DIGESTIVE SYSTEM

DEFINITION

• Inflammation of the oral tissues including lips, oral mucosa, gums and the posterior pharyngeal wall.

CAUSES

• Bacteria• Virus

• herpes simplex virus• Cosackie virus

• Fungal infections• Candida

Stomatitis

• fever (often very high in the case of herpetic infection);

• drooling;

• dysphagia;

• loss of appetite;

• erythema;

• vesicles;

• ulcers: confluent ulcers can take the shape of large and irregular white areas;

• submanidbular lymph nodes;

• herpetic stomatitis usually lasts ten days; herpangina lasts only a few days.

Stomatitis - symptomatology

Disease CauseType of lesion Site Size

Other clinical signs

Herpangina or hand-foot-and mouth syndrome

VirusCoxsackieEchovirus,Enterovirus

71

Vesicles and ulcers

accompanied by erythema

Anterior column, posterior palate;

pharynx and oral mucosa

1-3 mm

Dysphagia, vesicles on the palm of the hands, on the sole of the feet and in

the mouth

Herpetic stomatitis

Herpex simplex virus

Superficial vesicles and ulcers which

could be confluent

Gums, oral mucosa,

tongue, lips> 5 mm

Drooling, coalescence of

lesionsDuration of

approximately 10 days

Aphthous stomatitis Unknown Ulcers with

exudate

Oral mucosa, lateral surface of the tongue

> 5 mm

Otalgia, afebrile state

In general, there are just one or two

lesions

DIFFERENTIAL DIAGNOSIS

• ulcerative-necrotizing angina (Vincent’s angina)• mononucleosis.

COMPLICATIONS

• dehydration• secondary infection (e.g. gangrenous stomatitis).

TREATMENT

• increase the oral fluid intake;• nutritional changes (consumption of tasteless and non-acid liquids);• antipyretics: paracetamol 20-50 mg/kg/ day in 3-4 intakes, PO (oral administration) or ibuprofen 20-40 mg/kg/day in 3-4 intakes, PO;• mouthwashes with an anesthetic solution (benzocaine) + borax glycerine;• antibiotic therapy in case of secondary bacterial infection.

Stomatitis

• caused by Candida albicans;

• 2-5% of the normal newborns

• thrush after the 1st year of life: frequent use of antibiotics/immunodeficiency/diabetes.

Oral Thrush (“Muguet”)

SYMPTOMATOLOGY

• multiple white plagues + hyperthermic oral mucosa (lips, palate, tongue)• removal of plagues " punctiform areas with slight bleeding;• pains + food problems

DIAGNOSTIC

• clinical

TREATMENT

• paint the mouth with a nystatin solution or with sodium bicarbonate;• fluconazole 3-6 mg/kg/ day in one dose, PO.

DEFINITION

• reflux of stomach contents into the esophagus " gastrointestinal, respiratory and neurobehavioral manifestations.

Physiologic reflux

• appears most often at the age of 1-4 months;• short episodes (small quantities) after meals.

Pathologic reflux

• unusually high quantity of regurgitated food;• episodes with high frequency/ extended periods of time.

Gastroesophageal Reflux (Ger)

CAUSES

• disturbance of the normal functioning of the esophagus and related structures (dysfunction of the esophageal sphincter)

Predisposing factors

• dorsal decubitus position;• certain food and drugs.

Gastroesophageal Reflux (Ger)

Ger - symptomatology

Digestive manifestations

• regurgitations;• vomiting: dietary/

sanguineous/ hematemesis;

• esophagitis;• consequences:

underdevelopment, malnutrition, anaemia.

Respiratory manifestations

• chronic cough;• recurrent

wheezing• recurrent

bronchopneumopathies

• cyanotic attack or apnea (obstructive).

Neurobehavioral manifestations

• irritability;• neck

hyperextension or marked flexion of the neck on one side (torticollis - Sandifer syndrome)

Infants

Gastrointestinal manifestations (esophagitis)

•halitosis (caused by the reflux liquid in the mouth);•odynophagy;•dysphagia;•regurgitations;•chest pain (“burns”)•hematemesis;•consequences: anemia (caused by an iron deficiency).

Ger - symptomatology

Children and adolescents

Respiratory manifestations – the same

DIFFERENTIAL DIAGNOSIS

• gastroenteritis;• vomiting of central origin: hydrocephalus, brain tumor;• metabolic diseases: galactosemia, phenylketonuria;• food intolerance (e.g. milk allergy, celiac disease);• pyloric stenosis, esophageal atresia, intussusception.

COMPLICATIONS

• narrowing of the esophagus;• growth delay;• anemia;• aspiration pneumonia;• asthma (25-80% of asthmatic children have a GER);• apnea/ sudden infant death.

Ger

• hemogoblin dosage;

• esophageal transit with contrast medium;

• pH probe monitoring of the esophagus: Ph<4 for a period >5% in the total recording time; > 2 reflux episodes/hour

• endoscopy

• upper digestive endoscopy: Savary classification of the esophagitis:• Grade 1 – non-confluent erosions

• Grade 2 – longitudinal non-circumferential erosions

• Grade 3 – longitudinal confluent circumferential erosions without stenosis

• Grade 4 – ulcerations with stenosis or metaplasia

• Grade 5 – stenosis without ulcerations or metaplasia

• esophageal manometry;

• scintigraphy with 99Tc.

Diagnostic Tests

Posture

• place the child in upright position;• avoid the dorsal decubitus;• elevate the head of the bed with 30 grade

Food

• prepare smaller meals, but more often;• thicken the baby food (add rice cereals)

Ger - Treatment

Medical treatment

• Antacids• H2 receptor-antagonists of the histamine: ranitidine 5-10mg/kg/day, 2 doses, PO; famotidine 0,5 – 1(1,5)mg/kg/day, 2 doses, PO (max. 40mg/day).• Proton pump inhibitors: omeprazole 0,7 -3,3 mg/kg/day, PO; lansoprazole 1mg/kg/day, PO; esomeprazole 10-20mg/day, PO; pantoprazole 20-40 mg/day, PO.• Prokinetics: domperidone (MotiliumR) 0,2 -0,3 mg/kg/day, PO, in 3 doses before meals.• These drugs act by raising the base pressure of the lower esophageal sphincter, by improving the esophageal evacuation and by accelerating the gastric emptying. The usual

duration of the treatment is of 6-8 weeks.

Surgery

• failure of medical treatment;• severe or refractory effects of the treatment (growth delay, recurrent pneumonia, peptic stenosis);• Nissen fundoplication

Ger - Treatment

DEFINITION

• the gastritides are inflammatory acute and chronic affections of the gastric mucosa with specific histological changes: the inflammation, the edema and the hyperemia of the mucosa, without the breaking of the latter one;

• the gastric and duodenal ulcers are deep lesions of the epithelium, which penetrate through muscularis mucosae.

FREQUENCY

• an admission over 2500 is due to a gastric or duodenal ulcers (in the pediatric environment).

Gastritis And Ulcer (Gastric And Duodenal)

acute:

•bacterial (H. Pylori, staphylococcus – phlegmonous aspect, streptococcus, E. coli);•viral (herpes, cytomegalovirus);•medicinal (aspirin, NSAID, corticosteroids, potassium and iron preparations);•corrosive

chronic:

•bacterial (H. Pylori);•granulomatous (Crohn’s disease);•eosinipohilic;•autoimmune;•hypertrophic (Menetrier’s gastritis);•lymphocytic – erosions, vesicular aspect;•athropic + megaloblastic anemia " risk of evolution towards cancer;•chemical (reflux gastritis).

Gastritis - Classification

primary (H. pylori)

secondary:

stress ulcers (hypoxia, respiratory distress, septicemia,

traumas, burns);

medicinal ulcers: aspirin, NSAID, corticosteroids;

corrosives.

Ulcers - Classification

The primary peptic ulcer is a multifactorial disease, produced by:

• the imbalance between the defense factors (layer of mucus) and the attacking factors (acid hypersecretion + pepsin);

• H. pylori: a gram-negative, spiral, very mobile bacteria;• the infection with H pylori is more frequent in the developing countries where approximately 65% of the

children are infected before the age of two years;

• H. pylori is incriminated for 90% of the cases of duodenal ulcers; very rarely, H. pylori (type 1 carcinogen) is associated with a lymphoma at the child.

• hereditary factors (OI blood type)

• psychological stress

• alcohol, cigarettes

Pathogenesis

Primary ulcer is rare between 3-5 years; its frequency higher after 10-12 years.

* 2 main symptoms:• abdominal pain (diffuse, periumbilical, epigastric);

• vomiting (dietary, bilious, hematemesis);

• other: anorexia, nausea, heartburn, melena.

• Preschool children can present nausea, vomiting, abdominal pains incorrectly located, weight loss and irritability. Older children present epigastric pains being sometimes waken at night, or even worse, in the morning, on an empty stomach and relieved by food, manifestations which are similar to the ones of an adult.

• Secondary ulcer is specific to young ages (including newborns) and manifests especially through a complication (hemorrhage/perforation)

Symptomatology

X-ray examination

• direct signs: niche on the lesser curvature/ at the level of the bulb;• indirect signs: convergence of the folds of mucosa, bulbar deformations, motility disorders, stasis liquid.

Upper digestive endoscopy

• allows the direct visualization of the lesion (form, dimensions, base, existence of hemorrhage), of the associated lesions (e.g. nodular gastritis) and the biopsy sampling (3-5)

Diagnosis of infection with H. pylori

• invasive methods - rapid test of the urease• histopathological examination;• culture.

• non-invasive methods - serology: ELISA IgG;• urea breath test 13C;• test of H pylori antigen in the stools.

Diagnostic Tests

Normal diet! - carbonated drinks, coffee, alcohol and cigarettes are prohibited.

Medical treatment

• antacids

• H2 receptor-antagonists of the histamine: ranitidine (4)5-(6)10 mg/kg/day, 2 doses, PO, famotidine 0,5 – 1(1,5)mg/kg/day, 2 doses, PO (max. 40mg/day).

• proton pump inhibitors: omeprazole 0,7 -3,3 mg/kg/day, PO; lansoprazole 1mg/kg/day, PO, esomeprazole 10-20mg/day, PO; pantoprazole 20-40 mg/day, PO.

• sucralfate: used in the prophylaxis of the stress ulcer, 0,5 – 1 g/6 hours.

• the infection with H pylori: we appeal to a triple therapy = a proton pump inhibitor combined with a double antibiotic therapy (e.g. clarithromycin and amoxicillin or metronidazole) for 7 days.

• ”there is no ulcer without acid” - “there is no ulcer without H. pylori”

• eradication of H. pylori → peptic ulcer recurrence

Surgery - perforation; pyloric stenosis.

Interventional endoscopy - hemorrhages.

Treatment

DEFINITION

• inflammatory process (usually infectious) related to the alimentary tract and causing diarrhea and vomiting.

Gastroenteritis

Virus• rotavirus: the most frequent case at children from 6 to 24 months;• enteric adenovirus;• echovirus;• Coxsakie.

Bacteria• Salmonella;• Shigella;• Escherichia coli;• Campylobacter.

Parasites • Giardia lamblia.

Fungus infection • Candida.

Other causes• misfeed/ overeating (at newborns);• undesirable reaction to antibiotic therapy, causing an infection with Clostridium difficile.

Causes

• high temperature in the cases of infectious gastroenteritis;

• pallor/cyanosis;

• vomiting: frequency, color and quantity;

• thirst;

• abdominal pain: light sensitivity, diffused and generalized;

• abdominal distension and bowel sounds;

• stools: frequency, quantity, consistence (formed or watery), color, presence of blood and mucus;

• note the liveliness and the level of activity and the change of the mental status (e.g. irritability, lethargy).

Symptomatology

The dehydration which can be attributed to diarrhea is much higher at the child than at the adult taking into account the difference of the water content of the body and the weight/body surface ratio.

• dryness of mucosae;

• fontanelle depression;

• persistence of the cutaneous fold: when pinched, the skin sometimes preserves the shape of a tent for several seconds before taking its normal shape;

• mental status (e.g. irritability, apathy);

• the breathing is normal, except for the cases of shock; metabolic acidosis can cause a tachypnea with deep breathing = Kussmaul breathing (“dispnee sine materia”).

Dehidration

viral/bacterial gastroenteritis;

infections outside the alimentary tract can also cause diarrhea and vomiting (otitis media, pneumonia and urinary infections) ;

bronchopneumonia of the infant (fever, cyanosis, tachypnea, dehydration); common mistake of the diagnosis!

Differential Diagnosis

• CBC: hyperleukocytosis with polynucleosis in case of infectious gastroenteritis;

• blood electrolytogram:• natremia (Na=133-143 mmol/ L): iso/hypo/hyper-natremia

• kalemia (3,5-5 mmol/L): hypokalemia;

• bicarbonate (HCO3= 23-29 mmol/L): decrease of biocarbonates (metabolic acidosis);

• high urea and blood creatinine (in case of dehydration);

• ASTRUP: PaO2, PaCO2, pH, SaO2;

• urine analysis in order to detect the presence of ketones;

• the research of leucocytes and bacteria in the stools, stool culture;

• ELISA: diagnostic technique of choice of the infection with rotavirus for routine.

Laboratory

Rule: breastfeeding must continue!

Rule: stopping oral nutrition is a serious mistake (collapse of the digestive tolerance)!

Oral re-hydration (RVO)

• We must not administer only the oral re-hydration solution for more than 12-24 hours.

• “Transition” food: rice porridge, carrot soup (no more than 24 hours).

• The return of the previous alimentation must be progressive, 30-60ml/meal without exceeding 120-150 ml/kg/day.

The intravenous re-hydration

Symptomatic treatment: antipyretics; you must not use spasmolytics; the role of antiemetics is also very limited.

Etiological treatment → antibiotic therapy 5-7(10) days;

Treatment

DEFINITION

• allergic reaction to proteins of cow milk;

• 1-7,5% of infants with artificial feeding.

Sensitivity To Milk Proteins

the acute form

• jet-like vomiting;• diarrhea, with

dehydration;• abdominal pain;• respiratory symptoms

(wheezing, dyspnea);• state of shock

(gastrointestinal anaphylaxis).

the chronic form

• eczema• the form with colitis:

diarrhea with mucus and blood + ferriprive anemia;

• chronic diarrhea + malabsorption: poor weight gain and steatorrhea;

• the family history of allergy must be investigated.

Symptomatology

DIFFERENTIAL DIAGNOSIS• lactose intolerance;• malabsorption syndrome;• gastroenteritis.

COMPLICATIONS• acute dehydration with metabolic acidosis;• digestive hemorrhage  → anemia;• protein malabsorption → growth delay;• hypoproteinemia → edemas.

Sensitivity To Milk Proteins

• high rate of serum of eosinophils and in the stools;

• high rate of serum immunogoblin E (IgE);

• the provocation is best way to confirm the diagnosis!

• *the provocation should be attempted only towards the age of one year, after at least six months of a regime of exclusion;

• *the rapid progressive re-introduction, for 24 to 72 hours, is the most common practice (we start with 1-5 ml);

• *the oral desensitization is based on the ingestion of milk as drops, with a higher dose everyday;

• *Goldman’s criteria: the symptoms must disappear after the elimination of the antigen and reappear after its re-introduction.

• intestinal biopsy: intestinal villous atrophy

Diagnostic Tests

Prevention• identify rapidly the children at-risk and record the highly atopical family cases;• recommend breastfeeding;• delay the introduction of cow milk in the child’s diet (e.g. not before the age of 12

months)

Treatment• the treatment consists in the exclusion of the food in question, even the traces;• a certain quantity of dietary proteins ingested by the mother can be found in the

mother’s milk;• soy-based proteins diet;• up to 25% of the children sensitive to the proteins of cow milk are also allergic to

soy proteins → the replacement of cow milk with a milk formula for the infant which is soy-based might be useless.

• casein hydrolysate-based milk• amino acids-based milk.

Treatment

Thank you!