Among the countless factors that may play a role in perpetuating diarrheal illness, small bowel bacterial overgrowth caused by colonization of the small intestine by colonic flora most certainly has a major impact. This pathophysiological phenomenon, which is particularly associated with anaerobic bacteria such as Veillonella and Bacteroides species, predisposes to intestinal mucosal injury. Furthermore, the presence of secondary and unconjugated bile salts in the small bowel prevents formation of mixed micelles, which play an essential role in ensuring solubilization of dietary fats.
This pathological mechanism thus contributes to poor digestion and malabsorption of lipids, leading to steatorrhea. Patients may therefore develop other clinical complications, such as allergy to dietary proteins or multiple food intolerance, particularly to lactose and even to monosaccharides; this further perpetuates bowel injury and the vicious circle of diarrhea, malabsorption, and protein-energy malnutrition, which is the single greatest determinant of jejunal mucosal recovery failure, as well as specific micronutrient deficiencies.
Characterization of the damage caused by PD, with identification of the changes in digestion, absorption, secretion, and resorption of minerals, carbohydrates, proteins, and lipids induced by chronic enteropathy, is extremely important for gaining a better understanding of this condition. Secondary infections can also play an important role in prolonging diarrheal illness. Examination of the mucosa showed villus stunting, effacement of intercellular spaces which hampered individual visualization of enterocytes , and presence of lymphocytes and fat droplets in the small bowel lumen. In most patients, vast amounts of mucus covered the epithelial surface of the jejunum, and in some cases, a mucus-fibrinoid pseudomembrane was found in direct contact with enterocytes.
This most probably led to severe impairment of nutrient absorption due to enterocytes obstruction, thus perpetuating a malabsorption syndrome, which was present in nearly all patients in the study. It is important to distinguish the enteropathy caused by persistent bacterial colonization from the post-infections enteropathy that occurs secondary to failed or delayed regeneration of the bowel mucosa. Malabsorption and malnutrition are common factors in PD.
Diarrhoea and malnutrition
The former is defined as the presence of nutrients in stool with concomitant weight loss or failure to thrive, despite an age-appropriate diet. As PD has a presumably infectious etiology and is perpetuated in the form of multifactorial complications, precise diagnosis and determination of the causative agent and potential secondary complications will require detailed information on the following topics: a comprehensive clinical history extending as far back as the onset of the diarrheal illness; prior dietary history; breastfeeding history; socioeconomic status and living conditions; prior medical history, including prior infectious diseases; and family history.
History and physical examination can outline a profile of the patient's nutritional status and other consequences of the diarrheal illness. Some authors, who believe no single enteric pathogen is associated with PD in developing countries and that pathogens are isolated as often in children with diarrhea as in healthy controls, which would indicate that enteropathogenic agents are not the cause of PD, suggest that stool cultures are only warranted in conditions amenable to routine investigation.
Stool samples should also be tested for pH, reducing substances, white blood cells, occult blood, alpha 1-antitrypsin, and steatocrit. In light of the high prevalence of dietary carbohydrate intolerance as a factor perpetuating diarrhea in patients with PD, the laboratory workup should include challenge tests with the various carbohydrates consumed as part of a regular diet, including lactose, glucose, and fructose.
A lactulose challenge test should also be performed to detect potential small bowel bacterial overgrowth. All challenges should preferably be performed through the hydrogen breath test technique, as it is a noninvasive and highly sensitive and specific method. If possible, fecal electrolyte testing should also be performed, as it can distinguish osmotic from secretory diarrhea.
Once the intensity and extent of morphological injury have been established, dietary and therapeutic management can be planned more reliably. When rectal bleeding is present in addition to diarrhea, rectal biopsy is required for assessment of the degree and type of inflammatory process at hand. In , Lins et al. Regarding antimicrobial therapy in patients with established PD, the current evidence suggests that, in certain circumstances, antibiotics can shorten the duration of symptoms and, in some cases, reduce the likelihood of transmission.
Some pharmaceuticals have been employed in an attempt to prevent prolongation of acute diarrheal episodes. A 3-day course of Saccharomycis boulardii has been found to reduce duration of diarrhea, increase stool consistency and decrease the frequency of bowel movements. The management strategy of choice for this clinical picture is refeeding with formulas based on extensively hydrolyzed protein or, if necessary, an amino acid mixture.
In the event of persistent anorexia, the patient should be fed through a nasogastric or, if possible, a nasoenteral tube, preferably on a continuous drip, and always with the objective of transitioning back to oral feeding as soon as possible. If attempts at nasogastric or enteral feeding are unsuccessful, parenteral nutrition is indicated preferably through a peripheral line, to minimize the risk of systemic catheter-associated infection , again with the objective of transitioning back to oral feeding as soon as possible.
In light of the severity of diarrhea, which still poses a public health issue and cannot be overcome if patients' immune systems are compromised, Rocha et al. The authors conclude that zinc is not only an essential curative element in diarrheal episodes, but also an important prophylactic against diarrheal disease.
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Lukacik et al. Increased levels of brush border disaccharidases are indicative of a transporter effect for this electrolyte and of a potent immune response assisting intestinal defenses. This finding has also been described with adequate serum levels of zinc. In , the United Nations Children's Fund UNICEF and the WHO published a report proposing six measures for worldwide implementation as a strategy for control of diarrheal disease, namely: 1 fluid replacement to prevent dehydration; 2 zinc treatment; 3 rotavirus and measles vaccinations; 4 promotion of breastfeeding and vitamin A supplementation; 5 promotion of handwashing with soap; 6 improvement of water supply quantity and quality, including treatment and safe storage of household water; 7 community-wide sanitation promotion.
Achieving an adequate nutritional status is much more difficult in the setting of recurrent gastrointestinal infections ultimately leading to malabsorption. Infections are even more devastating in malnourished patients. Intestinal infection leads to malnutrition and malnutrition increases the risk of new intestinal infection. Breaking the vicious cycle of diarrhea and malnutrition should be the priority objective of all pediatricians if children are to develop to their fullest potential.
Measures required during an acute diarrheal episode include ensuring adequate hydration, zinc supplementation, and uninterrupted feeding. When an acute episode stretched over more than 7 days, it is termed prolonged diarrhea Pro-D, duration days. The epidemiology of Pro-D has yet to be studied in depth. This increased risk is due to the effects of prolonged diarrhea on nutritional status and immune function, and due to induction of changes in the intestinal barrier or gut flora. In conclusion, improvements in sanitation and hygiene are of the utmost importance if the incidence of diarrhea and, in particular, progression to PD is to be reduced.
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