Diarrhea (pediatrics)

Acute diarrheal diseases are among the most common diseases of childhood and are the most common cause of dehydration in infancy and toddler age, which can lead to life-threatening conditions. However, they usually have a mild, self-limiting course.

Acute diarrhea typically begins in full health. It may be accompanied by fever, which may indicate an inflammatory etiology, or may be due to dehydration. Children, especially infants, are much more prone to dehydration than adults due to the greater basal need for fluids and electrolytes per kilogram of weight, large body surface area and increased tendency to vomit.

The most common causes of diarrheal diseases in children are viruses (rotaviruses, caliciviruses, adenoviruses, astroviruses, noroviruses and others). Other causes of acute diarrhea can include alimentary bacterial (eg salmonella and campylobacter) and parasitic infections, medications, food allergies, vitamin deficiencies, heavy metals and resorption disorders.

Infectious diarrheal diseases are a serious problem, especially in developing countries, where 3-4 million children die of them each year. In developed countries, fatalities are much rarer and the economic impact of the disease is particularly significant.

Acute diarrhea is defined as:


 * a sudden change in the consistency and character of the stool with frequent emptying of sparse mushy to watery stools,
 * stool volume is more than 10 ml/kg/day.

In infants and toddlers, we define diarrhea as:


 * more frequent emptying of a larger volume of loose stools
 * stools more than 3 times a day (we cannot automatically consider diarrhea)
 * stool volume greater than 10 g/kg/day
 * acute diarrhea usually does not last longer than a week

Diarrheal disorders by etiology

 * Viral gastroenteritis (viral diarrheal diseases)
 * Rotavirus enteritis
 * Adenovirus enteritis
 * Bacterial gastroenteritis (bacterial diarrheal diseases)
 * Campylobacter enteritis (causative agent: Campylobacter jejuni)
 * Salmonella enteritis (causative agent: Salmonella enteritidis, S. typhimurium)
 * Typhoid fever (causative agent: Salmonella typhi)
 * Paratyphoid fever (causative agent: Salmonella paratyphi)
 * Shigellosis (causative agent: Shigella dysenteriae, flexneri, boydii, sonnei)
 * Cholera (causative agent: Vibrio cholerae)
 * Infections caused by Escherichia coli
 * Gastrointestinal parasitosis
 * protozoa: Toxoplasmosis (causative agent: Toxoplasma gondii), Toxocarosis (Toxocara canis / cati), Giardiasis (Giardia lamblia), Amoebiasis (Entamoeba histolytica), Cryptosporidiosis (Cryptosporidium parvum)
 * nematodes: Ascariasis (caused by: Ascaris lumbricoides), Trichuriosis (Trichuris trichiura), Trichinella spiralis, Enterobiosis (Enterobius vermicularis), Strongyloides stercoralis, Ancylostoma duodenale, Necator americanes, Dracunulus
 * cestodes: Teniosis (agents: Taenia solium, Taenia saginata), Diphyllobothrium latum, (Hymenolepis nana), Echinococcus granulosus,…
 * Enterotoxicosis - caused by enterotoxins
 * Drug-induced diarrhea
 * Pseudomembranous enterocolitis

More detailed information can be found on the page Differential diagnosis of diarrheal diseases.

Patophysiology

 * Changes in the intestinal mucosa (impaired resorption, digestion, secretion and motility) lead to excessive loss of water and electrolytes, especially sodium and potassium, metabolic acidosis and subsequent dehydration.
 * Two main pathophysiological mechanisms: osmotic and secretory diarrhea.
 * The viruses directly damage the intestinal villi and enterocyte brush border enzymes.
 * Osmotic and secretory diarrhea are combined in the pathogenesis of rotavirus diarrhea. Osmotic diarrhea causes villous destruction (cell lysis), NSP4-induced glucose malabsorption (SGLT-1 inhibition) and inflammation (NK-κB, IL-8). Secretory diarrhea is based on crypt cell proliferation (compensatory secretory cell proliferation), NSP4 - enterotoxin (increased intracellular calcium, chloride secretion), vascular ischemia (microcirculatory disorders) and inflammation.
 * Enteroinvasive bacteria (Salmonella spp., Shigella spp., Campylobacter jejuni, enteroinvasive E. coli) cause ulcerations and inflammatory infiltration of the intestinal mucosa.
 * Some bacteria (enterotoxigenic E. coli, staphylococcal enterotoxin) stimulate active secretion of ions and water into the intestinal lumen by their toxins (c-AMP, c-GMP).
 * Non-invasive bacteria and parasites adhere to the mucosa and cause inflammatory infiltration.

Pathophysiology of dehydration

 * In the acute phase, the deficiency of body fluids first concerns only the extracellular space. With further progression, intracellular dehydration and tissue hypoxia occur.
 * In about 70-80% of patients, water and sodium losses are proportional and isotonic dehydration occurs.
 * About 10-15% of patients have disproportionately large ion losses (mainly sodium) compared to water losses and hypotonic dehydration occurs. Hyponatremia can also develop or worsen if, during diarrhea, losses are covered by high fluid intake with little or no ion content.
 * About 10-20% of patients have a disproportionate large water loss compared to electrolyte loss and hypertonic dehydration occurs. Improperly prepared dairy products are a common cause, causing a large renal load of electrolytes and increased urine production. Another cause may be the incorrect treatment of an acute attack of diarrhea with home-prepared solutions with a high concentration of salts.
 * Hypernatremia and dehydration may also be exacerbated by increased fluid loss in fever, high ambient temperature, hyperventilation, and associated decreased free fluid availability.

Etiology

 * is very diverse, a division into infectious and non-infectious is recommended
 * the most common cause in infants is infection

Clinical manifestation

 * the symptomatology of diarrhea determines the severity of mucosal damage
 * they usually start by refusing food 2-3 days before diarrhea occurs
 * children stop gaining weight, vomit, are pale, lose interest in the environment, have a fever
 * diarrhea is sudden, first the stools are mushy, then watery
 * manifestations of dehydration:
 * entering the enteric phase reduces the turgor of the skin, eyes are halon, the abdomen is meteoric, mild hepatosplenomegaly may be present, urine production is reduced
 * the pulse gradually accelerates, with severe dehydration it is filamentous
 * the fontanelle falls, tears are missing when crying
 * the most severe form of infant enteritis - toxicosis
 * it begins with vomiting of green vomit with an admixture of hematin, at the same time frequent watery stools
 * significant dehydration occurs - halon eyes, sunken fontanelle, skin fold, standing, acrocyanosis, anuria
 * the decisive step of the therapeutic procedure is the estimation of water and electrolyte loss, because acute lethality is conditioned only by hypovolemic shock
 * the degree of dehydration can be determined by weight loss, the severity of dehydration by laboratory examination

Laboratory findings

 * acute diarrhea with weight loss below 5% with good oral fluid intake can be treated only on an outpatient basis without laboratory tests
 * in case of loss above 5%, in case of epidemic diarrhea and in case of bloody stools, a thorough examination is indicated
 * manifestations of hemoconcentration - increase in Hb and hematocrit
 * determination of sodium, potassium and chlorides, osmolality, acid-base homeostasis
 * picture of severe toxic enteritis - metabolic acidosis (mainly due to loss of bicarbonate in the stool)
 * oliguria develops, often with proteinuria, urea and creatinine rise in the serum
 * hypernatremic dehydration causes hyperglycemia (we do not treat this with insulin because there is a risk of cerebral edema)

Diagnostics

 * anamnesis (nutritional change, epidemic occurrence, administration of ATB and other drugs)
 * stool evaluation information:
 * secretory diarrhea (most often infectious) - watery, sparse, often with fever
 * malabsorption of carbohydrates - foamy, sour smelling, pH drop below 6
 * chronic eating disorders - bulky, greasy, putrid-smelling
 * colon inflammation (often infections - Salmonella, Shigella, Yersinia, Campylobacter) - mucus-bloody
 * right at the beginning we have to send the stool for microbiological examination (it must not be too thin, in watery stools we no longer have to cultivate pathogenic organisms)
 * stool coating - the presence of polymorphonuclear cells indicates a bacterial infection
 * in chronic disorders there is a positive stool test for fats, carbohydrates, reducing substances, trypsin, proteins
 * to exclude cystic fibrosis, we examine chlorides in sweat
 * serology is not relevant for acute diarrhea, it is important in recurrent and chronic diarrhea

Treatment
Most acute infectious gastroenteritis resolves spontaneously, so in the vast majority of cases, antibiotic therapy is not indicated. The key is to maintain adequate hydration of the child. With reduced hydration, rapid oral replacement of water and electrolyte losses is important. correction of metabolic acidosis, and subsequent maintenance of hydration and early initiation of realimentation, which prevents further damage to the intestinal mucosa and thus the development of prolonged gastroenteritis.

Rehydration
In the treatment of dehydration, oral (enteral) rehydration is preferred, which is as effective as intravenous rehydration, but has fewer side effects and shorter hospital stays.

Oral rehydration solutions (PRR):


 * hypoosmolar, sodium content 60 mmol / l, composition according to ESPGHAN recommendations;
 * e.g. Kulíšek®, Kulíšek forte®, HIPP ORS 200®, Vodníček Baby®, Vodníček Jahoda®, Enhydrol Banán®;
 * if the child is unable to drink the solution, it is given by nasogastric tube;
 * fluid and ion loss is compensated in a short interval - depending on the dehydration rate of 30-80 ml / kg within 4 hours.

Hydration maintenance:


 * after correction of dehydration, the recommended daily volume of fluids is given frequently and in small doses in the form of usual drinks (breast milk, infant formulas, tea, mineral water,…);
 * hyperosmolar drinks such as juices or cola are not suitable;
 * PRR compensates for the accompanying losses of fluids and ions through diarrhea and vomiting - 10 ml PRR / kg and each stool, up to a maximum volume of 100–150 ml.

Recommended composition of glucose rehydration solution:


 * 60 mmol / l Na, 20 mmol / l K, min. 25 mmol / l Cl, 10 mmol / l citrate, 74-111 mmol / l glc
 * osmolality 200–250 mOsmol / l
 * are produced ready, or according to the recipe:
 * Rp.
 * Natrii chorati 0,4375
 * Kalii chlorati 0,373
 * Natrii citrici dihydrati 0,735
 * Glucosi 5,0
 * M. f. pulv.
 * D. ad. sacc. pap.
 * D. S. dissolve the contents of the bag in 250 ml of boiled water


 * rehydration solution is administered cooled to 4–8 ° C in spoons (5–10 min. always 5–10 ml of solution or continuously by nasogastric tube)
 * mild conditions (with a decrease of up to 5%) can be treated on an outpatient basis (for 4 hours we give 50–100 ml / kg)
 * moderate conditions must be hospitalized
 * in case of repeated vomiting or diarrhea, we add the amount lost (according to weight, or we count on one watery stool 50–100 ml)
 * after 4 hours we check the hydration, if it has adjusted, we start with timely realimentation
 * during diarrhea, we then give 10 ml of solution per kg and each aqueous stool
 * it is fundamentally wrong to use juice or cola to rehydrate - high osmolality and few ions

Realimentation
Early loading of the digestive tract reduces increased intestinal permeability through digestive enzymes, contributes to maintaining the integrity of the mucosa, prevents bacterial overgrowth and the possibility of developing a serious intestinal lesion, event. to atrophic mucosa.

Breastfeeding is not interrupted - breast milk is given continuously even during the child's current dehydration. In non-breastfed infants, resuscitation begins after 4 hours of exclusive rehydration solution administration. Infants on artificial nutrition are realized with infant formulas based on cow's milk, which they were fed before the onset of acute gastroenteritis. Infant formulas are given in full concentration, not diluted. Lactose-free, soy or hydrolysed milk formulas are not indicated. Toddlers and older children receive an age-appropriate diet - optimally first food containing starches (rice, potatoes, pasta, pastries), then lean meat, carrot soups, apple and banana puree, etc. Drinks high in fructose, sucrose or sorbitol and very sweet foods are not suitable. It is advisable to quickly transfer children to their normal diet, especially if they have not vomited.

Medications
Most acute gastroenteritis does not require medication. In the vast majority of cases, antibiotics are not indicated.

Indications for antibiotics:


 * presumed or confirmed bacterial infection (especially Salmonella enteritidis)
 * in infants less than 3 months of age,
 * in premature babies under 1 year of age,
 * in immunodeficient or immunosuppressed children,
 * in the current serious illness or malnutrition,
 * with signs of sepsis;
 * severe campylobacter enteritis;
 * severe Giardia lamblia infection;
 * infections Vibrio cholerae, Shigella dysenteriae, Salmonella typhi, Entamoeba histolytica etc.

Antibiotics:


 * the drug of choice is cotrimoxazole - for salmonella, shigella, yersinia, ETEC, EIEC - for about 7 days
 * for campylobacter we administer erythromycin, for clostridium difficile vancomycin
 * giardia and entamoeba are treated with metronidazole

Pharmacotherapy:


 * antiemetics (severe vomiting): ondansetron;
 * absorbency: smectite;
 * drugs that reduce increased intestinal secretion in infectious acute gastroenteritis: racecadotril (does not affect intestinal motility);
 * probiotics: Lactobacillus GG and Saccharomyces boulardii strains (as recommended by ESPGHAN / ESPID).

Micronutrients, disinfectants and motility suppressants are not indicated in developed countries.

Prevention

 * vaccination against rotavirus gastroenteritis

Related articles

 * Antidiarrheals

Source

 * BENEŠ, Jiří. Studijní materiály [online]. [cit. 2009]. 

Literature

 * HRODEK, Otto a Jan VAVŘINEC, et al. Pediatrie. 1. vydání. Praha : Galén, 2002.  ISBN 80-7262-178-5.
 * ŠAŠINKA, Miroslav, Tibor ŠAGÁT a László KOVÁCS, et al. Pediatria. 2. vydání. Bratislava : Herba, 2007.  ISBN 978-80-89171-49-1.