Methods of clinical examination of the digestive system in children (inspection, palpation, percussion, auscultation). Semiotics of digestive system.
Acute abdomen.
Embryogenesis
The digestive system develops from endoderm at 11-15 days since fertilization. Liver and pancreas appear as buds at 26-30 days since fertilization.
General overview
The digestive system consists of the digestive tract, a tube extending from the mouth to the anus, and its associated accessory organs (primary glands), which secrete fluids into the digestive tract. The digestive tract is also called the alimentary canal. The term gastrointestinal tract technically only refers to the stomach and intestines.
Image.1. Digestive system.
The first section of the digestive tract is the mouth, or oral cavity. It is surrounded by the lips, cheeks, teeth,and palate, and it contains to the tongue.
The salivary glands and tonsils are accessory organs of the oral cavity. The oral cavity opens posteriorly into the pharynx, which in turn,continues inferiorly into the esophagus. The major accessory structures are single-celled or small, simple tubular mucous glands distributed the length of the pharynx and the esophagus. The esophagus opens inferiorly into the stomach. The stomach wall contains many tubelike glands from which acid and enzymes are released into the stomach and are mixed with ingested food. The stomach opens inferiorly into the small intestine. The first segment of the small intestine is the duodenum. The major accessory structures in the segment of the digestive tract are the liver,the gallbladder.and the pancreas. The next segment of the small intestine is the jejunum. Small glands exist along its length and it is the major site of absorption. The last segment of the small intestine is the ileum, which is similar to the jejunum except that fewer digestive enzymes and more mucus are secreted and less absorption occurs in the ileum. The last section of the digestive tract is the large intestine. Its major accessory glands secrete mucus. Its absorb water and salts and concentrates undigested food into feces. The first segment is the cecum, with the attached veriform appendix. The cecum is followed by the ascending, transverse, descending, and sigmoid colons and the rectum. The rectum joints the anal canal, which ends at the anus, the inferior termination of the digestive tract.
Anatomy and function of digestive system
Functional and anatomical peculiarities of the digestive system
The main functions of the digestive system
1. To process and absorb nutrients.
2. The excretory function.
3. Detoxification.
4. Maintain fluid and electrolyte balance.
5. The mechanical function.
Morphology peculiarities of all parts of digestive system in infant
1. The mucous membrane is thin, soft, dry and easy to damage.
2. The submucosal layer is well vasculerised.
3. The submucosal layer consists of loose connective tissue.
4. Underdevelopment (immaturity) of muscular and elastic tissue.
Physiological peculiarities of digestive system in infant
1. The secretory function of digestive system is impaired.
2. Digestive system produces only small amounts of digestive juice.
3. Digestion is worsen when the food does not adequate of age of child.
Peculiarities of oral cavity in infant
1. It is relatively small.
2. Teeth are absent.
3. The palate is flat.
4. The tongue is relatively thick and wide.
5. The sucking fat in the cheeks fill the mouth and help maintaiegative pressure.
Peculiarities of pharynx in infant
1. It is relatively wide and short.
2. The oral part is on the same level as oral cavity.
3. The way which the food passage is lateral of larynx.
4. The baby can‘t breath and swallow the food at once.
Peculiarities of the oesophagus in infant
1. Average length of the oesophagus iewborn is
2. It is relatively narrow.
3. The entrance into the oesophagus is:
iewborn – between the III-IV cervical vertebra;
2 years old – IV-V cervical vertebra;
12 years old – VI-VII cervical vertebra;
4. The localization of lower oesophagus’ sphincter is the same in children of different age groups (X-XI thoracic vertebra).
5. Ratio between the length of the oesophagus and the length of the body is the same in children of different age groups (1:5).
Length of the oesophagus in children of different age groups
iewborn is 11-
in 1.5-2 years – 22-
in 15-17 years – 48-
The constriction of the oesophagus
Anatomical
1. Upper constriction – in place of entrance into the oesophagus.
2. Middle constriction – in place of adjacent the trachea to oesophagus.
3. Lower constriction – in place of entrance through the diaphragm.
Physiological
1. Upper constriction – at the begining of the esophagus
2. Middle constriction – in place of adjacent the aorta to esophagus
3. Lower constriction – in place of entrance into the cardial part of the stomach.
Peculiarities of the stomach in infant
1. The stomach lying horizontally, is round until approximately 2 year of age.
3. Gastroesophageal reflux is frequent.
4. Cardial sphincter has a poor development of mucous membrane and muscular tunic.
5. Pyloric part is developed well.
6. The fundus of stomach is under the left dome of diaphragm.
7. The weight of the stomach is 6-
The anatomical capacity of the stomach, cm3
Newborn – 30-35.
4 days – 45.
14 days – 90.
Iext months the anatomical capacity of the stomach increase for 25 cm3.
2 years – 500.
4 years – 700.
8 years – 1000.
An adult- 1200-160.
The physiological capacity of the stomach, cm3
Newborn – 7.
1 year – 250-350.
3 years – 400-600.
10 years – 1300-1500.
Peculiarities of the stomach in infant
1. The proteolytic function of the stomach juice in baby is 1/3 less than in adult.
2. Figures of common gastric acidity is in 2.5-3 times lower than in adult.
3. The fats of human’s milk is easy digestion by enzyme lipase of human’s milk, saliva and stomach juice.
4. Highly saturated fats is digestion only in a small intestine.
Peculiarities of the bowels in infant
1. The length is relatively longer then in adult.
2. Ratio of bowels length and body length are:
in newborn – 8.3:1;
1 year – 6.6:1;
16 years – 7.6 1;
an adult – 5.4:1.
3. The increasing of bowels length is slower than the increasing of length of the body.
4. The bowels are more mobile in infant.
Peculiarities of the small intestine in infant
1. The length is in two times less than in adult.
2. The length of small intestine mesentery is relatively longer.
3. The membrane is thin, is well vascularisied.
4. The intestinal glands are bigger then in adult.
5. The lymph cells are in each little parts of small intestine.
Peculiarities of the large intestine in infant
1. The large intestine is not completely developed.
2. The length of the large intestine is the same as the body length (in any age of a child).
3. Haustrumes appear after 6 month of life.
Peculiarities of the sigmoid colon in infant
1. It is longer.
2. It is mobile.
3. Increasing in size during the life.
4. The localization of sigmoid colon is something upper in children younger 5 years then in schoolchildren (in schoolchildren it is in the pelvic cavity).
Peculiarities of the rectum in infant
1. The localization is under the entrance into the small pelvis in preschoolchildren.
3. It is longer.
3. It is mobile.
4. The ampulla of rectum is absent iewborn.
Peculiarities of the liver in infant
1. Before the birth the liver is the largest organ of the body.
2. It is in the upper quadrant of the abdomen and one part of the left and epigastrium.
3. The left lobe is very large before the birth.
Liver functions
1. Bile salts emulsify fats making them aviable to intestinal lipases.
2. Help make and products soluble and aviable for absorption by the intestinal mucosa, aid peristalis, fluid on enzyme, bile, sodium glucoholate sodium taurocholate, cholesterol, biliverdin, mucus, fat, lecitin, cells and cell debris.
3. Detoxification.
4. Glucose exchanges.
Hepatocytes functions
1. Synthesis of bile.
2. Storage (glycogen, fat, vitamins, copper, iron).
3. Biotransformation.
4. Synthesis of blood components.
Disorders
Control signs:
1. Painful syndrome. Pain intensive, paroxysmal, after the meal, more often at night and on empty stomach. The pain is localized in epigastrium, umbilicus, right subcostal area, sometimes irradiates to waist or has spread character. Tenderness on palpation in pyloroduodenal area, muscular defence, and hyperesthesia of skin in tender zones (Zakhariev-Ged), positive sign of Mendel.
2. Dyspeptic syndrome: vomiting, nausea, heartburn, vomiting frequently causes relief, removing pain, decrease of appetite. Tendency to constipation (in patients with increased gastric acidity) or unstable stool (in patient with low gastric acidity).
3. Intoxication syndrome: weakness, lucidity, bad sleep, headaches, irritability, tearfulness, increased disposition to perspiration, blue shadows under the eyes.
Major symptoms and signs of digestive tract disorders
Disorders of organs outside the gastrointestinal (GI) tract can produce symptoms and signs that mimic digestive tract disorders and should be considered in the differential diagnosis (Table 1).
Table 1.
Some nondigestive tract causes of gastrointestinal symptoms in children
|
Symptoms |
Nondigestive tract causes |
|
Anorexia |
Systemic disease: inflammatory, neoplastic |
|
|
Cardiorespiratory compromise |
|
|
Iatrogenic: drug therapy, unpalatable therapeutic diets |
|
|
Depression |
|
|
Anorexia nervosa |
|
Vomiting |
Inborn errors of metabolism |
|
|
Medications: erythromycin, chemotherapy, nonsteroidal anti-inflammatory drugs |
|
|
Increased intracranial pressure |
|
|
Brain tumor |
|
|
Infection of the urinary tract |
|
|
Labyrinthitis |
|
|
Adrenal insufficiency |
|
|
Pregnancy |
|
|
Psychogenic |
|
|
Abdominal migraine |
|
|
Toxins |
|
|
Renal disease |
|
Diarrhea |
Infection: otitis media, urinary |
|
|
Uremia |
|
|
Medications: antibiotics, cisapride |
|
|
Tumors: neuroblastoma |
|
|
Pericarditis |
|
Constipation |
Hypothyroidism |
|
|
Spina bifida |
|
|
Psychomotor retardation |
|
|
Dehydration: diabetes insipidus, renal tubular lesions |
|
|
Medications: narcotics |
|
|
Lead poisoning |
|
|
Infant botulism |
|
Abdominal pain |
Pyelonephritis, hydronephrosis, renal colic |
|
|
Pneumonia |
|
|
Pelvic inflammatory disease |
|
|
Porphyria |
|
|
Angioedema |
|
|
Endocarditis |
|
|
Abdominal migraine |
|
|
Familial Mediterranean fever |
|
|
Sexual or physical abuse |
|
|
Systemic lupus erythematosus |
|
|
School phobia |
|
|
Sickle cell crisis |
|
|
Vertebral disk inflammation |
|
|
Psoas abscess |
|
|
Pelvic osteomyelitis |
|
|
Medications |
|
Abdominal distention |
Ascites: nephrotic syndrome, neoplasm, heart failure |
|
|
Discrete mass: Wilms tumor, hydronephrosis, neuroblastoma, mesenteric cyst, hepatoblastoma, lymphoma |
|
|
Pregnancy |
|
Jaundice |
Hemolytic disease |
|
|
Urinary tract infection |
|
|
Sepsis |
|
|
Hypothyroidism |
|
|
Panhypopituitarism |
Poor weight gain or weight loss is often associated with a significant pathologic process and usually necessitates a more formal evaluation.
Dysphagia
Difficulty in swallowing is termed dysphagia. Painful swallowing is termed odynophagia.
Swallowing is a complex process that starts in the mouth with mastication and lubrication of food that is formed into a bolus. The bolus is pushed to the pharynx by the tongue. The pharyngeal phase of swallowing is rapid and involves protective mechanisms to prevent food from entering the airway. The epiglottis is lowered over the larynx while the soft palate is elevated against the nasopharyngeal wall; respiration is temporarily arrested while the upper esophageal sphincter opens to allow the bolus to enter the esophagus. In the esophagus, peristaltic coordinated muscular contractions push the food bolus toward the stomach. The lower esophageal sphincter relaxes shortly after the upper esophageal sphincter, so liquids that rapidly clear the esophagus enter the stomach without resistance.
Dysphagia is classified as oropharyngeal dysphagia and esophageal dysphagia. Oropharyngeal dysphagia occurs when the transfer of the food bolus from the mouth to the esophagus is impaired (also termed transfer dysphagia). The striated muscles of the mouth, pharynx, and upper esophageal sphincter are affected in oropharyngeal dysphagia. Neurologic and muscular disorders can give rise to oropharyngeal dysphagia (Table 2). The most serious complication of oropharyngeal dysphagia is life-threatening aspiration.
Table 2. Causes of oropharyngeal dysphagia
1. Neuromuscular disorders:
– cerebral palsy;
– brain tumors;
– cerebrovascular accidents;
– polio and postpolio syndromes;
– multiple sclerosis;
– myositis;
– dermatomyositis;
– myasthenia gravis;
– muscular dystrophies.
2. Metabolic and autoimmune disorders:
– hyperthyroidism;
– systemic lupus erythematosus;
– sarcoidosis;
– amyloidosis.
3. Infectious disease:
– meningitis;
– botulism;
– diphtheria;
– lyme disease;
– neurosyphilis;
– viral infection: polio, coxsackievirus, herpes, cytomegalovirus.
4. Structural lesions:
– inflammatory: abscess, pharyngitis;
– congenital web;
– cricopharyngeal bar;
– dental problems;
– bullous skin lesions;
– plummer-vinson syndrome;
– zenker diverticulum;
– extrinsic compression: osteophytes, lymph nodes, thyroid swelling.
5. Other:
– corrosive injury;
– side effects of medications;
– after surgery;
– after radiation therapy
A complex sequence of neuromuscular events is involved in the transfer of foods to the upper esophagus. Abnormalities of the muscles involved in the ingestion process and their innervation, strength, or coordination are associated with transfer dysphagia in infants and children. In such cases, an oropharyngeal problem is usually part of a more generalized neurologic or muscular problem (botulism, diphtheria, neuromuscular disease). Painful oral lesions, such as acute viral stomatitis or trauma, occasionally interfere with ingestion. If the nasal air passage is seriously obstructed, the need for respiration causes severe distress when suckling. Although severe structural, dental, and salivary abnormalities would be expected to create difficulties, ingestion proceeds relatively well in most affected children if they are hungry.
Esophageal dysphagia occurs when there is difficulty in transporting the food bolus down the esophagus. Esophageal dysphagia can result from neuromuscular disorders or mechanical obstruction (Table 298-3).
Primary motility disorders causing impaired peristaltic function and dysphagia are rare in children. Achalasia is an esophageal motility disorder with associated inability of relaxation of the lower esophageal sphincter, and it rarely occurs in children. Motility of the distal esophagus is disordered after surgical repair of tracheoesophageal fistula or achalasia. Abnormal motility can accompany collagen vascular disorders. Mechanical obstruction can be intrinsic or extrinsic. Intrinsic structural defects cause a fixed impediment to the passage of food bolus due to a narrowing within the esophagus, as in a stricture, web, or tumor. Extrinsic obstruction is due to compression from vascular rings, mediastinal lesions, or vertebral abnormalities. Structural defects typically cause more problems in swallowing solids than liquids. In infants, esophageal web, tracheobronchial remnant, or vascular ring can cause dysphagia. An esophageal stricture secondary to esophagitis (chronic gastroesophageal reflux, eosinophilic esophagitis, chronic infections) occasionally has dysphagia as the first manifestation. An esophageal foreign body or a stricture secondary to a caustic ingestion also causes dysphagia. A Schatzki ring, a thin ring of mucosal tissue near the lower esophageal sphincter, is another mechanical cause of recurrent dysphagia, and again is rare in children.
When dysphagia is associated with a delay in passage through the esophagus, the patient may be able to point to the level of the chest where the delay occurs, but esophageal symptoms are usually referred to the suprasternal notch. When a patient points to the suprasternal notch, the impaction can be found anywhere in the esophagus.
Table 3 — CAUSES OF ESOPHAGEAL DYSPHAGIA
1. NEUROMUSCULAR DISORDERS
– Gastroesophageal reflux disease
– Achalasia cardia
– Diffuse esophageal spasm
– Scleroderma
2. MECHANICAL
– Intrinsic Lesions
– Foreign bodies
– Esophagitis: gastroesophageal reflux disease, eosinophilic esophagitis
– Stricture: corrosive injury, pill induced, peptic
– Esophageal webs
– Esophageal rings
– Esophageal diverticula
– Neoplasm
– Extrinsic Lesions
– Vascular compression
– Mediastinal lesion
– Cervical osteochondritis
– Vertebral abnormalities
Regurgitation
Regurgitation is the effortless movement of stomach contents into the esophagus and mouth. It is not associated with distress, and infants with regurgitation are often hungry immediately after an episode. The lower esophageal sphincter prevents reflux of gastric contents into the esophagus. Regurgitation is a result of gastroesophageal reflux through an incompetent or, in infants, immature lower esophageal sphincter. This is often a developmental process, and regurgitation or “spitting” resolves with maturity. Regurgitation should be differentiated from vomiting, which denotes an active reflex process with an extensive differential diagnosis (Table 4).
Table 4. DIFFERENTIAL DIAGNOSIS OF EMESIS DURING CHILDHOOD
|
INFANT |
CHILD |
ADOLESCENT |
|
COMMON |
||
|
Gastroenteritis |
Gastroenteritis |
Gastroenteritis Systemic infection |
|
RARE |
||
|
Adrenogenital syndrome |
Reye syndrome |
Reye syndrome |
* Includes malrotation, pyloric stenosis, intussusception
Anorexia
Anorexia means prolonged lack of appetite. Hunger and satiety centers are located in the hypothalamus; it seems likely that afferent nerves from the GI tract to these brain centers are important determinants of the anorexia that characterizes many diseases of the stomach and intestine. Satiety is stimulated by distention of the stomach or upper small bowel, the signal being transmitted by sensory afferents, which are especially dense in the upper gut. Chemoreceptors in the intestine, influenced by the assimilation of nutrients, also affect afferent flow to the appetite centers. Impulses reach the hypothalamus from higher centers, possibly influenced by pain or the emotional disturbance of an intestinal disease. Other regulatory factors include hormones, ghrelin, leptin, and plasma glucose, which, in turn, reflect intestinal function.
Vomiting is a highly coordinated reflex process that may be preceded by increased salivation and begins with involuntary retching. Violent descent of the diaphragm and constriction of the abdominal muscles with relaxation of the gastric cardia actively force gastric contents back up the esophagus. This process is coordinated in the medullary vomiting center, which is influenced directly by afferent innervation and indirectly by the chemoreceptor trigger zone and higher central nervous system (CNS) centers. Many acute or chronic processes can cause vomiting.
Vomiting caused by obstruction of the GI tract is probably mediated by intestinal visceral afferent nerves stimulating the vomiting center (Table 5). If obstruction occurs below the 2nd part of the duodenum, vomitus is usually bile stained. Emesis can also become bile stained with repeated vomiting in the absence of obstruction when duodenal contents are refluxed into the stomach. Nonobstructive lesions of the digestive tract can also cause vomiting; this includes diseases of the upper bowel, pancreas, liver, or biliary tree. CNS or metabolic derangements can lead to severe, persistent emesis.
Table 5. CAUSES OF GASTROINTESTINAL OBSTRUCTION
1. ESOPHAGUS
1.1. Congenital
– Esophageal atresia
– Vascular rings
– Schatzki ring
– Tracheobronchial remnant
1.2. Acquired
– Esophageal stricture
– Foreign body
– Achalasia
– Chagas disease
– Collagen vascular disease
2. STOMACH
2.1. Congenital
– Antral webs
– Pyloric stenosis
2. 2. Acquired
– Bezoar, foreign body
– Pyloric stricture (ulcer)
– Chronic granulomatous disease of childhood
– Eosinophilic gastroenteritis
– Crohn disease
– Epidermolysis bullosa
3. SMALL INTESTINE
3.1. Congenital
– Duodenal atresia
– Annular pancreas
– Malrotation/volvulus
– Malrotation/Ladd bands
– Ileal atresia
– Meconium ileus
– Meckel diverticulum with volvulus or intussusception
– Inguinal hernia
– Intestinal duplication
3.2. Acquired
– Postsurgical adhesions
– Crohn disease
– Intussusception
– Distal ileal obstruction syndrome (cystic fibrosis)
– Duodenal hematoma
– Superior mesenteric artery syndrome
4.
4.1. Congenital
– Meconium plug
– Hirschsprung disease
– Colonic atresia, stenosis
– Imperforate anus
– Rectal stenosis
– Pseudo-obstruction
– Volvulus
– Colonic duplication
4.2. Acquired
– Ulcerative colitis (toxic megacolon)
– Chagas disease
– Crohn disease
– Fibrosing colonopathy (cystic fibrosis)
Cyclic vomiting is a syndrome with numerous episodes of vomiting interspersed with well intervals. The North American Society for Pediatric Gastroenterology, Hepatology and Nutrition consensus statement on the diagnosis and management of cyclic vomiting criteria are listed in Table 6. Rome III criteria for Functional GI disorders (FGIDs) have 2 criteria for cyclic vomiting in children, and both these criteria have to be present for a diagnosis of cyclic vomiting: 2 or more periods of intense nausea and unremitting vomiting or retching lasting hours to days and return to usual state of health lasting weeks to months.
Table 6 — CRITERIA FOR CYCLICAL VOMITING SYNDROME
|
All of the criteria must be met for the consensus definition of cyclical vomiting syndrome: |
||||||||||||||||||
|
The onset of cyclic vomiting is usually between 2 and 5 yr of age but has been observed in infants and adults. The frequency of vomiting episodes is variable (average of 12 episodes per yr) with each episode typically lasting 2-3 days and 4 or more emesis episodes per hour. The episodes usually occur in the early hours of the morning or upon wakening. Patients can have a prodrome of nausea, pallor, intolerance of noise or light, lethargy, and headache. Epigastric pain, abdominal pain, diarrhea, and fever are seen in many patients, making the diagnosis difficult. Precipitants include infection, physical stress, and psychologic stress.
Several theories have been proposed as causative factors including a migraine-related mechanism, mitochondrial disorders, and autonomic dysfunction. More than 80% of affected children have a first-degree relative with migraines; many patients develop migraines later in life. Many children show evidence for sympathetic autonomic dysfunction of sudomotor systems. The differential diagnosis includes GI anomalies (malrotation, duplication cysts, choledochal cysts, recurrent intussusceptions), CNS disorders (neoplasm, epilepsy, vestibular pathology), nephrolithiasis, cholelithiasis, hydronephrosis, metabolic-endocrine disorders (urea cycle, fatty acid metabolism,
Diarrhea
Diarrhea is best defined as excessive loss of fluid and electrolyte in the stool. Acute diarrhea is defined as sudden onset of excessively loose stools of >10 mL/kg/day in infants and >200 g/24 hr in older children, which lasts <14 days. When the episode lasts >14 days, it is called chronic or persistent diarrhea.
Normally, a young infant has approximately 5 mL/kg/day of stool output; the volume increases to 200 g/24 hr in an adult. The greatest volume of intestinal water is absorbed in the small bowel; the colon concentrates intestinal contents against a high osmotic gradient. The small intestine of an adult can absorb 10-11 L/day of a combination of ingested and secreted fluid, whereas the colon absorbs approximately
The basis of all diarrheas is disturbed intestinal solute transport and water absorption. Water movement across intestinal membranes is passive and is determined by both active and passive fluxes of solutes, particularly sodium, chloride, and glucose. The pathogenesis of most episodes of diarrhea can be explained by secretory, osmotic, or motility abnormalities or a combination of these (Table 7).
Table 7 — MECHANISMS OF DIARRHEA
|
PRIMARY MECHANISM |
DEFECT |
STOOL EXAMINATION |
EXAMPLES |
COMMENT |
|
Secretory |
Decreased absorption, increased secretion, electrolyte transport |
Watery, normal osmolality with ion gap <100 mOsm/kg |
Cholera, toxigenic Escherichia coli; carcinoid, vasoactive intestinal peptide, neuroblastoma, congenital chloride diarrhea, Clostridium difficile, cryptosporidiosis (AIDS) |
Persists during fasting; bile salt malabsorption can also increase intestinal water secretion; no stool leukocytes |
|
Osmotic |
Maldigestion, transport defects ingestion of unabsorbable substances |
Watery, acidic, and reducing substances; increased osmolality with ion gap >100 mOsm/kg |
Lactase deficiency, glucose-galactose malabsorption, lactulose, laxative abuse |
Stops with fasting; increased breath hydrogen with carbohydrate malabsorption; no stool leukocytes |
|
Increased motility |
Decreased transit time |
Loose to normal-appearing stool, stimulated by gastrocolic reflex |
Irritable bowel syndrome, thyrotoxicosis, postvagotomy dumping syndrome |
Infection can also contribute to increased motility |
|
Decreased motility |
Defect ieuromuscular unit(s) stasis (bacterial overgrowth) |
Loose to normal-appearing stool |
Pseudo-obstruction, blind loop |
Possible bacterial overgrowth |
|
Decreased surface area (osmotic, motility) |
Decreased functional capacity |
Watery |
Short bowel syndrome, celiac disease, rotavirus enteritis |
Might require elemental diet plus parenteral alimentation |
|
Mucosal invasion |
Inflammation, decreased colonic reabsorption, increased motility |
Blood and increased WBCs in stool |
Salmonella, Shigella, infection; amebiasis; Yersinia, Campylobacter infections |
Dysentery evident in blood, mucus, and WBCs |
Secretory diarrhea occurs when the intestinal epithelial cell solute transport system is in an active state of secretion. It is often caused by a secretagogue, such as cholera toxin, binding to a receptor on the surface epithelium of the bowel and thereby stimulating intracellular accumulation of cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP). Some intraluminal fatty acids and bile salts cause the colonic mucosa to secrete through this mechanism. Diarrhea not associated with an exogenous secretagogue can also have a secretory component (congenital microvillus inclusion disease). Secretory diarrhea is usually of large volume and persists even with fasting. The stool osmolality is indicated by the electrolytes and the ion gap is 100 mOsm/kg or less. The ion gap is calculated by subtracting the concentration of electrolytes from total osmolality:
Osmotic diarrhea occurs after ingestion of a poorly absorbed solute. The solute may be one that is normally not well absorbed (magnesium, phosphate, lactulose, or sorbitol) or one that is not well absorbed because of a disorder of the small bowel (lactose with lactase deficiency or glucose with rotavirus diarrhea). Malabsorbed carbohydrate is fermented in the colon, and short-chain fatty acids (SCFAs) are produced. Although SCFAs can be absorbed in the colon and used as an energy source, the net effect is increase in the osmotic solute load. This form of diarrhea is usually of lesser volume than a secretory diarrhea and stops with fasting. The osmolality of the stool will not be explained by the electrolyte content, because another osmotic component is present and the anion gap is >100 mOsm.
Motility disorders can be associated with rapid or delayed transit and are not generally associated with large-volume diarrhea. Slow motility can be associated with bacterial overgrowth leading to diarrhea.
Any definition of constipation is relative and depends on stool consistency, stool frequency, and difficulty in passing the stool. A normal child might have a soft stool only every 2nd or 3rd day without difficulty; this is not constipation. A hard stool passed with difficulty every 3rd day should be treated as constipation. Constipation can arise from defects either in filling or emptying the rectum (Table 8).
Table 8 — CAUSES OF CONSTIPATION
2. Organic
– Anatomic
Anal stenosis, atresia with fistula
Imperforate anus
Intestinal stricture (post necrotizing enterocolitis)
– Abnormal musculature
Prune-belly syndrome
Muscular dystrophy
– Intestinal nerve or muscle abnormalities
Hirschsprung disease
Pseudo-obstruction (visceral myopathy or neuropathy)
Intestinal neuronal dysplasia
Tethered cord
Spinal cord trauma
Spina bifida
Anticholinergics
Narcotics
Methylphenidate
Antidepressants
Chemotherapeutic agents (vincristine)
Pancreatic enzymes (fibrosing colonopathy)
Vitamin D intoxication
Hypokalemia
Hypercalcemia
Hypothyroidism
Diabetes mellitus, diabetes insipidus
– Intestinal disorders
Celiac disease
Cow’s milk protein intolerance
Cystic fibrosis (meconium ileus equivalent)
Inflammatory bowel disease (stricture)
– Connective tissue disorders
Systemic lupus erythematosus
Anorexia nervosa
A nursing infant might have very infrequent stools of normal consistency; this is usually a normal pattern. True constipation in the neonatal period is most likely secondary to Hirschsprung disease, intestinal pseudo-obstruction, or hypothyroidism.
Defective rectal filling occurs when colonic peristalsis is ineffective (in cases of hypothyroidism or opiate use and when bowel obstruction is caused either by a structural anomaly or by Hirschsprung disease). The resultant colonic stasis leads to excessive drying of stool and a failure to initiate reflexes from the rectum that normally trigger evacuation. Emptying the rectum by spontaneous evacuation depends on a defecation reflex initiated by pressure receptors in the rectal muscle. Stool retention, therefore, can also result from lesions involving these rectal muscles, the sacral spinal cord afferent and efferent fibers, or the muscles of the abdomen and pelvic floor. Disorders of anal sphincter relaxation can also contribute to fecal retention.
Constipation tends to be self-perpetuating, whatever its cause. Hard, large stools in the rectum become difficult and even painful to evacuate; thus, more retention occurs and a vicious circle ensues. Distention of the rectum and colon lessens the sensitivity of the defecation reflex and the effectiveness of peristalsis. Eventually, watery content from the proximal colon might percolate around hard retained stool and pass per rectum unperceived by the child. This involuntary encopresis may be mistaken for diarrhea. Constipation itself does not have deleterious systemic organic effects, but urinary tract stasis can accompany severe long-standing cases and constipation can generate anxiety, having a marked emotional impact on the patient and family.
Abdominal Pain
There is considerable variation among children in their perception and tolerance for abdominal pain. This is one reason the evaluation of chronic abdominal pain is difficult. A child with functional abdominal pain (no identifiable organic cause) may be as uncomfortable as one with an organic cause. It is very important to distinguish between organic and nonorganic (functional) abdominal pain because the approach for the management is based on this. Normal growth and physical examination (including a rectal examination) are reassuring in a child who is suspected of having functional pain.
A specific cause may be difficult to find, but the nature and location of a pain-provoking lesion can usually be determined from the clinical description. Two types of nerve fibers transmit painful stimuli in the abdomen. In skin and muscle, A fibers mediate sharp localized pain; C fibers from viscera, peritoneum, and muscle transmit poorly localized, dull pain. These afferent fibers have cell bodies in the dorsal root ganglia, and some axons cross the midline and ascend to the medulla, midbrain, and thalamus. Pain is perceived in the cortex of the postcentral gyrus, which can receive impulses arising from both sides of the body. In the gut, the usual stimulus provoking pain is tension or stretching. Inflammatory lesions can lower the pain threshold, but the mechanisms producing pain of inflammation are not clear. Tissue metabolites released near nerve endings probably account for the pain caused by ischemia. Perception of these painful stimuli can be modulated by input from both cerebral and peripheral sources. Psychologic factors are particularly important. Features of abdominal pain are noted in Tables 9 and 10. Pain that suggests a potentially serious organic etiology is associated with age <5 yr; fever; weight loss; bile or blood-stained emesis; jaundice; hepatosplenomegaly; back or flank pain or pain in a location other than the umbilicus; awakening from sleep in pain; referred pain to shoulder, groin or back; elevated ESR, WBC, or CRP; anemia; edema; or a strong family history of inflammatory bowel disease (IBD) or celiac disease.
Table 9 — CHRONIC ABDOMINAL PAIN IN CHILDREN
|
DISORDER |
CHARACTERISTICS |
KEY EVALUATIONS |
|
NONORGANIC |
||
|
Functional abdominal pain |
Nonspecific pain, often periumbilical |
Hx and PE; tests as indicated |
|
Irritable bowel syndrome |
Intermittent cramps,diarrhea, and constipation |
Hx and PE |
|
Non-ulcer dyspepsia |
Peptic ulcer–like symptoms without abnormalities on evaluation of the upper GI tract |
Hx; esophagogastroduodenoscopy |
|
GASTROINTESTINAL TRACT |
||
|
Chronic constipation |
Hx of stool retention, evidence of constipation on examination |
Hx and PE; plain x-ray of abdomen |
|
Lactose intolerance |
Symptoms may be associated with lactose ingestion; bloating, gas, cramps, and diarrhea |
Trial of lactose-free diet; lactose breath hydrogen test |
|
Parasite infection (especially Giardia) |
Bloating, gas, cramps, and diarrhea |
Stool evaluation for O&P; specific immunoassays for Giardia |
|
Excess fructose or sorbitol ingestion |
Nonspecific abdominal pain, bloating, gas, and diarrhea |
Large intake of apples, fruit juice, or candy or chewing gum sweetened with sorbitol |
|
Peptic ulcer |
Burning or gnawing epigastric pain; worse on awakening or before meals; relieved with antacids |
Esophagogastroduodenoscopy or upper GI contrast x-rays |
|
Esophagitis |
Epigastric pain with substernal burning |
Esophagogastroduodenoscopy |
|
Meckel’s diverticulum |
Periumbilical or lower abdominal pain; may have blood in stool |
Meckel scan or enteroclysis |
|
Recurrent intussusception |
Paroxysmal severe cramping abdominal pain; blood may be present in stool with episode |
Identify intussusception during episode or lead point in intestine between episodes with contrast studies of GI tract |
|
Internal, inguinal, or abdominal wall hernia |
Dull abdomen or abdominal wall pain |
PE, CT of abdominal wall |
|
Chronic appendicitis or appendiceal mucocele |
Recurrent RLQ pain; often incorrectly diagnosed, may be rare cause of abdominal pain |
Barium enema, CT |
|
GALLBLADDER AND PANCREAS |
||
|
Cholelithiasis |
RUQ pain, might worsen with meals |
Ultrasound of gallbladder |
|
Choledochal cyst |
RUQ pain, mass ? elevated bilirubin |
Ultrasound or CT of RUQ |
|
Recurrent pancreatitis |
Persistent boring pain, might radiate to back, vomiting |
Serum amylase and lipase ? serum trypsinogen; ultrasound or CT of pancreas |
|
GENITOURINARY TRACT |
||
|
Urinary tract infection |
Dull suprapubic pain, flank pain |
Urinalysis and urine culture; renal scan |
|
Hydronephrosis |
Unilateral abdominal or flank pain |
Ultrasound of kidneys |
|
Urolithiasis |
Progressive, severe pain; flank to inguinal region to testicle |
Urinalysis, ultrasound, IVP, CT |
|
Other genitourinary disorders |
Suprapubic or lower abdominal pain; genitourinary symptoms |
Ultrasound of kidneys and pelvis; gynecologic evaluation |
|
MISCELLANEOUS CAUSES |
||
|
Abdominal migraine |
See text; nausea, family Hx migraine |
Hx |
|
Abdominal epilepsy |
Might have seizure prodrome |
EEG (can require >1 study, including sleep-deprived EEG) |
|
Gilbert syndrome |
Mild abdominal pain (causal or coincidental?); slightly elevated unconjugated bilirubin |
Serum bilirubin |
|
Familial Mediterranean fever |
Paroxysmal episodes of fever, severe abdominal pain, and tenderness with other evidence of polyserositis |
Hx and PE during an episode, DNA diagnosis |
|
Sickle cell crisis |
Anemia |
Hematologic evaluation |
|
Lead poisoning |
Vague abdominal pain, constipation |
Serum lead level |
|
Henoch-Schonlein purpura |
Recurrent, severe crampy abdominal pain, occult blood in stool, characteristic rash, arthritis |
Hx, PE, urinalysis |
|
Angioneurotic edema |
Swelling of face or airway, crampy pain |
|
|
Acute intermittent porphyria |
Severe pain precipitated by drugs, fasting, or infections |
Spot urine for porphyrins |
abd – abdominal; EEG – electroencephalogram; GI – gastrointestinal; Hx – history; IVP – intravenous pyelogrophy; O&P – ova and parasites; PE – physical exam; RLQ – right lower quadrant; RUQ – right upper quadrant
Table 10 — DISTINGUISHING FEATURES OF ACUTE GASTROINTESTINAL TRACT PAIN IN CHILDREN
|
DISEASE |
ONSET |
LOCATION |
REFERRAL |
QUALITY |
COMMENTS |
|
Pancreatitis |
Acute |
Epigastric, left upper quadrant |
Back |
Constant, sharp, boring |
Nausea, emesis, tenderness |
|
Intestinal obstruction |
Acute or gradual |
Periumbilical-lower abdomen |
Back |
Alternating cramping (colic) and painless periods |
Distention, obstipation, emesis, increased bowel sounds |
|
Appendicitis |
Acute |
Periumbilical, then localized to lower right quadrant; generalized with peritonitis |
Back or pelvis if retrocecal |
Sharp, steady |
Anorexia, nausea, emesis, local tenderness, fever with peritonitis |
|
Intussusception |
Acute |
Periumbilical-lower abdomen |
None |
Cramping, with painless periods |
Hematochezia, knees in pulled-up position |
|
Urolithiasis |
Acute, sudden |
Back (unilateral) |
Groin |
Sharp, intermittent, cramping |
Hematuria |
|
Urinary tract infection |
Acute |
Back |
Bladder |
Dull to sharp |
Fever, costo-vertebral angle tenderness, dysuria, urinary frequency |
Visceral pain tends to be dull and aching and is experienced in the dermatome from which the affected organ receives innervations. So, most often, the pain and tenderness is not felt over the site of the disease process. Painful stimuli originating in the liver, pancreas, biliary tree, stomach, or upper bowel are felt in the epigastrium; pain from the distal small bowel, cecum, appendix, or proximal colon is felt at the umbilicus; and pain from the distal large bowel, urinary tract, or pelvic organs is usually suprapubic. The pain from the cecum, ascending colon, and descending colon sometimes is felt at the site of the lesion due to the short mesocecum and corresponding mesocolon. The pain due to appendicitis is initially felt in the periumbilical region, and pain from the transverse colon is usually felt in the supra pubic region. The shifting (localization) of pain is a pointer toward diagnosis; for example, periumbilical pain of a few hours localizing to the right lower quadrant suggests appendicitis. Radiation of pain can be helpful in diagnosis; for example, in biliary colic the radiation of pain is toward the inferior angle of the right scapula, pancreatic pain radiated to the back, and the renal colic pain is radiated to the inguinal region on the same side.
Somatic pain is intense and is usually well localized. When the inflamed viscus comes in contact with the somatic organ like the parietal peritoneum or the abdominal wall, pain is localized to that site. Peritonitis gives rise to generalized abdominal pain with rigidity, involuntary guarding, rebound tenderness, and cutaneous hyperesthesia on physical examination.
Referred pain from extraintestinal locations, due to shared central projections with the sensory pathway from the abdominal wall, can give rise to abdominal pain, as in pneumonia when the parietal pleural pain is referred to the abdomen.
Gastrointestinal Hemorrhage
Bleeding can occur anywhere along the GI tract, and identification of the site may be challenging (Table 298-15). Bleeding that originates in the esophagus, stomach, or duodenum can cause hematemesis. When exposed to gastric or intestinal juices, blood quickly darkens to resemble coffee grounds; massive bleeding is likely to be red. Red or maroon blood in stools, hematochezia, signifies either a distal bleeding site or massive hemorrhage above the distal ileum. Moderate to mild bleeding from sites above the distal ileum tends to cause blackened stools of tarry consistency (melena); major hemorrhages in the duodenum or above can also cause melena.
Erosive damage to the mucosa of the GI tract is the most common cause of bleeding, although variceal bleeding secondary to portal hypertension occurs often enough to require consideration. Prolapse gastropathy producing subepithelial hemorrhage and Mallory-Weiss lesions secondary to mucosal tears associated with emesis are causes of upper intestinal bleeds. Vascular malformations are a rare cause in children; they are difficult to identify. Upper intestinal bleeding is evaluated with an EGD (esophagogastroduodenoscopy). Evaluation of the small intestine is facilitated by capsule endoscopy. The capsule-sized imaging device is swallowed in older children or placed endoscopically in younger children. Lower GI bleeding is investigated with a colonoscopy. In brisk intestinal bleeding of unknown location, a tagged red blood cell (RBC) scan is helpful in locating the site of the bleeding. Occult blood in stool is usually detected by using commercially available fecal occult blood testing cards, which are based on a chemical reaction between the chemical guaiac and oxidizing action of a substrate (hemoglobin), giving a blue color. The guaiac test is very sensitive, but random testing can miss chronic blood loss, which can lead to iron-deficiency anemia. GI hemorrhage can produce hypotension and tachycardia but rarely causes GI symptoms; brisk duodenal or gastric bleeding can lead to nausea, vomiting, or diarrhea. The breakdown products of intraluminal blood might tip patients into hepatic coma if liver function is already compromised and can lead to elevation of serum bilirubin.
Enlargement of the abdomen can result from diminished tone of the wall musculature or from increased content: fluid, gas, or solid. Ascites, the accumulation of fluid in the peritoneal cavity, distends the abdomen both in the flanks and anteriorly when it is large in volume. This fluid shifts with movement of the patient and conducts a percussion wave. Ascitic fluid is usually a transudate with a low protein concentration resulting from reduced plasma colloid osmotic pressure of hypoalbuminemia and/or from raised portal venous pressure. In cases of portal hypertension, the fluid leak probably occurs from lymphatics on the liver surface and from visceral peritoneal capillaries, but ascites does not usually develop until the serum albumin level falls. Sodium excretion in the urine decreases greatly as the ascitic fluid accumulates and, thus, additional dietary sodium goes directly to the peritoneal space, taking with it more water. When ascitic fluid contains a high protein concentration, it is usually an exudate caused by an inflammatory or neoplastic lesion.
When fluid distends the gut, either obstruction or imbalance between absorption and secretion should be suspected. The factors causing fluid accumulation in the bowel lumen often cause gas to accumulate, too. The result may be audible gurgling noises. The source of gas is usually swallowed air, but endogenous flora can increase considerably in malabsorptive states and produce excessive gas when substrate reaches the lower intestine. Gas in the peritoneal cavity (pneumoperitoneum) is usually due to perforated viscus and can cause abdominal distention depending on the amount of gas leak. A tympanitic percussioote, even over solid organs such as the liver, indicates a large collection of gas in the peritoneum.
An abdominal organ can enlarge diffusely or be affected by a discrete mass. In the digestive tract, such discrete masses can occur in the lumen, wall, omentum, or mesentery. In a constipated child, mobile, nontender fecal masses are often found. Congenital anomalies, cysts, or inflammatory processes can affect the wall of the gut. Gut wall neoplasms are extremely rare in children. The pathologic enlargement of liver, spleen, bladder, and kidneys can give rise to abdominal distention.
Physical examination
Mouth and throat.
The mouth is the beginning of the passageway to the digestive tract, but it also functions in the entry or exit of air. The examination of the mouth and throat is conducted with the patient sitting up either in bed, with the head resting comfortably back on pillows, or in a chair. A bright torch, a tongue depressor (spatula) and a pair of latex gloves are essential. The lips, teeth, gums, tongue, palate, fauces and oropharynx are then visualized systematically, and finally palpation of the sides of the tongue, floor of mouth and tonsillar regions is carried out.
The major structure of the exterior of the mouth is the lips.
Look closely at the philtrum (the shallow depression running from nose to upper lip) for the tell-tale scar of a repaired cleft lip. When present, particularly if associated with ‘nasal speech’, inspect the palate carefully for signs of a cleft. Next, look at the corners of the mouth for cracks or fissures (angular stomatitis). The cracks are reddish-brown, moist, superficial, linear ulcers radiating from the angles of the mouth. In children their origin is infective (perleche); they are common in the elderly when ill-fitting or deficient dentures result in overclosure of the mouth.
Image 2. Angular cheilitis (angular stomatitis or perleche).
Cheilosis is also seen in severe iron-deficiency anaemia; it also occurs in vitamin B2 (riboflavin) or niacin deficiency.
The doctor should note the presence of painful, inflamed, and dried cracks or fissures of the lips, called cheilitis. These may be caused by exposure to harsh climatic conditions, habitual licking or biting of the lips, mouth breathing from respiratory distress, or dehydration, particularly with fever in systemic disease. Grouped vesicles on the lips on a red base with crusted lesions are seen in herpes simplex labialis commonly associated with coryza. This infection is usually of short duration and the lack of induration and ulceration serves to distinguish it from other more serious conditions. Recurrent actinic cheilitis with small blisters and exfoliation, however, is a premalignant condition found in people constantly exposed to the sun and wind, such as farmers and fishermen.
Look for any ulcer on the lips. Carcinoma (epithelioma) usually occurs on the lower lip away from the midline; the ulcer is indolent, flat and shallow, although in time the edge may become heaped up and induration may be felt. Epithelioma must be differentiated from keratoacanthoma, pyogenic granuloma and the chancre of primary syphilis. A keratoacanthoma (molluscum sebaceum) is a lesion due to overgrowth of the stratum granulosum of the skin. It usually presents as a firm, rounded nodule sometimes with ulceration; it is more common on the upper lip and heals spontaneously without treatment. Pyogenic granuloma is a soft red raspberry-like nodule on the upper lip, which often follows minor trauma. The upper lip is the commonest site of an extragenital chancre, which appears as a small, round lesion that is firm and indurated. A ‘snail-track ulcer’ in secondary syphilis has a serpiginous outline and greyish-white non-purulent exudate. In both epithelioma and chancre enlarged, painless cervical nodes are commonly felt. Rhagades, white scars at the angles of the mouth that extend into the mouth, due to cheilosis associated with congenital syphilis, are now only of historical interest. A crack in the middle of the lower lip in cold weather is a common, painful problem, but is of no sinister significance.
Very occasionally multiple small brown or black spots are seen on the skin around the mouth (circumoral pigmentation) which may also extend on to the lips and buccal mucosa. This pigmentation constitutes one of the triad of cardinal features of the Peutz-Jeghers syndrome and signifies underlying small bowel polyposis, a condition inherited as a Mendelian dominant. On the buccal mucosa the pigmentation may look very like that seen in Addison’s disease. Look carefully at the lips and tongue for telangiectasia. Their presence may signal the existence of others elsewhere in the intestine, which occasionally bleeds.
Now gently grasp the lower lip with the index finger and thumb of both hands and evert it fully, to display the mucous surface of the lip. Two lesions are commonly seen in this site: aphthous ulcers and retention cysts. Aphthous ulcers are small, superficial, painful ulcers with a white or yellow base and a narrow halo of hyperaemia. Such ulcers are also seen on the tongue, buccal mucosa and palate.
Image 3. Typical aphthous ulcer in a common site, showing inflammatory halo surrounding a yellowish, round ulcer.
Retention cysts of the mucous glands of the lips and buccal mucosa appear as round, translucent swellings, elevated from the surface with a characteristic white or bluish appearance. They are also found on the mucous surface of the lower lip.
Image 4. Retention cysts
The mouth and throat are divided into three areas: (1) the oral cavity, which extends from the lips to the palatopharyngeal arches, (2) the oropharynx, which extends from the epiglottis to the lower edge of the adenoids, and (3) the nasopharynx, which extends from above the lower edge of the adenoids to the nasal cavity. The major structures that are visible on examination within the oral cavity and oropharynx are the mucosal lining of the lips and cheeks, gums or gingiva, teeth, tongue, palate, uvula, tonsils, and posterior oropharynx. Other pharyngeal structures that are not visible on examination are the epiglottis, lingual tonsils, and pharyngeal tonsils or adenoids.
With a cooperative child almost the entire examination can be done without the use of a tongue blade. The doctor asks the child to open his mouth wide, requests that he move his tongue in different directions for full visualization, and has him say “ahh” in order to depress the tongue for full view of the back of the mouth (tonsils, uvula, oropharynx). For a closer look at the buccal mucosa or lining of the cheeks, the nurse can ask the child to use his fingers to move the outer lip and cheek to one side. Performing the examination in front of a mirror is a great aid in enlisting children’s cooperation. Another approach is using a puppet and letting the child examine its wide-open mouth.
Infants and toddlers, however, usually resist attempts to keep the mouth open. Because it is an upsetting part of the examination, it is reserved until last (with examination of the ears) or performed during episodes of crying. However, the use of a tongue blade to depress the tongue is necessary. The tongue blade is placed along the side of the tongue, not the center back area where the gag reflex is elicited. If the child resists in opening his mouth, pinching the nostrils closed forces the child to breathe by mouth and, therefore, open the mouth.
All areas lined with mucous membranes (inside the lips and cheeks, gingiva, underside of tongue, palate, back of pharynx) are inspected, noting color, any areas of white patches or ulceration, bleeding, sensitivity, and moisture. The membranes should be bright pink, smooth, glistening, uniform, and moist. Any deviations are noted. For example, reddened areas with white ulcerated centers may be canker sores (aphthae), which may be caused by trauma to the gums during toothbrushing or chewing. Koplik’s spots, indicative of measles during the prodromal stage, appear as grayish areas surrounded with a red, irregular areola. They first appear on the buccal mucosa opposite the lower molars.
Image 5. Koplik’s spots
White curdy plaques or patches anywhere on the oral mucosa, but particularly on the surface of the tongue and hard palate, that bleed when scraped are signs of moniliasis or thrush.
Image 6. Oral moniliasis.
As the doctor observes the lining of the mouth, any odor (halitosis) is noted. Mouth odors are characteristic of a number of important health problems, such as poor dental hygiene, gingival disease, chronic constipation, dehydration, malnutrition, or systemic illness. A sudden, foul odor in the mouth may indicate a foreign body in the nose, particularly a bean or pea. The nurse should inspect the nose carefully and, if possible, remove the object with tweezers.
The teeth are inspected for number in each dental arch, hygiene, and occlusion or bite. The general rule for estimating the number of temporary teeth in children who are 2 years of age or younger is: the child’s age in months minus 6 months equals the number of teeth. Discoloration of tooth enamel with obvious plaque (whitish coating on the surface of the teeth) is a sign of poor dental hygiene and indicates a need for dental counseling. Brown spots in the crevices of the crown of the tooth or between the teeth may be caries. Teeth that appear greenish black may be stained from oral ingestion of supplemental iron. Although unsightly, this disappears after the iron is no longer given. Malocclusion or poor biting relationship of the teeth is evaluated in terms of (1) how the jaws relate to each other in vertical, transverse, and anteroposterior directions, for example, the “bucktoothed” appearance that results when the maxilla is forward in relation to the mandible, (2) how the teeth are aligned, and (3) how the teeth interdigitate when in occlusion. Although parents frequently express concern regarding thumb-sucking and the development of orthodontic problems, thumb-sucking that ceases before the age of 6 years probably does little harm.
The gums surrounding the teeth are examined. The color is normally coral pink, and the surface texture is stippled, similar to the appearance of orange peel. In dark-skinned children the gums are more deeply colored and a brownish area is often observed along the gum line.
Examine the gums at the same time as the teeth. Pink, healthy gums adhere closely to the necks of the teeth and have a sharp border. With increasing age gingival recession occurs, so making the teeth appear longer and exposing the cementum below the enamel. This makes it easier for infection to gain a hold.
In chronic marginal gingivitis, the gums are retracted, frequently bleed easily and lose their characteristic stippling. Sometimes pus can be squeezed from them (pyorrhoea alveolaris).
Acute herpetic gingivostomatitis due to the simplex virus occurs most commonly in infants and children. Many small vesicles appear on the gums, cheeks, palate, tongue and lips. The vesicles rupture to produce shallow ulcers with a yellowish floor and bright red margins. Vincent’s gingivostomatitis, an infection due to fusiform spirochaetes, characteristically destroys the interdental papillae. A thick, felted, greenish-grey sloughs is formed and halitosis is present. In patients exposed to lead compounds, a stippled blue line can often be observed running along the edge of the gum, especially opposite those teeth showing gingivitis. Similar lines may be produced by bismuth or mercury but these are uncommon signs. The gums in scurvy are swollen, irregular in outline, red, spongy and bleed easily. Hypertrophy of the gums may occur in pregnancy and in patients treated for long periods with phenytoin. Haemorrhages may be observed in the buccal mucous membrane in thrombocytopenic purpura and acute leukaemia.
The tongue is inspected for the presence of papillae, small projections that contain several taste buds each and give the tongue its characteristic rough appearance. Changes in the surface texture are noted, such as (1) “geographic tongue”, unusual patterns of papillae formation and denuded areas, (2) coated tongue, such as in thrush, or (3) an exceptionally beefy red and swollen tongue, which is a sign of various systemic diseases. Geographical tongue is another harmless anomaly characterized by localized irregular red areas of desquamated epithelium and filiform papillae surrounded by a whitish-yellow border; the papillae change in distribution and give the appearance of a map. The ‘false geographical tongue’ with a similar appearance occurs chiefly in children with fever.
Image 7. Geographic tongue
The doctor also notes the size and mobility of the tongue, especially protrusion, which is frequently seen in children with mental retardation. Normally the tip of the tongue should extend to the lips. If the child is unable to move the tongue forward to this point, the frenulum, or central band of mucous membrane, which attaches the tongue to the floor of the mouth, may be too short. “Tongue-tie” can result in speech problems.
The state of the tongue gives some indication of the state of hydration of the body, provided the patient is not a mouth breather. A dry, brown tongue may be found in the later stages of any severe illness, but is found particularly in advanced uraemia and acute intestinal obstruction.
Furring of the tongue is of little value as an indication of disease. It is often found in heavy smokers. A brown fur, the ‘black hairy tongue’, is due to a fungus infection and is of no special significance, though frequently a source of great alarm to its possessor. The tongue of scarlet fever at first shows bright red papillae standing out of a thick white fur. Later the white coat disappears leaving enlarged papillae on a bright red surface — the ‘strawberry tongue’. Hairy leukoplakia is a common feature in patients with HIV infection. In chronic superficial glossitis, areas of leukoplakia (whitish opaque areas of thickened epithelium) are separated by intervening smooth and scarred areas; there are no normal papillae to be seen and the fissures run mainly in a longitudinal direction.
Generalized atrophy of the papillae produces a smooth or bald tongue, which is characteristic of vitamin B12 deficiency but may also sometimes be found in iron-deficiency anaemia, coeliac disease and other gastrointestinal disorders and deficiency states, especially pellagra. In severe cases smoothness may be associated with wrinkling of the mucous membrane, which has then to be distinguished from fissuring of the tongue seen in chronic superficial glossitis due to syphilis, and congenital fissuring of the tongue or ‘scrotal tongue’, which is common and of no pathological significance. In congenital fissuring the papillae are normal but the surface is interrupted by numerous irregular but more or less symmetrical folds, which tend to run mainly horizontally. In median rhomboid glossitis a lozenge-shaped area of loss of papillae and fissuring is seen in the midline anterior to the foramen caecum. It feels nodular and may be mistaken for a carcinoma. It must also be distinguished from a lingual thyroid but this is situated posterior to the foramen caecum.
The roof of the mouth consists of the hard palate, near the front of the cavity, and the soft palate, toward the back of the pharynx, which has a small midline protrusion called the uvula. Both are carefully inspected to be sure that they are intact. Sometimes there is a pinpoint cleft in the soft palate, which may go undetected unless carefully inspected. Such a cleft is especially important if the uvula is bifid or separated into two appendages. A submucosal cleft may result in speech problems later on, since air cannot be effectively trapped for vocalization. The arch of the palate should be dome shaped. A narrow-flat roof or high-arched palate affects the placement of the tongue and can cause feeding and speech problems. Movement of the uvula is tested by eliciting a gag reflex. It moves upward to close off the nasopharynx from the oropharynx.
As the recesses of the oropharynx are inspected, the size and color of the palatine tonsils are also noted. They are normally the same color as the surrounding mucosa, glandular, rather than smooth in appearance, and barely visible over the edge of the palatoglossal arches. Enlargement, redness, and white patches on the tonsils and surrounding area are recorded. Such signs are indicative of suppurative tonsillitis or pharyngitis.
The breath
Carious teeth, infection or ulceration of the gum, stomatitis, and retention and decomposition of secretion in the follicles of enlarged tonsils are the commonest sources of offensive breath. Characteristic odorous may be recognized:
• in ketosis, the breath smells of acetone;
• in uraemia, there is a fishy or ammoniacal odour;
• in hepatic failure, the odour is described as ‘mousy’;
• in suppurative conditions of the lung the breath may have a putrid smell;
• in bronchiectasis the odour has been compared to that of apple blossom with a hint of stale faeces.
• Paraldehyde and alcohol also impart their characteristic smells to the breath.
Examination of abdomen.
Examination of the abdomen involves the usual four skills, except that the order is significantly changed. Inspection is followed by auscultation, percussion, and then palpation, which may distort the normal abdominal sounds. The nurse must have knowledge of the anatomic placement of the abdominal organs in order to differentiate normal, expected findings from abnormal ones.
The sequence of examining the abdomen changes according to the age and cooperativeness of the child. Frequently all four types of assessment are performed at different times. For example, the nurse may auscultate for bowel sounds following evaluation of heart and lung sounds at the beginning of the examination when the child is quiet. Inspection may occur at any time during the examination. Percussion usually follows lung percussion, and palpation may be done toward the end of the examination when the child is relaxed and more trusting of the nurse.
The abdominal cavity is the portion of the trunk from directly beneath the diaphragm and thoracic cavity to the region of the pelvic cavity. For descriptive purposes the abdominal cavity is divided into 9 quadrants.
Image 8. Anatomical areas of the anterior abdominal wall.
The abdominal cavity contains the major organs of digestion, and the pelvic cavity houses the internal reproductive organs, the lower parts of the digestive tract, and the urinary bladder. However, in infancy the bladder is an abdominal organ.
Inspection. The contour of the abdomen is inspected while the child is erect and supine. Normally the abdomen of infants and young children is quite cylindric and, in the erect position, fairly prominent because of the physiologic lordosis of the spine. In the supine position the abdomen appears flat. During adolescence the usual male and female contours of the pelvic cavity change the shape of the abdomen to form characteristic adult curves, especially in the female.
The size and tone of the abdomen also give some indication of general nutritional status and muscular development. A large, prominent, flabby abdomen is often seen in obese children, whereas a concave abdomen is frequently suggestive of undernutrition. However, careful note is made of a protruding abdomen, which may indicate pathologic states such as abdominal distention, ascites, tumors, or organomegaly. A protuberant abdomen with spindly extremities and flat, wasted buttocks suggests severe malnutrition that may occur from inadequate nutritional intake such as kwashiorkor or from diseases such as cystic fibrosis. Likewise, a scaphoid abdomen may indicate dehydration or diaphragmatic hernia, in which the abdominal organs rise into the thoracic cavity, or a “scaphoidlike” abdomen that only appears sunken in relationship to pneumothorax or high intestinal obstruction. A midline protrusion from the xiphoid to the umbilicus or pubic symphysis is usually diastasis recti, or failure of the rectus abdominis muscles to join in utero. In a healthy child a midline protrusion is usually a variation of normal muscular development. A tense, boardlike abdomen is a serious sign of paralytic ileus and intestinal obstruction.
The condition of the skin covering the abdomen should be noted. It should be uniformily taut, without wrinkles or creases. Sometimes silvery, whitish striae are seen, especially if the skin has been stretched as in obesity or with distention resulting from ascites. Any scars, ecchymotic areas, excessive hair distribution, or distended veins are noted.
Movement of the abdomen is observed. In infants and thin children peristaltic waves may be visible through the abdominal wall, and they always warrant careful evaluation. They are best observed by standing at eye level to and across from the abdomen. Visible peristaltic waves most often indicate pathologic states, particularly intestinal obstruction such as pyloric stenosis.
A doctor may observe pulsation of the descending aorta in the epigastric region (midline and below the xiphoid). Although visible pulsations are normally seen, especially in thin children, the nurse should auscultate and palpate the aorta for any evidence of an aneurysm, a saclike enlargement of the vessel.
In children under 7 or 8 years of age, breathing is primarily abdominal. If the abdomen fails to move with respiration, even in older children, this may indicate serious abdominal problems. Conversely, if the thoracic muscles fail to move, so that breathing is confined to abdominal movement, pulmonary problems may be at fault. Normally chest and abdominal movements are synchronous.
The umbilicus is inspected for hemiation, fistulas, such as a patent urachus (an abnormal connection between the umbilicus and bladder), discharge, and hygiene. If a hemiation is present the sac is palpated for abdominal contents and the approximate size of the opening is estimated. Umbilical hernias are common in infants, especially in black children. Since “home remedies” for treatment such as taping coins over the umbilicus or using “belly binders” may be harmful to the skin and actually delay natural closure, a doctor should ask parents whether such procedures have been used. Umbilical hernias normally protrude and expand when the child coughs, cries, or strains.
Hernias are looked for elsewhere on the abdominal wall, such as in the inguinal or femoral region. An inguinal hernia is a protrusion of peritoneum through the abdominal wall in the inguinal canal. It most often occurs in males, is frequently bilateral, and may be visible as a mass in the scrotum. It is palpated by sliding the little finger into the external inguinal ring at the base of the scrotum and asking the child to cough. If a hernia is present, it will hit the tip of the finger.
A femoral hernia, which occurs more frequently in girls, is felt or seen as a small mass on the anterior surface of the thigh just below the inguinal ligament in the femoral canal (a potential space medial to the femoral artery). Its location can be estimated by placing the index finger of the right hand on the child’s right femoral pulse (left hand for left pulse) and the middle ring finger flat against the skin toward the midline. The ring finger lies over the femoral canal, where the hemiation occurs. Palpation of hernias in the pelvic region, particularly inguinal ones, is often part of the examination of genitalia.
Auscultation. Each of the four quadrants should be auscultated using the diaphragm and bell chestpieces. Unlike listening to the heart or lungs, in which the stethoscope rests gently on the skin, to hear bowel sounds the stethoscope must be pressed firmly against the abdominal surface. With the diaphragm chestpiece this usually presents no difficulty, but with the bell chestpiece, especially one with a short cone, the skin may occlude the opening and prevent transmission of sound.
The most important sound to listen for is peristalsis, or bowel sounds, which sound like short metallic clicks and gurgles. Loud grumbling noises, known as borborygmi, are the familiar “stomach growls” usually denoting hunger. A sound may be heard every 10 to 30 seconds and its frequency per minute should be recorded (for example, 5 bowel sounds/minute). However, the nurse may need to listen for several seconds before audible peristalsis can be heard. Bowel sounds may be stimulated by stroking the abdominal surface with a fingernail. Absent bowel sounds or hyperperistalsis is recorded and reported, since either usually denotes abdominal disorder.
Various other sounds may be heard in the abdominal cavity. Normally the pulsation of the aorta is heard in the epigastrium. Sounds that resemble murmurs (called bruits), hums, or rubs are always referred for further evaluation.
Percussion. Percussion of the abdomen is performed in the same manner as percussion of the lungs and heart. Normally dullness or flatness is heard on the right side at the lower costal margin because of the location of the liver. Tympany is typically heard over the stomach on the left side and usually in the rest of the abdomen. An unusually tympanitic sound, like the beating of a tight drum, usually denotes air in the stomach, a common cause of which is mouth breathing. However, it can also denote a pathologic condition such as low intestinal obstruction or paralytic ileus. Lack of tympany may occur normally when the stomach is full after a meal, but in other situations it may denote the presence of fluid or solid masses.
Palpation.
It is necessary that the abdominal cavity should be accessible to palpation, i.e. that its muscles (prelum) be relaxed and that the examiner should not provoke their straining by his. manipulations. The patient should relax in his bed. (The bed should not be too soft.) His legs should be stretched and the arms flexed on the chest; The patient’s breathing should not be deep; his head should rest against a small firm pillow. This position ensures relaxation of the abdominal muscles. The physician takes his place by the right side of the bed, facing the patient. The chair should be firm and level with the patient’s bed. The ambient temperature should be comfortable for the patient, and the hands of the doctor should be warm and dry.
The examining movements should be careful and gentle so as not to hurt the patient. Touching the abdomen roughly with cold hands will cause reflex contraction of the prelum to interfere with palpation of the abdomen. The patient with distended abdomen should first be given cathartics or enema to empty the bowels. These are the conditions for palpation of the patient in the recumbent position. But some organs or their parts can only be palpated when they hang by gravity with the patient in the erect position. Thus the left lobe of the liver, the lesser curvature of the stomach, the spleen, the kidneys, the caecum, or tumors can become palpable. The epigastrium and the lateral parts of the abdominal cavity should also be palpated with the patient in the erect position.
Palpation is used to establish normal topographic relations between the abdominal organs and their normal physical condition; the other object is to detect any possible pathology that changes the morphological condition of the organs and their topographic relations responsible for their dysfunction, to locate the defect, and to determine its nature. Surface and deep palpation are used. Deep palpation gives information on the physical and sometimes functional condition of the organs and also on their position in the abdominal cavity. In other words, deep palpation gives information on the topography of the abdominal cavity (topographic palpation).
In superficial palpation a doctor lightly places the hand against the skin and feels each quadrant, noting any areas of tenderness, muscle tone, and superficial lesions, such as cysts. Superficial palpation is often perceived as “tickling” by the child, which can interfere with its effectiveness. The nurse can avoid this problem by having the child “help” with the palpation by placing his hand over the doctor’s palpating hand or by distracting him with statements such as, “I am trying to feel what you had for lunch”. Admonishing the child to stop laughing only draws attention to the sensation and decreases cooperation. Positioning the child supine with the legs flexed at the hips and knees helps relax the abdominal muscles.
Tenderness anywhere in the abdomen during superficial palpation is always noted. There are two types of abdominal pain: (1) visceral, which arises from the viscera or internal organs such as the intestines, and (2) somatic, which arises from the walls or linings of the abdominal cavity such as the peritoneum. Visceral pain is usually dull, poorly localized, and difficult for the patient to describe. Somatic pain is generally sharp, well localized, and more easily described. When assessing abdominal pain, it is important to remember that the child will often respond with an “all-or-none” reaction – either there is no pain or great pain. Therefore all aspects of the examination must be carefully considered when ruling out conditions such as appendicitis.
A special phenomenon called rebound tenderness, or Blumberg’s sign, may be performed if the child complains of abdominal pain. It is produced by pressing firmly over part of the abdomen distal to the area of tenderness. When the pressure is suddenly released, the child feels pain in the original area of tenderness. This response is only found when the peritoneum overlying a diseased viscus or organ is inflamed, such as in appendicitis.
Deep palpation is used for palpating organs and large blood vessels and for detecting masses and tenderness that were not discovered during superficial palpation. If the child complains of abdominal pain, that area of the abdomen is palpated last. Normally palpation of the midepigastrium causes pain as pressure is exerted over the aorta, but this should not be confused with visceral or somatic tenderness.
The doctor palpates the abdominal organs by pressing them against the free hand, which is placed on the child’s back. Palpation begins in the lower quadrants and proceeds upward. In this way the edge of an enlarged liver or spleen is not missed. Except for palpating the liver, successful identification of other organs, such as the spleen, kidney, and part of the colon, requires considerable practice with tutored supervision.
Surface tentative palpation.
The physician assumes his position by the bedside as described above and places his right hand flat on the abdomen of the patient (the fingers may be slightly flexed) to examine carefully and gradually the entire abdomen without trying to penetrate the deep parts of the abdomen. By this examination the physician should establish the strain of the prelum, its tenderness, and location of the painful site. The left inguinal area should be examined first, provided the patient does not complain of pain in this region. Palpation is then continued by examining symmetrical points of the abdomen on its left and right sides to end in the epigastric region. If the patient complains of pain in the left inguinal area, the sequence of palpation should be so changed that the least painful site on the anterior abdomen should first be examined. The physician should simultaneously assess the condition of the abdominal skin and sub-cutaneous connective tissue, the strain of the abdominal wall, the zones of superficial and deeper painful areas to locate them accurately. Hernial separation of muscles and protrusions, and also other anatomical changes should be revealed, if any. Resistance and marked strain of muscles of the abdominal wall are usually palpated over the organ affected by inflammation, especially so if the peritoneum is involved. In the presence of acute inflammation of the peritoneum (local inflammation included, e.g. in purulent ppendicitis, cholecystitis, and the like), local pressure causes strong pain but it becomes even more severe when the pressure is released (Shchetkin-Blumberg symptom). In the presence of pronounced enlargement of the parenchymatous organs, in strained abdomen or intestinal loops, and also in the presence of large tumors, even surface palpation can give much diagnostic information. But only deep systematic palpation can give full information about the condition of the abdominal cavity and its organs, as well as their topography.
Deep sliding palpation (according to Obraztsov and Strazhesko).
When starting deep palpation the examiner should always be aware of the anatomical relations in the abdominal cavity, the shape and physical properties of the organs, their supporting structures and possible deviations in topographical relations that may depend on the constitution of the patient, his special condition, nutrition, relaxation of the abdominal muscles, etc.
Obraztsov used the double-checking principle in his examinations. For example, in order to make sure that a given section of the intestine is actually ileum terminale it is necessary to locate the caecum; to determine the size of the stomach, the palpatory findings are checked by percussion and percussive palpation of the stomach. Respiratory excursions of the organs should be taken into consideration during palpation according to a strictly predetermined plan, beginning with more readily accessible parts. The following sequence is recommended: the sigmoid, the caecum_with the appendix, pars coecalis ilii, the ascending and descending colon, the stomach with its parts, the transverse colon, the liver, the spleen, the duodenum, the pancreas, and the kidneys.
Success of palpation depends on strict observation of the rules. The posture of the patient and the physician should be the same as in surface palpation. Palpation should be carried out by the apt hand. In some cases the other hand should be placed on the examining hand to increase pressure. Palpation can also be bimanual (palpation with both hands simultaneously). If only one hand is used, the other hand presses the prelum laterally to the palpated zone in order to lessen or overcome resistance of the abdominal wall and hence to promote relaxation of the prelum in the palpated zone. The other hand can be used to move the palpated organ closer to the examining hand or in order to perform bimanual palpation.
The palpation technique includes the following four steps. First: proper positioning of the physician’s hands. The right hand is placed flat on the anterior abdominal wall, perpendicular to the axis of the examined part or the edge of the examined organ. Second: formation of a skin fold to facilitate further movements of the examining hand. Third: moving the hand inside the abdomen. Deep palpation is when the fingers are moved gradually, with each expiration, into the abdomen when the abdominal wall is relaxed. The examining hand thus reaches the posterior wall of the abdomen or the underlying organ. Fourth: sliding movement of the fingertips in the direction perpendicular to the transverse axis of the examined organ. The organ is pressed against the posterior wall and the examining fingers continue moving over the examined intestine or the stomach direction (the sigmoid, caecum) or in the downward direction (the stomach, transverse colon); the movements should then be more oblique in accordance with the deviation of the organ from the horizontal or vertical course. The examining hand should always move together with the skin and not over its surface.
By palpating the intestine, the physician establishes its localization, mobility, tenderness, consistency, diameter, the condition of the surface (smooth, tubercular), the absence or presence of rumbling sounds during palpation. All these signs indicate the presence or absence of pathology.
The sigmoid is palpated from top right to medial left, downward and laterally, perpendicularly to the axis of the intestine, which runs obliquely in the left iliac space at the border of median and the outer third of the linea umbilico-iliacae. Palpations is carried out by four fingers, placed together and slightly flexed, or by the ulnar edge of the right little finger. The fingers are immersed medially of the expected position of the intestine and as soon as the posterior wall of the abdomen is reached, the fingers slide along the intestine in the given direction, i.e. laterally and downward. The intestine is pressed against the posterior wall and first slides along it (to the extent allowed by the mesenteric length) but later it slips from under the examining fingers. The sigmoid can be palpated by the described technique in 90-95 per cent of cases. The sigmoid is only impalpable in excess inflation of the abdomen and in obese patients. If the sigmoid is not found where it belongs, it may be displaced to some other location because of long mesenterium ,which accounts for the high sigmoid mobility. It is then usually displaced closer to the navel and to the right. The sigmoid can usually be found by deep palpation of the infraumbilical and suprapubic areas. Normally the sigmoid can be palpated over the length of 20—25 cm as a smooth firm cylinder, its thickness being that of a thumb or an index finger; the sigmoid is painless to palpation, it does not produce rumbling sounds, its peristalsis is rather flaccid and infrequent. The sigmoid can be displaced 3—5 cm to either side.
The caecum is palpated by the same technique except that the direction is different. Since the caecum is situated at the border of the median and lateral third of the umbilico-iliac line (
The ascending and descending colons are palpated by two hands . The left hand is placed under the left and then the right lumbar side, while the fingers of the right hand press on the anterior wall of the abdominal cavity until the examiner feels his right and left hands meet. The examining fingers then slide laterally, perpendicularly to the axis of the intestine (Vasilenko).
The transverse colon is palpated by four fingers of the right hand held together and slightly flexed . Bimanual palpation can also be used. Since the position of the transverse colon is unstable, it is useful first to determine by percussive palpation (after Obraztsov) the lower border of the stomach, and only then to search for the colon some 2-
In addition to the mentioned portions of the intestine, the horizontal parts of the duodenum and the curvature of the colon can in rare cases be palpated; an occasional loop of the small intestine that may happen in the iliac cavity can also be palpated. But the small intestine is usually impalpable because of its deep location, high mobility, and thin walls; it cannot be pressed against the posterior abdominal wall, which is the necessary condition for palpation of normal intestine.
The rectum can be probed by a finger after cleansing it with enema. The patient should assume the knee-chest position. The examining index finger should first be coated with vaseline oil and then introduced carefully into the rectum to the maximum possible depth. If the patient is especially sensitive, or the rectum and the ampulla are affected with inflammation or fissures, the sphincter and the ampulla should be anaesthetized before the intervention. As the examining finger passes the sphincter, it feels anteriorly the prostate in men and the vaginal part of the uterus in women. The finger should be moved upwards to pass the sacrococcygeal plica and to reach, if possible, the terminal rectal plica that closes the entrance to the sigmoid (11-
The lower edge of the liver is sometimes palpable in infants and young children as a superficial mass 1 to
The spleen is palpated by feeling it between the hand placed against the back and the one palpating the left upper quadrant. The spleen is much smaller than the liver and positioned behind the fundus of the stomach. The tip of the spleen is normally felt during inspiration as it descends within the abdominal cavity. It is sometimes palpable 1 to
Although most of these structures are not routinely felt, one should be aware of their relative location and characteristics in order not to mistake them for abnormal masses. The most common palpable mass in children is feces. It may be associated with pain in the right lower quadrant because with constipation the left colon fills with stool and gas until the ileocecal valve is reached. Then the cecum becomes distended, causing pain, which may be erroneously associated with appendicitis.
Paediatrics : Clinical Examinations – Examination of the Abdomen
Digestive Diagnostic Procedures for Children
In order to reach a diagnosis for digestive and liver problems, a thorough and accurate medical history must be taken by the doctor, noting the symptoms your child has experienced and any other pertinent information. A physical examination is also done to help assess the problem more completely.
Some patients need to undergo a more extensive diagnostic evaluation, which may include laboratory tests, imaging tests, or endoscopic procedures. These tests may include any, or all, of the following:
Laboratory tests:
· Albumin level. A sample of blood is obtained from your child’s vein. Below-normal levels of albumin, a protein made by the liver, found in the bloodstream are associated with many chronic liver disorders.
· Bilirubin level. A sample of blood is taken from your child’s vein. Bilirubin is produced by the liver and is excreted in the bile. Elevated levels of bilirubin may indicate an obstruction of bile flow or a defect in the processing of bile by the liver.
· Complete blood count (CBC). A sample of blood is taken from your child’s finger or vein, and the different types of cells in the bloodstream are examined. White blood cells multiply when infection is present. Red blood cells will be present in smaller amounts than normal if blood has been lost, if the diet has been inadequate, or with certain diseases.
· Electrolyte tests. A sample of blood is taken from your child’s vein, and the amounts of minerals known as electrolytes are measured, including sodium, potassium, calcium, and glucose. These minerals are important for the body to function properly. Children who have lost large amounts of fluid due to vomiting or diarrhea often lose large amounts of the various electrolytes as well. Your child’s doctor uses electrolyte tests to help determine when your child might need extra fluids given intravenously or other medications to help with dehydration and mineral loss.
· Fecal fat test. With this test, you child is asked to eat a high-fat diet for several days. You collect small samples of stool in sealed containers for three days. Your child’s doctor will send them to a laboratory. The amount of fat contained in your child’s stool is measured. If the digestive tract is working properly, only small amounts of fat will be present in the stool; the rest of the fat that was in the diet will have been digested and reabsorbed by the body. If your child has a condition known as malabsorption, then the intestinal tract cannot digest fats as well as it should, and elevated amounts of fat will pass through into the stool.
· Fecal occult blood test. A fecal occult blood test checks for hidden (occult) blood in the stool. It involves placing a very small amount of stool on a special card, which is then tested in the doctor’s office or sent to a laboratory.
· Hydrogen breath test. This test measures the amount of hydrogen in the breath, and helps diagnose several digestive problems, including carbohydrate intolerance, bacterial overgrowth of the small intestine, and rapid transit of food through the small intestine. Normally, digestive enzymes in the stomach and upper small intestine digest carbohydrates in the food we eat.
Bacteria in the lower small intestine digest the rest of the carbohydrates, and produce hydrogen gas in the process. If carbohydrates are largely undigested by the time they reach the small intestine, bacteria will complete the digestive process; however, hydrogen gas being produced will cause cramps and bloating. This can happen if the carbohydrates are not digested properly, if food moves through the digestive system quickly, or if there are large numbers of bacteria present. The amount of hydrogen in the breath is greater than usual when bacteria in the intestines digest carbohydrates instead of digestion being done by the normal digestive enzymes.
The child is told to fast overnight, and then breath samples are obtained by having the child blow into a balloon periodically. He or she will be given samples of a carbohydrate (such as lactose or sorbitol) to drink. The amount of hydrogen produced in the breath will be measured at the start of the test, and at intervals after carbohydrates are given.
· Lactose tolerance test. This test helps determine if a child has trouble digesting lactose properly. Your child is given a liquid containing lactose to drink. Several blood samples are taken over a two-hour period to measure the amount of glucose (sugar) present in the bloodstream. If lactose is digested normally, blood glucose rises. If lactose is not digested as it should be, then the blood glucose level does not change throughout the test.
· Liver enzymes. A sample of blood is taken from your child’s vein, and the amounts of enzymes that the liver normally makes are measured. Elevated levels of liver enzymes can alert doctors to liver damage or injury, since the enzymes leak from the liver into the bloodstream under these circumstances.
· Prothrombin time (PT) test. This test measures the time it takes for blood to clot. Blood clotting requires vitamin K and a protein made by the liver. Liver cell damage and bile flow obstruction can both interfere with proper blood clotting.
· Stool culture. A stool culture checks for the presence of abnormal bacteria in the digestive tract that may cause diarrhea and other problems. A small sample of stool is collected and sent to a laboratory by your doctor’s office. In two or three days, the test will show whether abnormal bacteria are present.
· Urea breath test. This test helps diagnose the presence of Helicobacter pylori (H. pylori) in the digestive tract. Your child swallows a capsule containing urea. If H. pylori is present in the stomach, then the urea will be converted into nitrogen and carbon. The carbon changes to carbon dioxide and moves into the bloodstream, and then into the lungs where it is exhaled. Your child breathes into a balloon, and the amount of carbon in the breath is measured. A positive test, meaning carbon is present, indicates the presence of H. pylori. A negative test, meaning no carbon is detected, indicates no H. pylori is present.
Imaging tests:
· Computed tomography scan (CT or CAT scan). A diagnostic imaging procedure that uses a combination of X-rays and computer technology to produce horizontal, or axial, images (often called slices) of the body.
scan shows detailed images of any part of the body, including the bones, muscles, fat, and organs. CT scans are more detailed than general X-rays. Your child will lie on a bed that moves into a doughnut shaped machine that takes many pictures of different areas of the body. Because the machine is noisy, and because your child may need to lie still for awhile with his or her arms over the head, a sedative might be given to help your child rest during the procedure.
· Lower GI (gastrointestinal) series (also called barium enema). A procedure that examines the rectum, the large intestine, and the lower part of the small intestine. A fluid called barium (a metallic, chemical, chalky, liquid used to coat the inside of organs so that they will show up on an X-ray) is given into the rectum as an enema. An X-ray of the abdomen shows strictures (narrowed areas), obstructions (blockages), and other problems.
· Magnetic resonance imaging (MRI). A diagnostic procedure that uses a combination of large magnets, radiofrequencies, and a computer to produce detailed images of organs and structures within the body. Your child lies on a bed that moves into the cylindrical CT scanner. The machine takes a series of pictures of the inside of the body using a magnetic field and radio waves. The computer enhances the pictures produced. The test is painless, and does not involve exposure to radiation. Because the CT scanner is like a tunnel, some children are claustrophobic or unable to hold still during the test, and may be given medication to help them relax or sleep. Metal objects cannot be present in the MRI room, so children with pacemakers or metal clips or rods inside the body cannot have this test done. All jewelry must be removed before the procedure.
· Magnetic resonance cholangiopancreatography (MRCP). A special type of magnetic resonance imaging (MRI) that uses radio waves and magnets to obtain pictures of the bile ducts and internal organs.
· Oropharyngeal motility (swallowing) study. Your child is given small amounts of a liquid containing barium to drink with a bottle, spoon, or cup. Barium shows up well on X-ray. A series of X-rays are taken to evaluate what happens as your child swallows the liquid. This procedure is also called a modified barium swallow.
· Ultrasound. A diagnostic imaging technique that uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs. Ultrasounds are used to view internal organs as they function, and to assess blood flow through various vessels. Gel is applied to the area of the body being studied, such as the abdomen, and a wand called a transducer is placed on the skin. The transducer sends sound waves into the body that bounce off organs and return to the ultrasound machine, producing an image on the monitor. A picture or video tape of the test is also made so it can be reviewed in the future.
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· Gallblader Ultrasound Part 1
· Gallblader Ultrasound Part 2 – Gallstones
· Gallblader Ultrasound Part 3 – Cholecystitis
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· Upper GI (gastrointestinal) series. A diagnostic test that examines the organs of the upper part of the digestive system: the esophagus, stomach, and duodenum (the first section of the small intestine). A fluid called barium (a metallic, chemical, chalky, liquid used to coat the inside of organs so that they will show up on an X-ray) is swallowed. X-rays are then taken to evaluate the digestive organs.
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Image 9. Abdominal X-ray showing severe faecal retention in
the rectum of a child with functional constipation.
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Endoscopic procedures:
· Colonoscopy. Colonoscopy is a procedure that allows the doctor to view the entire length of the large intestine (colon), and can often help identify abnormal growths, inflamed tissue, ulcers, and bleeding. It involves inserting a colonoscope, a long, flexible lighted tube, in through the rectum up into the colon. The colonoscope allows the doctor to see the lining of the colon, remove tissue for further examination, and possibly treat some problems that are discovered.
· Endoscopic retrograde cholangiopancreatography (ERCP). ERCP is a procedure that allows the doctor to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas. The procedure combines X-ray and the use of an endoscope, which is a long, flexible, lighted tube. The scope is guided through the patient’s mouth and throat, then through the esophagus, stomach, and duodenum (the first part of the small intestine). The doctor can examine the inside of these organs and detect any abnormalities. A tube is then passed through the scope, and a dye is injected which will allow the internal organs to appear on X-ray.
· Esophagogastroduodenoscopy (EGD) (also called upper endoscopy). EGD (upper endoscopy) is a procedure that allows the doctor to look at the inside of the esophagus, stomach, and duodenum. A thin, flexible, lighted tube called an endoscope is guided into the mouth and throat, then into the esophagus, stomach, and duodenum. The endoscope allows the doctor to view the inside of this area of the body, as well as to insert instruments through a scope for the removal of a sample of tissue for biopsy (if necessary).
Other procedures:
· Anorectal manometry. This test helps determine the strength of the muscles in the rectum and anus. These muscles normally tighten to hold in a bowel movement and relax when a bowel movement is passed. Anorectal manometry is helpful in evaluating anorectal malformations and Hirschsprung’s disease, among other problems. A small tube is placed into the rectum, and the pressures inside the anus and rectum are measured.
· Esophageal manometry. This test helps determine the strength of the muscles in the esophagus. It is useful in evaluating gastroesophageal reflux and swallowing abnormalities. A small tube is guided into the nostril, then passed into the throat and finally into the esophagus. The pressure the esophageal muscles produce at rest is then measured.
· Esophageal pH monitoring. An esophageal pH monitor measures the acidity inside of the esophagus. It is helpful in evaluating gastroesophageal reflux disease (GERD). A thin plastic tube is placed into a nostril, guided down the throat and then into the esophagus. The tube stops just above the lower esophageal sphincter, which is at the connection between the esophagus and the stomach. At the end of the tube inside the esophagus is a sensor that measures pH, or acidity. The other end of the tube outside the body is connected to a monitor that records the pH levels for a 24 to 48 hour period. Normal activity is encouraged during the study, and a diary is kept of symptoms experienced or activity that might be suspicious for reflux, such as gagging or coughing. It is also recommended to keep a record of the time, type, and amount of food eaten. The pH readings are evaluated and compared to the child’s activity for that time period.
· Magnetic resonance cholangiopancreatography (MRCP). This uses magnetic resonance imaging (MRI) to obtain pictures of the bile ducts. The machine uses radio waves and magnets to scan internal organs and tissues.
· Capsule endoscopy. A capsule endoscopy helps doctors examine the small intestine, because traditional procedures, such as an upper endoscopy or colonoscopy, cannot reach this part of the bowel. This procedure is helpful in identifying causes of bleeding, detecting polyps, inflammatory bowel disease, ulcers, and tumors of the small intestine. A sensor device is placed on a patient’s abdomen and a pillcam (capsule endoscope) is swallowed. The pillcam passes naturally through the digestive tract while transmitting video images to a data recorder. The data recorder is secured to a patient’s waist by a belt for eight hours. Images of the small bowel are downloaded on a computer from the data recorder. The images are reviewed by a doctor on a computer screen. Normally, the pillcam passes through the colon and is eliminated in the stool within 24 hours.
· Liver biopsy. A liver biopsy helps diagnose liver diseases. A small sample of liver tissue is obtained with a special biopsy needle and examined for abnormalities. Children are sometimes given medication to minimize their anxiety during the procedure. A small area of skin over the liver is numbed with a local anesthetic. The anesthetic is then injected deeper under the skin to numb the area that the biopsy needle will pass through and reduce the discomfort of the test. The biopsy needle is quickly inserted through the skin and into the liver, and then withdrawn. Sometimes, an ultrasound of the liver is done at the same time to help the doctor know exactly where to obtain the tissue samples. After a liver biopsy, a health care professional will observe the child for bleeding problems for a few hours. Pain medications will be given, if needed.
DISEASES of digestive system
Pylorostenosis
Pylorostenosis is a disease of infants of the first month of life due to a narrowing of the pyloric canal’s aperture because of muscular hypertrophy of the pylorus.
Clinical manifestation
– latent period,
– regurgitations up to abundant vomit without bile,
– dehydration,
– malnutrition,
– stomach peristalsis in a form of sand –glass,
– constipation.
Gastroesophageal reflux (GER, chalasia, cardiochalasia) denotes relaxation or incompetence of the lower esophageal sphincter, causing frequent return of stomach contents into the esophagus. In newborns this is considered a normal phenomenon because of immature neuromuscular control of the gastroesophageal sphincter. However, in a small percentage of infants reflux continues, producing symptoms that warrant investigation. The exact cause is not known, although it is thought to result from delayed maturation of lower esophageal neuromuscular function or impaired local hormonal control mechanisms.
Clinical manifestations
– vomiting,
– weight loss,
– respiratory problems,
– bleeding.
Vomiting is the most frequent symptom and in infants is quite forceful. It is frequently so severe that there is a loss of calories sufficient to cause weight loss and failure to thrive.
Reflux of stomach contents to the pharynx predisposes to aspiration and the development of respiratory symptoms, especially pneumonia. Repeated irritation of the esophageal lining with gastric acid can lead to esophagitis and consequently bleeding. Blood loss in turn causes anemia and is seen as hematemesis or melena (blood in stools). Heartburn is also a frequent symptom in older children who can describe it but may go unrecognized in infants.
Malabsorption syndromes
The term “malabsorption syndrome” is applied to a long list of disorders associated with some degree of impaired digestion and/or absorption. Most are classified according to the locations of the supposed anatomic and biochemical defect.
Digestive defects mainly include those conditions in which the enzymes necessary for digestion are diminished or absent, such as cystic fibrosis, in which pancreatic enzymes are absent biliary or liver disease, in which bile production is affected, or lactase deficiency, in which there is congenital or secondary lactose intolerance.
Absorptive defects include those conditions in which the intestinal mucosal transport system is impaired. It may be because of a primary defect, such as in celiac disease or gluten enteropathy, or secondary to inflammatory disease of the bowel, hat results in impaired absorption because bowel motility is accelerated, such as ulcerative colitis.
Obstructive disorders, such as Hirschsprung’s disease, can also cause secondary malabsorption from enterocolitis, chronic inflammation of the distended small and large bowel, megacolon or large colon.
In addition, there is failure of the internal rectal sphincter to relax, which adds to the clinical manifestations because it prevents evacuation of solids, liquids, and gas.
Clinical manifestations
Clinical manifestations vary according to the age.
In the newborn the chief signs and symptoms are failure to pass meconium within 24 to 48 hours after birth, reluctance to ingest fluids, bile-stained vomitus, abdominal distention.
If the disorder is allowed to progress, other signs of intestinal obstruction, such as respiratory distress and shock, develop.
During infancy the child does not thrive and has constipation, abdominal distention, episodes of diarrhea and vomiting.
The occurrence of explosive, watery diarrhea, fever, and severe prostration is ominous because it often signifies the presence of enterocolitis, which greatly increases the risk of fatality. Enterocolitis may also be present without diarrhea and is first evidenced with unexplained fever and poor feeding.
During childhood the symptoms include: constipation, passage of ribbonlike, foul-smelling stools, abdominal distention, visible peristalsis. Fecal masses are easily palpable. The child is usually poorly nourished, anemic, and hypoproteinemic from malabsorption of nutrients.
Peptic ulcer
A peptic ulcer is an erosion of the mucosal wall of the stomach, pylorus, or duodenum. A gastric ulcer affects the lining of the stomach, whereas a duodenal ulcer involves the pylorus or duodenum. Although peptic ulcers are more common in adults, they are also a significant pediatric problem, occurring most frequently between 12 and 18 years. Males are affected more than three times as often as females or duodenum. Although peptic ulcers are more common in adults; they are also a significant pediatric problem, occurring most frequently between 12 and 18 years.
Clinical manifestations
Signs and symptoms of peptic ulcers vary according to the age of the child and the location of the ulcer.
1. The typical pain-food-relief syndrome.
2. Chronic abdominal pain, especially when the stomach is empty, during the night or early morning.
3. Recurrent vomiting after meals.
4. Chronic anemia with occult blood in the stools.
5. Vague gastrointestinal complaints with a positive family history for peptic ulcer.
6. Children with chronic illness and especially those undergoing steroid therapy are prone to develop peptic ulcers.
Acute appendicitis
Appendicitis, inflammation of the vermiform appendix, or blind sac, at the end of the cecum, is the most common reason for abdominal surgery during childhood. It is rare in children younger than 2 years of age group.
Progressive peritoneal inflammation results in functional intestinal obstruction of the small bowel, since intense gastrointestinal reflexes severely inhibit bowel motility.
Clinical manifestations
1. Abdominal pain, initially the pain generalized or periumbilical.
2. Localized tenderness, usually descends to the lower right quadrant.
3. Fever.
4. The intense site of pain may be at McBumey’s point, which is located about
5. Rebound tenderness.
6. A rigid abdomen, and decreased or absent bowel sounds are important signs of appendicitis.
7. Vomiting is a common early sign.
8. Constipation may be present, diarrhea can also occur.
Low-grade fever is typically seen early in the disease but can rise sharply once peritonitis has begun.
Other signs of peritonitis include sudden relief from pain after perforation, subsequent increase in pain, which is usually diffuse and accompanied by rigid guarding of the abdomen, progressive abdominal distention, tachycardia, rapid shallow breathing as the child refrains from using abdominal muscles, pallor, chills, irritability, and restlessness.
– A change in the child’s behavior,
– a characteristic side-lying position with the knees flexed to the abdomen,
-a rigid, motionless posture should alert one to abdominal pain.
The older child may exhibit all of these behaviors, while complaining of abdominal pain.
Diagnostic evaluation
· Diagnosis is based primarily on history and examination.
· The chief clues that should alert the practitioner to appendicitis are the progression of abdominal pain.
· Location of abdominal tenderness.
· Decreased peristalsis.
· Pain on rectal examination.
· Absence of any other symptoms or findings suggesting another disorder, such as pneumonia.
Laboratory evaluation
– white blood cell count, which is usually elevated but is seldom higher than 15,000 to 20,000/mm3,
– roentgenographic studies of the abdomen.
Therapeutic management
– surgical removal of the appendix (appendectomy).
For child with peritonitis:
a) medical management for shock,
b) dehydration (this includes intravenous administration of fluid and electrolytes, blood volume replacement with plasma or albumin)
c) systemic antibiotics,
e) nasogastric suctioning, and positioning in Fowler’s position to facilitate drainage into the pelvic area,
f) antibiotic therapy.
Ulcerative colitis is a disease characterized by a chronic inflammatory reaction involving the mucosa and submucosa of the large intestine. It occurs in both sexes and in all age-groups. It is basically a disease of young adults, although close to 15% of the cases begin in children younger than 16 years. The peak onset in children is between ages 10 and 19. This disorder and Crohn’s disease are together referred to as inflammatory bowel disease.
Etiology. The cause of ulcerative colitis is unknown, although infectious, nutritional, immunologic, and psychogenic etiologies have been proposed but not substantiated. At present the feeling is that ulcerative colitis is an organic disease caused by a combination of physical and emotional factors. Psychologic influences, such as stress, significantly affect the exacerbation and chronicity of the illness.
Several genetic and environmental factors influence the incidence of ulcerative colitis: (1) there is a familial tendency in about 5% to 15% of the cases, (2) individuals from higher socioeconomic levels and more whites thaonwhites are affected, (3) the incidence is four times greater in Jewish populations than in the general population, and (4) there is a higher occurrence of allergic disease in relatives of these patients.
Pathophysiology. The mucous membranes of the bowel become hyperemic and edematous with the formation of patchy granulations over the intestinal surface that bleed easily and eventually develop irregular areas of superficial ulcerations. In longstanding disease the bowel becomes narrowed, smooth, and inflexible with thin or absent mucosa heavily infiltrated by scar tissue. The greatly reduced absorptive surface results in loose, watery, and sometimes bloody stools.
Clinical manifestations
The most common feature of ulcerative colitis is persistent or recurring diarrhea. In the acute, fulminating disease there is bloody diarrhea preceded by cramping abdominal pain and followed by abdominal distention. Diarrhea may be very severe with marked urgency and frequency (20 to 30 stools daily). It is usually associated with fever, weight loss, anorexia, and sometimes nausea and vomiting. Pallor and anemia may result from bleeding and reduced dietary intake, and the numerous watery bowel movements often cause depletion of water and electrolytes.
The clinical course varies markedly in terms of severity, response to therapy, and prognosis. In general the disease follows one of two patterns: acute remitting type or chronic continuous course. Children afflicted with either type have usually been healthy before the onset of the disease.
The acute remitting type is more common and follows a pattern of remissions and exacerbations. During the period of remission, the child is usually well, with few or no symptoms of the disease. However, periods of exacerbation are severe and acute, although they usually respond well to medical treatment. The disease may terminate in a permanent remission or ultimately follow the course of chronic colitis.
In chronic continuous colitis there are no definitive periods of severe disease with intermittent good health. Intestinal symptoms tend to be less severe, but chronic malnutrition and anemia are common. These children often respond poorly to medical therapy and are more likely to suffer from complications, especially carcinoma of the colon.
Therapeutic management
Medical treatment is based on a combination of therapies: (1) dietary management to allow the colon a rest and improve the child’s nutritional status, (2) medication to reduce the abdominal pain and rectal spasm, (3) steroids to reduce bowel inflammation, and (4) antibacterial agents (sulfasalazine) to prevent infection. The child is usually hospitalized both to ensure proper medical management and to reduce the familial/environmental factors that may be contributing to the disease.
Other medical therapies that may be warranted include intravenous fluids, to correct dehydration and associated electrolyte imbalances, and parenteral alimentation when malnutrition is severe and the colitis is further aggravated by oral diet. Emergency surgical intervention is required for complications such as perforation, massive hemorrhage, or toxic megacolon (fulminating distention of the colon with progressive inflammation).
In some instances a poor response to medical treatment necessitates elective surgery either to allow the bowel a period of rest, in which a temporary colostomy is performed, or to arrest the disease process by removing the entire section of ulcerated bowel, in which case a total colectomy or ileostomy is usually required. In some centers a prophylactic colectomy is considered in those children with chronic colitis of 10 years or more duration to eliminate the high risk of coionic cancer.
A possible alternative to a permanent colostomy or ileostomy is the continent (Koch) ileostomy. In this procedure an intraabdominal pouch or reservoir is constructed from the terminal ileum. The feces are stored in the pouch until the patient drains it with a catheter. A surgically implanted valve prevents leakage of feces. The stoma is less than an inch in diameter, is almost level with the skin, and requires no appliance. These are obvious advantages, especially to an adolescent who is concerned with body image and self-identity.
Psychotherapy or family counseling may also prove helpful in reducing stresses that existed before the disease and those that have resulted from the colitis. A particularly difficult stress for these children to cope with is the consequent growth retardation and delayed sexual maturation from chronic colitis. Supportive therapy may also be of benefit to those children facing the adjustment of a permanent ileostomy.
Syndromes of digestive system
1. Painful syndrome.
2. Dyspeptic syndrome.
3. Intoxication syndrome.
4. Malabsorption.
5. Acute abdomen.
6. Exicosis.
7. Toxicosis.
8. Hypotrophy.
9. Obesity.
10. Jaundice.
11. Hepatolienal syndrome.
12. Cholestasis.
13. Cytolysis.
14. Portal hypertension.
15. Pylorospasm.
16. Pylorostenosis.
17. Hypovitaminosis.
18. Dyskinesia
а) Basic
1. Manual of Propaedeutic Pediatrics / S.O. Nykytyuk, N.I. Balatska, N.B. Galyash, N.O. Lishchenko, O.Y. Nykytyuk – Ternopil: TSMU, 2005. – 468 pp.
2. Kapitan T. Propaedeutics of children’s diseases and nursing of the child : [Textbook for students of higher medical educational institutions] ; Fourth edition, updated and
translated in English / T. Kapitan – Vinnitsa: The State Cartographical Factory, 2010. – 808 pp.
3. Nelson Textbook of Pediatrics /edited by Richard E. Behrman, Robert M. Kliegman; senior editor, Waldo E. Nelson – 19th ed. – W.B.Saunders Company, 2011. – 2680 p.
b) Additional
1. www.bookfinder.com/author/american-academy-of-pediatrics
3. http://www.nlm.nih.gov/medlineplus/medlineplus.html
4. Gasiorowska A, R Faas R: Current approach to dysphagia. Gastroenterol Hepatol 2009; 5:269-279.
