Themes:
Theme 1: Functional gastrointestinal disturbances in the early age children. Classification by Roman criterions ІІІ.
Theme 2: Diarrheal diseases, cyclic vomiting, functional constipation. Etiology, pathogenesis, clinical features, diagnostics, treatment.
Theme 3: Protein-vitamin insufficiency in children. Malnutrition. Clinical features, diagnostics, treatment and prophylaxis.
Theme 1: Dyspepsia syndrome – pain or discomfort sensation (distension, overload, early saturation), localized in epigastria more to the midline.
Roman criterions ІІІ of functional disorders of gastrointestinal tract – nonulcer dyspepsia syndrome
1.Permanent (constant) or relapsing dyspepsia (or pain, discomfort, which is localized in upper part of the abdomen on the midline)with duratioot less than 12 weeks for the last 12 months.
2. Absense of the organic disease evidences, proved by accurately taken anamnesis, endoscopic examination of the upper parts gastrointestinal tract and ultrasonic investigation of the abdominal cavity organs.
3. Absence of the evidence, that dyspepsia is decreased by defecation or is connected with the feces quantity or form (which is typical for irritable bowel syndrome).
Classification of dyspepsia syndrome
1. Ulcer like dyspepsia
2. Dyskinetic dyspepsia
3. Nonspecific dyspepsia
Criterions of different type of dyspepsia
І. Ulcer like dyspepsia:
1. Pain is localized in epigastria region
2. Pain relief after food intake, antacids, antisecretion medicine
3. Empty stomach pain
4. Night pain
5. Periodic pain.
ІІ. Dyskinetic dyspepsia
Sensation of overload, distension in epigastria region after meal
Sensation of meteorism in the upper part of abdomen
Rapid saturation
Loss of appetite
Nausea
ІІІ. Nonspecific dyspepsia
Signs and symptoms which are combined
TREATMENT.
Ulcer like dyspepsia: Antacids (Maalox), antisecretory agents: H2-receptor antagonists (Famotidine, Ranitidine), Proton pump inhibitors (Omeprazole), Eradication of H pylori infection
(Metronidazole, Amoxicillin or clarithromycin ).
Dyskinetic dyspepsia: prokinetics (motilium)
Nonspecific dyspepsia: Antacids (Maalox), prokinetics (motilium)
Theme 2: Diarrheal diseases, cyclic vomiting, functional constipation. Etiology, pathogenesis, clinical features, diagnostics, treatment.
Diarrhea-loose, watery stools occurring more than three times in one day-is a common problem that usually lasts a day or two and goes away on its own without any special treatment. However, prolonged diarrhea can be a sign of other problems.Diarrhea can cause dehydration, which means the body lacks enough fluid to function properly. Water is vital to the normal working of the body and a shortage is always serious.Diarrheal disorders may be a result of bacterial pathogens (Escherichia coli, Campylobacter, Salmonella, Shigella), viral pathogens or cow‘s milk and soy protein intolerance, dietary disturbances, secondary malabsorption syndrome.

INTRODUCTION
Dehydration is particularly dangerous in children and the elderly, and it must be treated promptly to avoid serious health problems.
People of all ages can get diarrhea. The average adult has a bout of diarrhea about four times a year.
Each year diarrhea disease causes an estimated 3 million deaths in children under five.
Diarrhea remains one of the most common illnesses affecting infants and children in the world. Although most children have mild symptoms with little or no dehydration, a substantial number are affected more seriously. Almost 10% of hospitalizations of children younger than 5 years of age are because of diarrhea and it is estimated that almost ¼ of a million children are hospitalized each year with gastroenteritis. The average child under age 5 experiences 2.2 diarrheal episodes per year; children attending Day Care Centers have an even higher incidence. There are surveys to show that many health care providers do not follow recommended procedures for the optimal management of children with diarrhea.
The water loss associated with conditions such as gastroenteritis can impose a relatively greater stress on the young infant due to the higher percentage of body water. A term baby is 80% water, which reduces to a proportion of 60% at a year.
It is very important to note that it is both easy for an infant to become dehydrated, and easy to rehydrate that infant with oral rehydration therapy in the vast majority of cases.
Infectious diarrhoea in children is a very common problem, most of which is viral, principally rotavirus. The important features of management are: recognition of more serious causes of diarrhoea, for example, if there is blood in the stool – ie the possibility of intussusception appropriate treatment is usually conservative, antibiotics and gut motility inhibitors are rarely required adequate oral rehydration at an early stage
ETIOLOGY
INFECTION DIARRHEA
More than 90% of infectious diarrhoea in infants has a viral aetiology – in fact 90% is caused by rotavirus, a virus which can cause infections of both the GIT and URT. Other viruses include Echo and Enteroviruses.
A bacterial aetiology is suggested by high pyrexia and bloody diarrhoea. This is principally Enteropathic E. coli, although Shigella, Salmonella and Campylobacter should be borne in mind. World-wide, cholera must be considered, especially currently in South America.
Chronic infections might suggest protozoans, for example Giardia lamblia. This causes three or four episodes of foul smelling diarrhoea a day, and a diagnosis is made on the basis of cysts found in the stool.
Rotavirus gastroenteritis
Rotavirus gastroenteritis is an important cause of diarrhoea and vomiting in children, affecting boys more often than girls. It is the most common cause of gastroenteritis in children, but is not a notifiable illness and therefore not recorded as frequently as bacterial gastroenteritis.
There are winter and spring peaks, which fall off in the summer. Usually the patient is less than one year old; rotavirus is only seen in the under fives and in the elderly.
Diagnosis is made from examination of faecal suspensions or faecal fluids. Treatment is with oral rehydration therapy.
Escherichia coli (diarrhoea)
Various strains of E. coli may cause diarrhoea by differing mechanisms.
The organism is isolated by stool culture. Traditionally, the specific strain is identified by serotype – ‘O’ somatic antigen – but increasingly, diagnosis is based on the direct demonstration of toxins – either their effect on cell cultures or immunologically – or by detection of the genes coding for them.
Treatment is usually supportive. Adequate fluid intake must be ensured. Codeine phosphate or loperamide may be given for symptom control but must never be used in children. Antibiotics may be administered for enterohaemorrhagic E. coli.
Enteroinvasive E. Coli
Enteroinvasive E. coli cause a dysentery-like illness by invading the epithelial cells of the large intestine where they cause necrosis, ulceration and inflammation.
They cause sporadic outbreaks of diarrhoea in older children and adults, some of which are food-borne.
Enteroinvasive serotypes include 0124, 0136, 0143 etc.
Enterohaemorrhagic E. Coli
Enterohaemorrhagic E. coli cause a haemorrhagic colitis, haemolytic uraemic syndrome and thrombotic thrombocytopaenic purpura by the production of verotoxins.
They colonise the large intestine where they cause diffuse mucosal haemorrhages.
Enterohaemorrhagic serotypes include O157.H7.
Treatment is mainly supportive. Antibiotics such as co-trimoxazole, ciprofloxacin, or gentamicin, may be helpful but their use is controversial since there is evidence linking antibiotic treatment of this condition to the development of haemolytic uraemic syndrome.
Enterotoxigenic E. Coli
Enterotoxigenic E. coli cause traveller’s and infant diarrhoea via the production of enterotoxins. The heat stable form stimulates guanyl cyclase; the heat labile form closely resembles the cholera toxin and stimulates adenyl cyclase. Primarily they affect the small intestine, causing hyperaemia of the mucosa.
Food and water contaminated by human faeces are chiefly responsible.
Enterotoxigenic serotypes of E. coli include 0115, 0148 and 0153.
Enteropathogenic E. Coli
Enteropathogenic E. coli cause diarrhoea by an unknown mechanism. It is known that they cause destruction of the microvilli, and that adherence is important, mediated through the production of characteristic fimbrial adhesins. It is a cause of sporadic diarrhoea in infants and outbreaks iurseries, associated with cross-infection via staff hands.
Enteropathogenic serotypes include 044, 0111, 0114, 0125, etc.
Shigella spp dysentery
Bacillary dysentery is caused by Shigella, with Shigella sonnei responsible for more than 90% of cases in UK, but causing the mildest form of the condition, S. flexneri, S. boydii and S. dysenteriae causing progressively more severe dysentery.
The inoculating dose is small – about 200 organisms.
The organisms invade the superficial colonic mucosa causing inflammation. Local multiplication and invasion is possible via a virulence factor, together with the production of a toxin. A cholera-like presentation may occur if the disease is due to S. dysenteriae, which produces a cytotoxin, Shiga toxin. The shiga-like toxins are related, but less potent, and are produced by Shigella sp. and also by enterohaemorrhagic E. Coli.
Outbreaks occur iurseries, mental and geriatric institutions – the latter two are on the decline – underlining the fact that the faecal-oral route is needed. Some 50% of cases occur in children less than 10 years old.
Salmonella spp
The salmonella species of bacteria are gram negative bacilli responsible for three distinct clinical syndromes:
enteric fevers:
typhoid and paratyphoid fever
caused by S. typhi or S. paratyphi respectively
are systemic bacteraemic infections
salmonellosis:
is a form food poisoning, caused by non-typhoid Salmonellae
bowel symptoms e.g. diarrhoea, are predominant
salmonella osteomyelitis:
particularly common in patients with sickle cell anaemia
About 3% of patients will become chronic carriers.

Campylobacter jejuni
Campylobacter jejuni food poisoning is characterised by a prodromal malaise, abdominal pain, diarrhoea, with vomiting being uncommon. The problems are due to multiplication organisms within the gut and the release of endotoxin, with symptoms occurring after 2 to 5 days. It was the most common cause of gastroenteritis in England and Wales in 1991. The organism comes from poultry and unpasteurised milk.
The loading dose is 10,000 organisms, which colonise the jejunum, ileum, and colon with local invasion of the epithelium. There is sometimes production of a cholera- like toxin and cytotoxins.
Campylobacter is cultured at 42øC in selective media.
The condition is usually self limiting but may be treated if severe with oral erythromycin. Principally this is to reduce the risk of bacteraemia.
Cholera
Cholera is an acute infectious disease endemic and epidemic in Asia.
It is caused by Vibrio cholerae in two biotypes – classic and El Tor. The latter is able to survive longer iature, can cause subclinical cases, has a longer faecal excretion of the organism, and can be transmitted from case to case or via food and water.
Giardiasis
This is a chronic diarrhoeal disease that is due to the flagellate protozoal parasite, Giardia lamblia, which attaches to, but does not invade, the small bowel.
This disease is associated with malabsorption, particularly of carbohydrate and fat. Presentation is of chronic persistent, or recurrent diarrhoea with very offensive stools, abdominal distension and weight loss. Children may show failure to thrive from lack of fat soluble vitamins.
Epidemiology
Environmental factors include:
poverty and overcrowding, in the absence of clean water supply, proper sewerage disposal and appropriate personal hygiene are important internationally
malnutrition is a strong contributory factor
bottle feeding, with incorrect sterilisation
The highest risk groups are children under six months old in the developed, or infants bottle fed or between weaning and the second year in the developing world.
Pathophysiology of infective diarrhoea
Infective organisms are able to cause diarrhoea in a variety of ways:
mucosal damage caused by direct attack
toxin production after ingestion
toxin production before ingestion
The diarrhoea itself can be:
secretory, where deranged membrane transport results in decreased electrolyte absorption and thus decreased water absorption
decreased absorption, itself a result of mucosal damage, osmosis, or increased gut motility
Non-infectious diarrhoea in children
Non infectious causes of diarrhoea would tend to cause a more chronic diarrhoea. Causes include:
monosaccharide intolerance
disaccharide intolerance
cow’s milk intolerance
coeliac disease
ulcerative colitis and Crohn’s disease
cystic fibrosis
agammaglobulinaemia
acrodermatitis enteropathica – zinc deficiency
Monosaccharide intolerance
Monosaccharide intolerance occurs probably as a result of an inability to transport these molecules across the gut wall. Of these, the best documented type is glucose-galactose intolerance where fructose is the only monosaccharide that can be transported.
Disaccharide intolerance
Disaccharide intolerance results from inability to enzymatically split disaccharides into monosaccharides. An example is lactase inactivity, as in the lactose intolerance conditions.
Cow’s milk protein intolerance
Cow’s milk intolerance is mainly a clinical diagnosis that is made as the result of acute or chronic symptoms related to ingestion of cow’s milk.
The incidence is roughly one in two hundred, although there is considerable variation between studies; there may be differences in criteria for diagnosis.
Toddler’s diarrhoea
Toddler’s diarrhoea is a chronic non-specific diarrhoea seen in small children, between about one and four years. This condition accounts for a large proportion of children with chronic diarrhoea, but should be regarded as a diagnosis of exclusion.
Coeliac disease
Coeliac disease is clinically very variable and so is defined pathologically as a permanent gluten-sensitive enteropathy.
The mucosal lesions seen on upper GI biopsy are the result of an abnormal, genetically determined, cell-mediated immune response to gliadin, a constituent of the gluten found in wheat. A similar response occurs to comparable proteins found in rye and barley. Gluten is not found in oats, rice and maize.
Coeliac disease was first identifed by Samuel Gee in 1888. However, it was W. Dicke in the 1950s who identified the dietary link, noting that patients with this condition were apparently cured by the deprivations of World War II, but relapsed when rationing was abolished.
Ulcerative colitis
Ulcerative colitis is a chronic disease of unknown aetiology in which a part or the whole of the mucosa of the large bowel becomes diffusely inflamed and may ulcerate, as a result of which the patient suffers from diarrhoea which may be bloody.
It is characterised by exacerbations and remissions.
The highest incidence of this disease is in adulthood, although it may occur in childhood.
The cause of ulcerative colitis is unknown but genetic, immunological, dietary, and psychological factors have all been implicated.
Crohn’s disease
Crohn’s disease is a disorder of unknown aetiology that is characterised pathologically by involvement of all bowel wall layers in a chronic inflammatory process with non-caseating granulomas. The granulomatous inflammation most frequently affects the terminal ileum but it may affect any part of the gastrointestinal tract and frequently affected areas are in discontinuity. There is a tendency to form fistulae.
Cystic fibrosis
Cystic fibrosis is the most common potentially lethal autosomal recessive disorder in Caucasian populations, characterised by chronic suppurative lung disease and chronic exocrine pancreatic insufficiency.
It affects
The predominant symptoms of CF are attributed to epithelial abnormalities in the respiratory, digestive and reproductive tracts:
although lungs are normal at birth, recurrent respiratory infection is a major presenting feature
85% of CF patients have pancreatic insufficiency
10% of CF newborns suffer meconium ileus
patients are also prone to hepatic cirrhosis and male infertility
DEHYDRATATION
Dehydration leads to a change in the vital balance of chemical substances dissolved in the blood and tissue fluids, especially sodium (salt) and potassium. The function of many cells depends critically on these substances being maintained at the correct levels; serious effects follow any change and often lead to death. The risk is especially great in babies and infants, whose high death rate from conditions such as gastroenteritis is largely due to dehydration.
Dehydration is loss of water and important blood salts like potassium (K+) and sodium (Na+). Vital organs like the kidneys, brain, and heart can’t function without a certain minimum of water and salt. In underdeveloped countries, dehydration from diseases like cholera and dysentery kills millions every year (usually infants and children). Still, with severe vomiting or diarrhea and occasionally with excessive sweating, you can become dangerously dehydrated right here in the U.S.A. Below are some warning signs for dehydration.
Causes and risks
Because of their smaller body weights and higher turnover rates for water and electrolytes, infants and children are more susceptible to dehydration than adults. Causes of dehydration include excessive fluid losses, inadequate fluid intake, or a combination of these factors.
Causes of acute fluid loss include:
diarrhea (especially well recognized in cholera)
excessive urine output (polyuria) such as with uncontrolled diabetes
fever
Dehydration can also occur from inadequate intake as in:
refusing to drink because of mouth sores (stomatitis) or a sore throat (pharyngitis)
acute illness with loss of appetite
Dehydration in children is most often a combination of both as in:
gastroenteritis with vomiting and diarrhea
acute illness where the child refuses fluids and loses excessive fluid through sweating with fever.
Types of Dehydration
|
xx |
Isotonic |
Hypotonic |
Hypertonic |
|
Serum Na (mEq/L) |
130 to 150 |
<130 |
>150 |
|
Serum osmolality |
280 to 300 |
decreased |
increased |
|
Physical Signs: |
gray |
gray |
gray |
|
Temperature |
cold |
cold |
cold |
|
Turgor |
poor |
very poor |
fair |
|
feel |
dry |
clammy |
thick, doughy |
|
Mucous membrane |
dry |
dry |
parched |
|
Sunken eyes |
+ |
+ |
+ |
|
Depressed Anterior Fontanel |
+ |
+ |
+ |
|
Mental status |
lethargic |
coma/seizure |
irritable/seizure |
|
Increased pulse |
++ |
++ |
+ |
|
Decreased BP |
++ |
+++ |
+ |
|
Etiology |
vomiting, diarrhea, DKA |
electrolyte in excess of water loss |
water loss in excess of electrolyte loss |
|
Table 2 Clinical Signs Associated With Various Degrees of Dehydration
|
|
|
Dehydration (%) |
Clinical Observation |
|
5-6 |
Heart rate (10% to 15% above baseline value) |
|
7-8 |
Increased severity of above |
|
>9 |
Pronounced severity of above signs |
|
* These signs may be less sensitive indicators of dehydration than the others. |
|
|
|
|
SIGNS AND SYMPTOMS OF DEHYDRATATION
|
|
DEGREE of DEHYDRATION |
||
|
SIGNS and SYMPTOMS |
Mild (5%) |
Moderate (10%) |
Severe (15% or greater) |
|
Dry mucous membranes |
+/- |
+ |
+ |
|
Reduced skin turgor |
– |
+/- |
+ |
|
Depressed anterior fontanel |
– |
+ |
+ |
|
Sunken eyes; no tears |
– |
+ |
+ |
|
Hyperpnea |
– |
+/- |
+ |
|
Hypotension (orthostatic) |
– |
+/- |
+ |
|
Increased pulse |
– |
+ |
+ |
|
Laboratory Studies |
|
|
|
|
Urine – volume |
small |
Oliguria |
oliguria/anuria |
|
Specific gravity |
<1.020 |
>1.030 |
>1.035 |
|
Blood – BUN |
WNL |
Elevated |
very high |
|
pH (arterial) |
7.30-7.40 |
7.00-7.30 |
<7.10 |

clinical features of dehydration in an child
It may help to think of childhood dehydration in terms of borrowing from various sources. Thus mild dehydration results in thirst, oliguria and restlessness. Moderate dehydration borrows from reserves; severe dehydration results in circulatory collapse.
5% dehydration in a child
5% dehydation refers to a loss of body weight of 5%; it is mild dehydration.
Features are as follows:
skin – decreased turgor
fontanelle – may be slighly depressed
eyes – slightly sunken
pulses – normal
mental state – may be normal
5% dehydration can be treated with oral rehydration therapy.
10% dehydration in a child
10% dehydration, ie a loss of 10% of body weight as moderate dehydration, is characterised by:
skin – decreased turgor with poor capillary return – a reduced capillary filling time
fontanelle – depressed
eyes – sunken
pulses – poor volume
mental state – lethargic
oliguria may be noted
Capillary filling time
Capillary filling time is used to assess dehydration, usually in infants.
Pressure is applied for five seconds to a pink area of skin at the extremities – for example the sole of the foot. This area should be held five centimetres above the heart. When the pressure is released the time taken for blood to return to the area of skin is measured.
Ordinarily the blood should return in two seconds or less. More time than this implies underperfusion of the limb, which, provided the limb is not cold, may be attributed to peripheral shutdown secondary to hypovolaemia.
Sometimes it is possible to use pressure to the skin on the sternum if the peripheries are cool from a cold environment.
More than 10% dehydration in a child

If a child loses more than 10% body weight in severe dehydration features are as follows:
shock – falling blood pressure with tachycardia
coma
anuria
In addition the features of less dehydrated states – reduced skin turgor, lengthened capillary filling time and sunken eyes will be present.
Evaluation OF dIARRHEA.
History. Acute versus chronic. Volume, frequency, character of stools, presence of blood or mucus. Associated symptoms (vomiting, fever, malaise, etc.). Epidemiologic data (travel, day care, family history).
Exam. Estimate dehydration (see section on dehydration below). Examine for other infectious process or source. Determine if nutritional status is compromised. Neurologic symptoms, mental status changes or seizures suggest Shigella or Rotavirus.
Lab tests. Culture is indicated for acute bloody or guaiac positive diarrhea. Fecal leukocytes and RBCs are not sensitive or specific enough to be useful in the diagnosis of infectious diarrhea; there is a high degree of false negative tests. O&P for prolonged diarrhea or as indicated. Studies for chronic disease as appropriate. An ELISA test is available for Rotavirus (Rotazyme). .
Evaluation Dehydration.
Clinical observation. Clinical signs and symptoms are neither sensitive nor specific (only about 75% sensitive) and have a high index of suspicion for dehydration given the proper history.
Laboratory diagnosis. BUN/Creatinine ratio of >20 is 92% sensitive but only 33% specific for dehydration. Serum bicarbonate, urine specific gravity, etc. are all poor predictors of dehydration.
of dehydration. Because is it clinically very difficult to determine the percent dehydration, the World Health Organization has suggested categorizing patients as having “none,” “some,” or “severe,” rather than trying to predict a percentage.
In hypotonic dehydration (Na+ <130 mEq/L) all manifestations appear with less fluid deficit, whereas in hypertonic dehydration (Na+ >150 mEq/L) the circulating volume is relatively preserved, and so circulatory disturbances are seen later.
Calculation of electrolyte deficits. .
Epidemiology
Environmental factors include:
poverty and overcrowding, in the absence of clean water supply, proper sewerage disposal and appropriate personal hygiene are important internationally
malnutrition is a strong contributory factor
bottle feeding, with incorrect sterilisation
The highest risk groups are children under six months old in the developed, or infants bottle fed or between weaning and the second year in the developing world.
Pathophysiology of infective diarrhoea
Infective organisms are able to cause diarrhoea in a variety of ways:
mucosal damage caused by direct attack
toxin production after ingestion
toxin production before ingestion
The diarrhoea itself can be:
secretory, where deranged membrane transport results in decreased electrolyte absorption and thus decreased water absorption
decreased absorption, itself a result of mucosal damage, osmosis, or increased gut motility
Non-infectious diarrhoea in children
Non infectious causes of diarrhoea would tend to cause a more chronic diarrhoea. Causes include:
monosaccharide intolerance
disaccharide intolerance
cow’s milk intolerance
coeliac disease
ulcerative colitis and Crohn’s disease
cystic fibrosis
agammaglobulinaemia
acrodermatitis enteropathica – zinc deficiency
Reasons
infective diarrhoea
1. Bacterial pathogens (Escherichia coli, Campylobacter, Salmonella, Shigella)
viral pathogens
Non-infectious diarrhoea
1. Cow’s milk (monosaccharide and disaccharide intolerance) and soy protein intolerance
dietary disturbances
secondary malabsorption syndrome.
poverty and overcrowding, in the absence of clean water supply, proper sewerage disposal and appropriate personal hygiene
bottle feeding, with incorrect sterilisation
coeliac disease
ulcerative colitis and Crohn’s disease
cystic fibrosis
DEHYDRATATION
Dehydration leads to a change in the vital balance of chemical substances dissolved in the blood and tissue fluids, especially sodium (salt) and potassium. The function of many cells depends critically on these substances being maintained at the correct levels; serious effects follow any change and often lead to death. The risk is especially great in babies and infants, whose high death rate from conditions such as gastroenteritis is largely due to dehydration.
Dehydration is loss of water and important blood salts like potassium (K+) and sodium (Na+). Vital organs like the kidneys, brain, and heart can’t function without a certain minimum of water and salt.Causes of dehydration include excessive fluid losses, inadequate fluid intake, or a combination of these factors.
Causes of acute fluid loss include:
diarrhea (especially well recognized in cholera)
excessive urine output (polyuria<!–[if !supportNestedAnchors]
such as with uncontrolled diabetes
fever
Dehydration can also occur from inadequate intake as in:
refusing to drink because of mouth sores (stomatitis) or a sore throat (pharyngitis)
acute illness with loss of appetite
Dehydration in children is most often a combination of both as in:
gastroenteritis with vomiting and diarrhea
acute illness where the child refuses fluids and loses excessive fluid through sweating with fever.
Clinical signs of dehydration severity (present 2 or more from the noted signs)
|
Sign
|
Mild (1st degree)
|
Moderate (2nd degree)
|
Severe (3rd degree)
|
|
|
Loss of body weight
|
Children aged before 3 yrs |
3-5% |
6-9% |
10% and more |
|
Children aged 3-14 years |
To 3% |
3-6% |
6-9% |
|
|
General condition |
Disturbance |
Disturbance or somnolence |
Languor, somnolence |
|
|
Thirst |
Drinks voraciously |
Drinks voraciously |
Does not drink |
|
|
Anterior fontanel |
Not changed |
Slightly sunken |
Sunken |
|
|
Eyeballs |
Not changed |
Soft |
Sunken expressively |
|
|
Mucus membranes of the mouth |
Moist |
Slightly dry |
Dry |
|
|
Skin fold |
Disappears at once |
Disappears slowly
|
It can disappear slowly (> 2 sec.) or does not disappear at all |
|
|
Arterial pressure |
Norm |
Hypotonia |
Severe hypotonia |
|
|
Urination
|
|
Decreased
|
Considerably decreased to 10 ml/kg day |
|
Types of Dehydration
|
xx |
Isotonic |
Hypotonic |
Hypertonic |
|
Serum Na (mEq/L) |
130 to 150 |
<130 |
>150 |
|
Serum osmolality |
280 to 300 |
decreased |
Increased |
|
Physical Signs: |
gray |
gray |
Gray |
|
Temperature |
cold |
cold |
Cold |
|
turgor |
poor |
very poor |
Fair |
|
feel |
dry |
clammy |
thick, doughy |
|
Mucous membrane |
dry |
dry |
Parched |
|
Sunken eyes |
+ |
+ |
+ |
|
Depressed Anterior Fontanel |
+ |
+ |
+ |
|
Mental status |
Lethargic |
coma/seizure |
Irritable/seizure |
|
Increased pulse |
++ |
++ |
+ |
|
Decreased BP |
++ |
+++ |
+ |
|
Etiology |
Vomiting, diarrhea, DKA |
electrolyte in excess of water loss |
water loss in excess of electrolyte loss |
|
xx |
DEGREE of DEHYDRATION |
||
|
SIGNS and SYMPTOMS |
Mild (5%) |
Moderate (10%) |
Severe (15% or greater) |
|
Dry mucous membranes |
+/- |
+ |
+ |
|
Reduced skin turgor |
– |
+/- |
+ |
|
Depressed anterior fontanel |
– |
+ |
+ |
|
Sunken eyes; no tears |
– |
+ |
+ |
|
Hyperpnea |
– |
+/- |
+ |
|
Hypotension (orthostatic) |
– |
+/- |
+ |
|
Increased pulse |
– |
+ |
+ |
|
Laboratory Studies |
|
|
|
|
Urine – volume |
small |
oliguria |
oliguria/anuria |
|
specific gravity |
<1.020 |
>1.030 |
>1.035 |
|
Blood – BUN |
WNL |
elevated |
very high |
|
pH (arterial) |
7.30-7.40 |
7.00-7.30 |
<7.10 |
clinical features of dehydration in an child
It may help to think of childhood dehydration in terms of borrowing from various sources. Thus mild dehydration results in thirst, oliguria and restlessness. Moderate dehydration borrows from reserves; severe dehydration results in circulatory collapse.
VOLUME OF REGIDRATATION THERAPY
|
AGE |
1 STAGE-Isotonic Exicosis |
2 STAGE-Hypotonic Salt deficiency Exicosis |
3 STAGE Hypertonic Water deficiency Exicosis |
|
Till 1 year |
130-150 ml kg |
170-200 ml kg |
200-300 ml kg |
|
1-5 years |
100-125 ml kg |
130-170 ml kg |
175-200 ml kg |
|
6-10 years |
75-100 ml kg |
100-110 ml kg |
110-150 ml kg |

Medicinal intervention in diarrhoea is not often recommended, since antibiotic treatment in itself may lead to pseudomembranous colitis.
In cases of Giardia lamblia and of amoebic dysentry metronidazole is given.
In treatment of diarrhoea, the most important factor is to maintain hydration, thus oral rehydration therapy.
Perhaps an important prophylactic treatment of diarrhoea is to encourage breast feeding – maternal IgA, lactoferrin, neutrophils and macrophages all contribute to protection from diarrhoea.
Acute diarrhea with dehydration in the absence of vomiting is treated with large amounts of osmotically balanced clear liquids such as Pedialyte, Ricelyte, or the WHO rehydration formula until rehydration is complete. See dehydration and oral rehydration section.
There is abundant evidence that early reinstitution of a lactose-free general diet will decrease the duration and severity of diarrhea. Foods provided should be the same as those in the child’s normal diet with the exclusion of high-sugar foods such as apple juice, which may cause an osmotic diarrhea, and milk products with lactose. Breast-fed infants should continue to nurse without restrictions; lactose-free soybean formulas may be used in those who are bottle fed.
Avoid the use of antiperistaltic agents in infants and children.
Most episodes of diarrhea do not benefit from antimicrobial therapy. Bacterial diarrhea should be treated appropriately after culture results are available, although many would treat heme positive diarrhea presumptively once cultures have been obtained. Caution should be used in the treatment of diarrhea caused by Salmonella species because this may prolong the carrier state. However, antibiotics should be used for Salmonella in infants <3 months old, patients with symptoms of toxicity, patients with metastatic foci, or with Salmonella typhi. Avoid treating enterohemorrhagic E. coli (0157:H7) with antibiotics, since it increases the risk of hemolytic uremic syndrome (NEJM 342:2000.)
Diarrhea with vomiting is treated as for vomiting until patient is able to tolerate oral feedings.
Racecadotril (acetorphan) has been used successfully in children as young as 3 mon with watery, heme-negative diarrhea (NEJM 343:463, 2000.)
Oral rehydration. There is no role for weak tea, flat soda, Jell-O (gelatin) water, etc.
Concept of “gut rest,” that is, stopping oral intake for several hours before refeeding, has been found to have several negative effects, such as increased intestinal permeability and worsening of starvation and dehydration. Studies have shown that stool production is actually less with early refeeding.
Oral rehydration is appropriate in most cases of mild to moderate dehydration.
Currently only two fluids meet the recommendations of the World Health Organization (WHO) and the American Academy of Pediatrics for the rehydration phase of the treatment of diarrhea&endash;Rehydralyte. (Ross) and the WHO-ORS product (oral rehydration solution). These are the only two products that contain the 75 to 90 mEq/L of sodium recommended for rehydration. A simple alternative for making a rehydration solution is to mix half a teaspoon of table salt and 8 teaspoons of sugar in
Oral rehydration should be accomplished over 4 hours. The dose for mild dehydration is 50 ml/kg, or 100 ml/kg for moderate dehydration. If vomiting is occurring, the child may be given frequent small doses of the rehydration fluid and then subsequent maintenance fluids by using a teaspoon or a small oral syringe to provide a rate of approximately 5 ml/min.
For replacement of ongoing losses, it is recommended that a fluid with a lower sodium content than the rehydration fluid be used. Pedialyte (Ross) or Ricelyte (Mead Johnson) are examples of appropriate maintenance fluids. Other solutions, such as weak tea, dilute or full-strength soft drinks, Jell-O (gelatin) water, tap water, apple juice, etc., are contraindicated and may lead to hyponatremia. Alternatively, the rehydration fluid may be given along with other low-sodium fluids, such as breast milk or formula. Replacement of ongoing losses is advised at a rate of 10 ml/kg or 1/2 to 1 cup of ORS for each diarrheal stool.
Principles of Therapy for Fluid and Electrolyte Losses
First of all it is necessary to evaluate the degree of dehydration. For these perposes:
1. Look for a recent weight change, it available.
2. Gauge clinical appearance.
For most patients, while you’re waiting for lab results, it is appropriate to begin fluid resuscitation with 0.33% NaCl, 0.45% NaCl, or even 0.9% NaCl solution at a 1.5 x maintenance rate. When laboratory information is available, calculations for volume and electrolytes losses can take into account what has already been given to the child.
Important point: If a child is in shock, give volume (crystalloid: 0.9% NaCl or Ringer’s Lactate as a bolus of 20 mL/kg) irrespective of the serum sodium level.
|
xx |
DEGREE of DEHYDRATION |
||
|
SIGNS and SYMPTOMS |
Mild (5%) |
Moderate (10%) |
Severe (15% or greater) |
|
Dry mucous membranes |
+/- |
+ |
+ |
|
Reduced skin turgor |
– |
+/- |
+ |
|
Depressed anterior fontanel |
– |
+ |
+ |
|
Sunken eyes; no tears |
– |
+ |
+ |
|
Hyperpnea |
– |
+/- |
+ |
|
Hypotension (orthostatic) |
– |
+/- |
+ |
|
Increased pulse |
– |
+ |
+ |
|
Laboratory Studies |
|
|
|
|
Urine – volume |
small |
oliguria |
oliguria/anuria |
|
specific gravity |
<1.020 |
>1.030 |
>1.035 |
|
Blood – BUN |
WNL |
elevated |
very high |
|
pH (arterial) |
7.30-7.40 |
7.00-7.30 |
<7.10 |
Management of mild dehydration
Oral hydration is usually adequate in the child that is less than 5 percent dehydrated if the patient can tolerate oral intake.
If oral fluids are not retained, parenteral fluids should be given. Many children can tolerate fluids after an initial IV bolus of 10-20 mL/kg of normal saline. However, if the child continues to vomit, then consider fluid resuscitation as outlined below.
Patients require careful monitoring of intake, output and weight (or change in weight). If initial labs are normal and if the child continues to improve, then additional lab studies may not be necessary.
Orally, use clear fluids (i.e., Pedialyte, Lytren, Resol). In a child whose emesis is abating or who is being managed as an outpatient, drinking an ounce an hour of a rehydration fluid will often prevent significant dehydration. Do not use tea or boiled milk. Fruit juices may worsen the diarrhea secondary to their hyperosmolarity.
Once ongoing losses have ceased, diet may be advanced. Recommend do not prescribe the BRAT (bread, rice, applesauce, and toast) diet. See the section on pediatric diarrhea for a discussion on this subject.
Examples
Isotonic Dehydration: Normal serum sodium. Calculations of deficit and maintenance requirements require three variables: wet weight; water deficit; and sodium deficit
Some practitioners use a simpler method, skipping the calculation of wet weight and calculating the deficit based on the dry weight. In this example then, the deficit, using the simpler method would be 1000 mL (10 percent of
After calculating the fluid deficit, next calculate the Na+ deficit. In isotonic dehydration, the patient has lost water and sodium in such a way that the serum sodium remains normal. However, some sodium has been lost and must be replaced. A simple approach is demonstrated in the following table:
|
Percent dehydration |
5 percent |
10 percent |
15 percent |
|
Na+ deficit in mEq/kg |
4 |
8 |
12 |
<!–[if !vml]–><!–[endif]–>
Since this patient is 10 percent dehydrated, the Na+ deficit is 8 mEq per kg of wet weight or 8 x 11.1 or 89 mEq.
Thus the three required variables for calculating fluid resuscitation in this patient are:
Wet weight
Water deficit 1100 mL
Sodium deficit 89 mEq
There are two phases to the resuscitation; (1) an initial phase, lasting 8 hours, in which 50 percent of the deficit is replaced and standard maintenance fluid and electrolytes are provided. The second phase lasts 16 hours (total 24 hours), and the remaining deficit as well as maintenance fluid and electrolytes are given. For ease of calculation, assume that you are almost always going to use a glucose-containing solution (D5W) with added electrolytes (exception: DKA). This allows you to skip calculations for glucose. Further assume that you are going to provide K+ at 2 mEq per 100 mL (20 mEq/L) in most cases. This allows you to skip calculations for potassium. Many practitioners choose to add the potassium only after the patient’s first void.
First phase:
Maintenance for 8 hours plus replacement of half of the deficits.
|
xx |
Maintenance for 8 hrs |
Repair of 1/2 deficit |
Total |
|
Water |
350 mL (1050 x 1/3) |
550 (1100 x 1/2) |
900 mL |
|
Sodium |
11 mEq (33 x 1/3) |
44 mEq (89 x 1/2) |
55 mEq |
Thus, in the first 8 hours of resuscitation, this patient needs a total of 900 mL of water and 55 mEq of sodium. To convert this into a liter-based equivalent, divide both the volume and the sodium by 0.9, yielding a sodium concentration of ~ 60mEq/L. There is no standard off-the-shelf solution with this concentration, but note that a 0.33% NaCl solution has 57 mEq of sodium per liter – close enough so that you don’t have to break the seal on the sterile IV solution and add sodium. Your rate of administration will be 900 mL/ 8 hrs or 112 mL/ hr. Your order for this first phase would then read:
IV with D5 + 0.33% NaCl at 112 mL / hr for 8 hrs. Add KCl 20 mEq / L after first void.
Second phase:
Maintenance solutions for 16 hours plus replacement of the remaining deficit.
|
xx |
Maintenance for 8 hrs |
Repair of 1/2 deficit |
Total |
|
Water |
700 mL (1050 x 2/3) |
550 (1100 x 1/2) |
1250 mL |
|
Sodium |
22 mEq (33 x 2/3) |
44 mEq (89 x 1/2) |
66 mEq |
Thus, in the second phase of resuscitation, this patient needs a total of 1250 mL of water and 66 mEq of sodium. To convert this into a liter-based equivalent, divide both the volume and the sodium by 1.25, yielding a sodium concentration of ~ 50 mEq/L. There is no standard off-the-shelf solution with this concentration, but note that a 0.33% NaCl solution has 57 mEq of sodium per liter again, close enough, and you don’t have to prepare a special solution. Your rate of administration will be 1250/ 16 hrs or 78 mL/hr. Your order for this second phase would then read:
After 8 hours, decrease IV rate to 78 mL / hr.
Writing these orders is not enough. Reassess the patient periodically based on clinical appearance and urine output.
Hypotonic Dehydration (Na <125 mEq/L).
Symptomatic earlier than in isotonic or hypertonic dehydration. Therefore use weight loss of 3% = mild, 6% = moderate, and 9% = severe dehydration as a guide.
Hypotonic dehydration usually results from replacing losses (vomit- ing and diarrhea) with low-solute fluids, such as dilute juice, cola, weak tea.
Lethargy and irritability are common, and vascular collapse can occur early.
Therapy. Calculate total fluid and electrolyte needs according to the maintenance and deficit replacement formulas in section C.
Do not try to raise serum Na more than 10 mEq/L (that is, if the current serum sodium is 125, use 135 as the desired serum Na level in the calculation) in first 24 hours.
To calculate the milliequivalents of Na needed in each liter during the first 24 hours of therapy: mEq of Na per liter of IV fluid 5 total sodium needed in the first 24 hours divided by total volume of fluid needed. (Normal saline 5 154 mEq of Na/liter).
Usually D5 1/2 NS or D5 NS is used. Potassium can be added after urine output is established. Give half of the calculated total fluid and electrolyte requirements for the first 24 hours over the first 8 hours and the other half over the subsequent 16 hours.
When the serum sodium is low in a dehydrated patient, the patient has lost more sodium than water. In addition to the predicted sodium loss based on the percent dehydration, there have been additional losses, calculated as:
Additional sodium deficit = Wet weight in kg x 0.6 x 135 – measured sodium
Given a
Wet weight
Water deficit 1100 mL
Sodium deficit 89 mEq + (11.1) (0.6) (135-120) = 89 + 99 = 188 mEq
In treating a patient with hypotonic dehydration, most practitioners will use a 24-hour treatment period rather than a 2-phase approach. Calculations would be as follows:
|
xx |
Maintenance |
Repair |
Total |
|
Water |
1050 mL |
1100 mL |
2150 mL |
|
Sodium |
33 mEq |
188 mEq |
221 mEq |
Thus, in this example, the patient needs a total of 2150 mL of water and 221 mEq of sodium over a 24-hour period. To convert this into a liter-based equivalent, divide both the volume and the sodium by 2.15, yielding a sodium concentration of ~ 103 mEq /L. There is no standard off-the-shelf solution with this concentration, but note that a 0.45% NaCI solution has 77 mEq of sodium per liter – not quite close enough, so you’ll have to prepare a special solution. Add 26 mEq of NaCl to each liter of fluid, and you have a sodium concentration of 103 mEq/ L. Your rate of administration will be 2150 mL/ 24 hrs or 90 mL/ hr. Your order for this patient would then read:
IV D5 + 0.45% NaCI at 90 mL/hr. Add NaCl 26 mEq / L Add KCl 20 mEq/ L after first void.
Again, simply writing these orders is not enough. Reassess the patient periodically based on clinical appearance and urine output.
Warning: Correcting hyponatremia too quickly, especially in adults, can result in central pontine myelinolysis leading to virtual destruction of the central pons. Go slow with sodium replacement. The only exception would be in the patient who is having seizures related to the hypernatremia.
Hypertonic Dehydration:
Elevated serum sodium
Water loss in excess of sodium loss
This type of dehydration requires skill and experience in management. Discussion is beyond the scope of this manual. If you encounter this type of dehydration in a pediatric patient, in the absence of shock (requiring a fluid bolus), start an IV with D5 + 0.2 % NaCl at a 1.5 x maintenance rate and refer or transport.
ORAL REGIDRATATION THERAPY
Oral rehydration therapy was developed in the 1950s for developing countries, where diarrhea is common. Ukrainian children average only one or two bouts with diarrhea yearly. But those illnesses can still be dangerous. The best way for parents to keep their children from getting dehydrated is by stocking the medicine chest with at least one bottle of oral rehydration fluid.
“I think it’s very reasonable for every family to have it at home,” says John Snyder, M.D., a researcher in the field of ORT and professor of pediatrics at the University of California Medical School in San Francisco. “Diarrhea frequently starts at night, and a small child can get dehydrated very quickly.”
Yet many physicians do not recommend ORT for children suffering from diarrhea. According to a 1991 study published in the medical journal, Pediatrics, most pediatricians don’t follow the guidelines for treating diarrhea set by the American Academy of Pediatrics in 1985.
More commonly, doctors frequently tell parents to withhold food from a child and give clear liquids such as fruit juice, chicken broth, and sports drinks. Neither of these practices is recommended by the academy.
Common clear liquids don’t contain the proper balance of sodium, chloride and potassium salts that the body needs. These and other minerals change in the body into electrically charged particles called ions. If electrolytes are not perfectly balanced in the body, many organs, including the heart, cannot function properly. Children under 5 are especially vulnerable to diarrhea because their bodies are small. It doesn’t take much fluid loss to get their electrolytes out of balance.
Only a physician can diagnose dehydration, but parents can watch for some obvious signs: a dry mouth, no tears, sunken eyes, a reduction in urination, and skin that stays compressed when pinched.
The AAP guidelines are:
<!–[if !supportLists]–>· <!–[endif]–>For diarrhea with no dehydration, feed the child normally and give supplemental commercial rehydration fluids within four to six hours after a diarrheal episode. If the diarrhea persists, call the child’s doctor.
<!–[if !supportLists]–>· <!–[endif]–>For diarrhea with mild dehydration, take the child to a physician. The child should be given oral rehydration fluids in the doctor’s office, with food and rehydration fluid continued at home.
<!–[if !supportLists]–>· <!–[endif]–>For moderate or severe dehydration, the child should be treated in a health-care facility. Moderate dehydration may be treated orally, but severe dehydration requires intravenous fluids.
The old advice to let the intestine “rest” after a bout with diarrhea is now not recommended by AAP.
“Early feeding isn’t just a good idea, it helps to make the diarrhea better,” says Snyder.
Food can help the intestine absorb more water, which helps slow down the diarrhea. A child should eat as soon as possible after a bout of diarrhea, and at least within six hours. A balanced diet rich in calories is recommended. Foods such as rice, wheat, potatoes, sorghum, corn, and chicken have all been proven helpful in slowing diarrhea. Just about anything the child tolerates is OK, except for foods high in sugar or salt.
Milk products, because they can be difficult to digest, can be withheld for 24 to 48 hours during significant bouts of diarrhea. Infants who are bottle-fed, however, should continue drinking formula diluted to half strength. Breast-fed infants should continue nursing.
The once favored “BRAT” diet–an acronym for bananas, rice, applesauce, and toast–is no longer recommended for children. Instead, parents should offer a more balanced diet that is higher in calories.
Giving anti-diarrhea medicine to children is not the best treatment, according to John Udall, M.D., Ph.D., chairman of pediatric nutrition and gastroenterology at the Children’s Hospital in New Orleans.
“Diarrhea is really a purging of the intestine,” he says. “Giving medicines to slow down the intestine actually gives the bacteria more time to grow, which prolongs the illness.”
Allowing the illness to run its course, while preventing dehydration with fluids, is usually the quickest way toward health.
Dosage information for ORT depends on weight and is listed on the label. Side effects with ORT are rare, but parents should watch for signs of too much sodium in the body: dizziness, a fast heartbeat, irritability, muscle twitching, restlessness, swelling of the feet or lower legs, weakness, and convulsions.
Rehydration fluids have a brief shelf life. Once a bottle has been opened or a mix prepared, it must be used or thrown out within 24 hours because bacteria rapidly grow in the solution. A child could easily drink three or four bottles of the fluid during an illness.
ORT is effective to a lesser degree when the child is vomiting. If the child can keep the liquid down, it will be absorbed. But if the child vomits it back up, intravenous rehydration may be necessary.
ORT is effective for all ages, although the brands available at most grocery stores and drugstores are usually formulated just for children. Adults are usually able to tolerate a bout with diarrhea better than small children because they have more fluid reserves in their bodies. But older adults and those weakened by diseases like cancer and AIDS are at a greater risk for complications from diarrhea. These patients should call their doctors if diarrhea and vomiting persist.
Parents should also remember that ORT will not stop the diarrheal illness. In fact, the child may have even more episodes of vomiting and diarrhea until the illness runs its course. As long as the child is keeping some rehydration fluid down, however, the chances of dehydration are greatly reduced.
If a child under 5 has diarrhea and vomiting for longer than an hour or so, it’s always a good idea to call a physician.
According to Snyder, “Parents should have a low threshold of concern to [prompt them to] phone the pediatrician.”
Parents don’t have to wait for a prescription to use oral rehydration fluids, however. The products are available at grocery stores and drugstores in premixed bottles. National brands can cost as much as $6 per liter, but less expensive generic brands are available as well for as little as $2.
According to a 1991 study in the Journal of the American Medical Association, cost is one reason why more parents do not use ORT for their children suffering from diarrhea. Deaths from diarrhea are most common in the South and in low-income, African-American families headed by young single mothers.
To help with that expense, the federally funded and state-administered WIC (Women, Infants and Children) Program pays for ORT along with certain foods for pregnant women, new mothers, and children under
As the use of ORT increases, the number of deaths from diarrhea is slowly declining in the United States. This simple solution of water, minerals and carbohydrates will not eliminate the problem of stomach viruses and flu, but perhaps it will make diarrhea less of a life-threatening risk to America’s children.
What is the mechanism of action of ORT?
Oral rehydration takes advantage of the glucose-coupled sodium transport system. This is a process for sodium absorption which remains intact in infective diarrheas due to viruses or enteropathogenic bacteria. It has been shown that glucose enhances sodium and secondarily water transport across the mucosa of the upper intestine. The amount of fluid absorbed depends on three factors which makes the composition of rehydration solutions critical. Maximal water uptake occurs with a sodium concentration from 40 to 90 mmol/L, a glucose concentration from 110 to 140 mmol/L and in a solution with an osmolality of about 290 mOsm/L.
What are the consequences of altering the composition of the rehydration fluid?
Increasing the sodium beyond 90 mmol/L may result in hypernatremia (chicken broth may contain 250 mmol/L of sodium and is contraindicated as a rehydration fluid). Increasing the glucose concentration beyond 200 mOsm/L will increase the osmolality of the solution and may result in a net loss of water. For these reasons the following clear liquids are not appropriate for oral rehydration therapy:
Cola has approximately 700 mmol/L of fructose and glucose and has an osmolality of 750mOsm/L.
Undiluted apple juice has approximately 690 mmol/L of fructose, glucose and sucrose and has an osmolality of 730mOsm/L
Sports beverages have approximately 255 mmol/L of sucrose and glucose with an osmolality of 330mOsm/L.
Another reason why fruit juices and pop are not efficacious in the treatment of diarrhea is because their sodium content is too low (cola 2 mmol/L, apple juice 3 mmol/L, sports beverages 20 mmol/L) For optimal therapy the carbohydrates: sodium ratio should not exceed 2:1 in the rehydraton solution.
How should children be managed who have diarrhea but are not dehydrated?
These children should continue to be fed age appropriate diets. Several studies have now demonstrated that unrestricted diets do not worsen the course or symptoms of mild diarrhea. In fact a recent meta-analysis was performed to evaluate the use of lactose-containing feedings in children with diarrhea and concluded that 80% or more of children with acute diarrhea can tolerate full strength milk safely. Although reduction in intestinal brush border lactase levels is often associated with diarrhea, most infants with decreased lactase levels will not have clinical signs or symptoms of malabsorption. Infants fed breast milk can be nursed safely during episodes of diarrhea. In the past, the American Academy of Pediatrics recommended gradual re-introduction of milk-based formulas or cow’s milk in the management of acute diarrhea beginning with diluted mixtures; this recommendation has been re-evaluated in the light of these recent data.
Which foods are best for re-feeding children with gastroenteritis?
The classic BRAT diet which consist of bananas, rice, apple sauce and toast is well tolerated in infants with diarrhea but it is now considered that this diet is limited iutritional quality because of low energy density, protein and fat. Current recommendations include age appropriate foods including complex carbohydrates (rice, potatoes, bread and cereals), lean meats, yogurt, fruits and vegetables. Foods to be avoided include fatty foods or foods high in simple sugars (juices and soft drinks).
What clinical criteria does the clinician use to evaluate the degree of dehydration?
The only objective measure of dehydration is the degree of the child’s weight loss. If a recent accurate weight is available this is the most useful measure to calculate the percentage of weight loss and dehydration. All children with diarrhea must be weighed at the time of their initial presentation to a physician since this weight can be used for comparison over the next few days if the diarrhea is not mild and self limiting. Delayed capillary refill-time (although affected by temperature and age) should be considered a sign of significant dehydration. Urinary output and specific gravity are also helpful measures to confirm the degree of dehydration.
Should serum electrolytes be measured in patients with diarrhea?
Since most episodes of dehydration caused by diarrhea are isonatremic, serum electrolyte measurements are considered unnecessary. However electrolytes should be measured in all children with severe dehydration and in those with moderate dehydration where the physical findings are inconsistent with the history obtained. Children with hypernatremic dehydration are often inappropriately assessed because of it’s unusual clinical presentation; these children do not appear to be as unwell and as dehydrated as the history suggests, irritability and fever may be present, a doughy feel to the skin is a distinctive feature and the typical skin tenting usually associated with the more common isotonic dehydration may not be present. Hypernatremic dehydration can result from the ingestion of hypertonic liquids such as boiled milk and home made solutions to which salt has been added.
How should the vomiting child be managed?
Vomiting may be an early symptom of gastroenteritis and sometimes may be the only manifestation (gastritis). The combination of vomiting and diarrhea at the same time is potentially the most serious symptoms in a child with gastroenteritis because of the combined upper and lower intestinal fluid loss. Most children with vomiting and dehydration can in fact be treated with ORT. The mainstay of therapy in the vomiting child is to administer small amounts of fluid frequently. Therapy should be initiated with 5ml aliquots given every 1 to 2 minutes. Although this technique is labor intensive it can be done by a parent and will deliver 150 to 300 ml/hour. As the vomiting lessens, larger amounts of ORT can be given after longer intervals. Once rehydration is accomplished, other fluids including milk and age appropriate foods can be introduced. If the vomiting continues despite efforts to administer ORT intravenous hydration is indicated.
What should parents do if the child refuses to take an oral rehydration fluid solution?
It appears that children who are dehydrated rarely refuse ORT; however those who are not dehydrated may refuse the solution because of its salty taste. Consequently, children with mild diarrhea and no dehydration should be fed a regular diet and do not require ORT solutions. There are some practical techniques that can be used to induce the reluctant child to drink glucose electrolyte solutions by offering small amounts at first; this may allow the child to get accustomed to the taste. Some commercial preparations are flavored, without altering the basic composition of the fluid, and this may be more palatable for some children. Frozen ORT solutions may be given to children in the form of a Popsicle.
How much oral rehydration therapy should be given?
In children who are not dehydrated an ORT solution may not be required. These children can be continued on age appropriate feeding with an increase in their normal fluid consumption. These children are the least likely to ingest ORT. It is estimated that they should receive approximately 10 ml/kg for each stool passed. In children with mild dehydration (3-5%) 50 ml/kg of ORT should be given over a period of 4 hours. The replacement of continuing losses from stool and vomiting requires an additional 10 ml/kg for each stool passed and an estimate for the amount of vomiting. For moderate dehydration (6-9%) 100 ml/kg of ORT replacement should be administered as well as continuing losses over a 4 hour period. Children with moderate dehydration should be monitored in a supervised setting such as an emergency room, or a physician’s office which has the capability of observing the child. Severe dehydration (>10%) is a medical emergency and should be treated with immediate intravenous therapy.
Is there any indication to treat children who have diarrhea with anti-diarrheal compounds?
There are four classes of anti-diarrheal pharmacological agents, and as a general rule none should be used to treat acute diarrhea in children. These medications include the following, and are effective by altering:
Intestinal motility, e.g. Loperamide (Imodium)
Secretions e.g. Bismuth subsalicyclate (Pepto-Bismol)
Adsorption of toxins and water e.g. Donnagel or Kaopectate
Intestinal microflora e.g. lactobacillus.
Antiemetic drugs are not indicated for the management of vomiting in children with gastroenteritis.
|
PEARLS |
|
Acute gastroenteritis in children is common and has a high morbidity |
|
The use of oral rehydration solutions (ORT) have advantages over conventional therapy |
|
ORT solutions should be encouraged for rehydration purposes over fruit juices and pop which are not efficacious because of their high carbohydrate concentration, high osmolality and inadequate sodium concentration. |
|
Early re-feeding of age-appropriate foods should be encouraged. |
|
Pharmacological agents should not be used to treat acute diarrhea in children |
Intravenous rehydration.
Correction of free-water deficit in hypernatremic dehydration. Free-water deficit = 4 ml/kg for every mEq that the serum Na exceeds 145 mEq/L.
Maintenance requirements for fluids and electrolytes.
Fluid maintenance.
Weight <10 kg: 100 ml/kg/day
Weight 11 to 20 kg: 1000 ml + 50 ml/kg/day for every kg over
Weight >20 kg: 1500 ml + 20 ml/kg/day for every kg over
Adult: 2000 to 2400 ml/day
Total body water. 60% of body weight.
Maintenance electrolyte requirements.
Na+: 3 mEq/kg/day, or 3 mEq/100 ml of H2O
K+: 2 mEq/kg/day or 2 mEq/100 ml of H2O (adult: 50 mEq/day)
Cl–: 3 mEq/100 ml of H2O
Glucose: 5 g/100 ml of H2O
Replacement of ongoing losses.
NG losses usually replaced with D5 1/2NS with 20 mEq/L of KCl.
Diarrhea usually replaced with D5 1/4NS with 40 mEq/L of KCl.
General principles in treating dehydration (Algorithm)
Weigh the child.
Be sure to add ongoing losses to maintenance + deficit fluids and electrolytes.
If moderately or severely dehydrated, give an initial fluid bolus of 20 ml/kg LR or NS over 20 minutes. Repeat bolus if response is inadequate. If poor response after three fluid boluses, that is, poor perfusion, no urine output, abnormal vital signs, may need CVP or PCWP to guide fluid resuscitation.
In hypotonic or isotonic dehydration, calculate the total fluids and electrolytes (maintenance + deficit replacement) for the first 24 hours, give half over the first 8 hours and the other half over the next 16 hours. In hypertonic dehydration, correct the fluid and electrolyte deficits slowly over about 48 hours.
Do not add potassium to IV until urine output is established. Diabetic ketoacidosis may be an exception, where correction of hyperglycemia and acidosis may lead to rapid development of hypokalemia.
Increase maintenance fluids by 12% for each Celsius degree of fever.
A. Hypotonic Dehydration (Na <125 mEq/L).
1. Symptomatic earlier than in isotonic or hypertonic dehydration. Therefore use weight loss of 3% = mild, 6% = moderate, and 9% = severe dehydration as a guide.
2. Hypotonic dehydration usually results from replacing losses (vomit- ing and diarrhea) with low-solute fluids, such as dilute juice, cola, weak tea.
3. Lethargy and irritability are common, and vascular collapse can occur early.
Therapy.
1. Calculate total fluid and electrolyte needs according to the maintenance and deficit replacement formulas in section C.
2. Do not try to raise serum Na more than 10 mEq/L (that is, if the current serum sodium is 125, use 135 as the desired serum Na level in the calculation) in first 24 hours.
3. To calculate the milliequivalents of Na needed in each liter during the first 24 hours of therapy: mEq of Na per liter of IV fluid 5 total sodium needed in the first 24 hours divided by total volume of fluid needed. (Normal saline 5 154 mEq of Na/liter).
4. Usually D5 1/2 NS or D5 NS is used. Potassium can be added after urine output is established. Give half of the calculated total fluid and electrolyte requirements for the first 24 hours over the first 8 hours and the other half over the subsequent 16 hours.
Symptoms are less dramatic than in hypotonic dehydration.
Use estimate (loss of weight) 5% = mild, 10% = moderate, 15% = severe dehydration.
Calculate total maintenance + deficit replacement fluids and electrolytes for first 24 hours.
Treatment is similar to treatment for hypotonic dehydration: give half of first 24 hours needs in first 8 hours, and give the remaining half over the next 16 hours.
Usually can use D5 1/4 NS or D5 1/2 NS; may add potassium after urine output established.
Remember to estimate and replace ongoing losses.
Usually occurs as a result of using inappropriately high solute load as replacement, renal concentrating defect with large free-water losses, heat exposure with large insensible losses, etc.
Typical symptoms include thick, doughy texture to skin (tenting is uncommon), shrill cry, weakness, tachypnea, intense thirst.
Shock is a very late manifestation. If severe dehydration or shock is present, the patient may need an initial fluid bolus of 20 ml/kg NS over the first 20 to 30 minutes.
Free-water deficit (ml) is estimated to be 4 ml/kg x (Actual serum Na (mEq/L) – 145 mEq/L).
Replace the free-water deficit slowly over 48 hours. Aim to decrease the serum sodium by about 10 mEq/L/day. Reducing serum sodium more rapidly can have severe repercussions, such as cerebral and pulmonary edema.
Usual replacement fluid is D5 1/4 NS or D5 1/2 NS.
If Na >180, may need dialysis.
Theme 3: Protein-vitamin insufficiency in children. Malnutrition. Clinical features, diagnostics, treatment and prophylaxis.
Malnutrition is absence of adequate caloric and volume feeding of the child There are numerous causes of malnutrition including recurrent bacterial diarrhea, often upper respiratory tract infections, congenital gastrointestinal diseases, diseases of the mother during pregnansy. This state is associated with anergy, infectious complications, high mortality.
Etiology: inadequate feeding, low level of ferments of gastrointestinal tract. Organic factors include congenital heart defects, neurologic lesions, microcephaly, chronic urinary tract infection, gastroesophageal reflux, renal insufficiency, endocrine dysfunction, cystic fibrosis. Malnutrition can also be caused by psychosocial factors, the problem being between the child and primary caregiver, usually the mother. In this situation the lack of physical growth and development is secondary to the lack of emotional and sensory stimulation.
Pathogenesis: 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 primary defect such as celiac disease or gluten enteropathy or secondary to inflammatory disease of the bowel, that results in impaired absorption because bowel motility is accelerated. Anatomic defects such as short bowel syndrome, affect digestion by decreasing the transit time of substances with the digestive juices and affect absorption by compromising the absorptive surface. All this causes leads to maldigestion and malabsorption syndrome, damage of function of all organs and systems of the organism.

Main clinical symptoms are: abdomen pain, regurgitation, periodic vomiting, bad appetite, frequent liquid stool, decreasing or absense of subcutaneous fat. Becides the obvious signs of malnutrition and delayed development, the child seems to have a characteristic posture of “body language”. The child may be unpliable, stiff and rigid. He is uncomforted by unyielding to cuddling and is very slow in smiling or social responding to others. The other extreme is the floppy infant, who is like the rag doll.
–>Frequently there is a history of difficult feeding, vomiting, sleep disturbances, excessive irritability. Difficulties of infant feeding may include poor appetite, poor suck, crying during feeding, vomiting, hoarding food in the mouth, ruminating after feeding, refuse of liquids and solids, aversion behavior such as turning from food or spitting food. In addition, chronic reduction in caloric intake can lead to appetite depression, which compounds the problem. Another outstanding feature of children with malnutrition is their irregularity in activities of daily living. Some of these children called as “difficult child pattern”. However, another type is the passive, sleepy, lethargic child who does not awake up for feeding.
Other clinical symptoms range from moderate growth failure ( a common occurance in underdeveloped countries ) to more severe conditions such as marasmus and kwashiorcor. The former results from an anadequate intake of a suitable diet; the latter resulrs from a diet with a low protein, energy ratio, frequently with protein of poor biologic quality. The three stages of protein-energy malnutrition are marasmus, marasmic-kwashiorcor and kwashiorcor.They are compounded by a whole spectrum of nutritional disorders that include deficiences of one or more vitamins, minerals and trace minerals. The three stages of protein-energy malnutrition can be differenciated most clearly on the basis of clinical findings. Intermediate forms known as marasmic-kwashiorcor also are seen. Growth retardation, weight loss, psychic changers, muscular atrophy, pellagroid dermatitis, hair changes, edema, gastrointestinal changers and other abnormalities are present in various combinations. Marasmus which predominate in infancy, is characterised by severe weight reduction , gross wasting of muscle and subcutaneous tissue, no detectable edema and marked stunting. Marasmus results from inadequate energy intake, impaired absorption of protein, energy, vitamins and minerals. The hair and skin changes and hepatomegaly resulting from fatty infiltration of the liver. The marasmic child, characteristically irritable and apathetic, is the skin and bones portrait of the skeleton.
Kwashiorcor results from either inadequate protein intake , or, more commonly, from acute or chronic infection. It appears predominantly in older infants and younger children. Clinically it is characterised by edema, skin lesions, hair changers, apathy, anorexia, a large fatty liver, and decreased a serum albumine. Weight loos is also usual, without a decrease of energy intake. The edema of kwashiorcor can only partially be explained by the low serum albumine, other contributing factors include increased capillary permeability, increase cortisol, and antidiuretic hormones lewel.

Marasmic – Kwashiorcor presents with the clinical findings of both marasmus and kwashiorcor. The child has edema, gross wasting and usually stunted. There may also be mild hair and skin changers and a palpable fatty-infiltrated liver. The child with marasmus-kwashiorcor is one who demonstrated the combined defects of an inadequate intake of nutrients to meet requirements plus superimposed infection.
3. General examination of the patient: patients have asthenic constitution, reduced degree of nourishment, weight loss, the abdomen is great, distended, meteorism, the skin and mucus membranes are dry, turgor of skin is decreased, muscular hypotonia, abdomen is asymmetrical, CNS dysfunktion (retardation of the development).
CLASSIFICATION OF MALNUTRITION
|
Origin |
Stage |
Period |
Prenatal malnutrition forms |
|
Alimentary factors Infection factors Regime breaking, care and upbringing defects Prenatal factors Hereditary pathology and congenital development defects
|
I ( mild) II (moderate) III ( severe) |
Initial Progressive Stabilization Reconvalecsention (recovery)
|
Neuropathic Neurodystrophic Encephalopathic Neuroendocrinilogical
|
MALNUTRITIONAL STAGES
|
STAGES |
WEIGHT DEFICITE |
LENTH DEFICITE |
CHULITSKA NUTRITIONAL INDEX |
|
І |
10-20% |
– |
10 – 15 |
|
ІІ |
20-30% |
2-4 sm |
0 – 10 |
|
ІІІ |
More than 30% |
7-10 sm |
negative |
Interpretation
|
|
Weight for Height (wasting) |
Height for Age (stunting) |
|
Normal |
> 90 |
> 95 |
|
Mild |
80 – 90 |
90 – 95 |
|
Moderate |
70 – 80 |
85 – 90 |
|
Severe |
< 70 |
< 85 |
CHULITSKA NUTRITIONAL INDEX (characterizes a degree of the child fattenies:
3 contours of a shoulder (sm.) + contour of thigh (sm.) + contour of shin (sm.) – growth (sm.);
Norm: by one year – 20-25 sm.; smaller 20 sm. – gipotrophija; greater 25 sm. – paratrophija.
Weight of a body: 1. I month – plus 600gr.
II month – plus 800 gr.
III month – plus 800 gr., for each next month on 50 gr.less, than for previous.
Growth: for І sq. – + 3 sm. monthly (for one quarter 9 sm.);
For ІІ sq. + 2,5 sm. monthly (for one quarter 7,5 sm.);
For ІІІ sq.+1,5 sm.monthly (for one quarter 4,5 sm.);
For IU sq. +1,0 sm monthly (for one quarter 3 sm).
A Scoring System for Classifying Severe Protein-Calorie Malnutrition in Young Children
|
Parameter |
Finding |
Points |
|
Edema and dermatitis |
edema plus dermatitis |
6 |
|
|
edema without dermatitis |
3 |
|
|
dermatitis without edema |
2 |
|
|
both absent |
0 |
|
Hair changes |
present |
1 |
|
|
absent |
0 |
|
Hepatosplenomegaly |
present |
1 |
|
|
absent |
0 |
|
Serum albumin or total serum protein |
< 1 g/dL albumin < 3.25 g/dL total protein |
7 |
|
|
1.00 – 1.49g/dL albumin 3.25 – 3.99 g/dL total protein |
6 |
|
|
1.50 – 1.99 g/dL albumin 4 – 4.74 g/dL total protein |
5 |
|
|
2.00 – 2.49 g/dL albumin 4.75 – 5.49 g/dL total protein |
4 |
|
|
2.50 – 2.99 g/dL albumin 5.5 – 6.24 g/dL total protein |
3 |
|
|
3.00 – 3.49 g/dL albumin 6.25 – 6.99 g/dL total protein |
2 |
|
|
3.50 – 3.00g/dL albumin 7 – 7.74 g/dL total protein |
1 |
|
|
> 4.0 g/dL albumin > 7.75 g/dL total protein |
0 |
nutrition score =
= SUM(points for the 4 parameters)
Interpretation
∙ minimum score: 0
∙ maximum score: 15
|
Score |
Type of Malnutrition |
|
||
|
0 – 3 |
Marasmic |
|
||
|
4 – 8 |
Marasmic kwashiorkor |
|
||
|
9 – 15 |
Kwashiorkor |
|
||
|
|
|
|
||
|
Parameter |
Finding |
Points |
||
|
Weight for height |
< 3rd percentile |
2 |
||
|
|
3rd to 10th percentile |
1 |
||
|
|
> 10th percentile |
0 |
||
|
Triceps skinfold thickness |
< |
2 |
||
|
|
5.6 √ |
1 |
||
|
|
> |
0 |
||
|
Serum albumin or prealbumin |
serum albumin < 3.0 g/dL or prealbumin < 8 mg/dL |
2 |
||
|
|
serum albumin 3.0 √ 3.5 g/dL or prealbumin 8-20 mg/dL |
1 |
||
|
|
serum albumin > 3.5 g/dL or prealbumin > 20 mg/dL |
0 |
||
|
Transferrin |
< 150 mg/dL |
2 |
||
|
|
150 √ 200 mg/dL |
1 |
||
|
|
> 200 mg/dL |
0 |
||
|
Serum alkaline phosphatase |
< 100 IU/L |
2 |
||
|
|
100 √ 600 IU/L |
1 |
||
|
|
> 600 IU/L |
0 |
||
|
Serum ferritin |
< 20 ng/mL (see note) |
1 |
||
|
|
>= 20 ng/mL (see note) |
0<!–[if !supportMisalignedColumns]–> |
||
|
|
|
|
|
<!–[endif]–> |
|
SENR |
Interpretation |
|
0 |
no malnutrition |
|
1 |
low risk for malnutrition |
|
2 or 3 |
high risk for malnutrition |
|
>= 4 |
child is malnourished |
Сlinical symptoms of malnutrition I stage – 10-20% weight loss.
The general condition of the patient is satisfactory; Psychomotorical development is adequate to age; coefficient weight / length is about 55-60;proportion index changes; the index degree of nourishment of Chulitskaya reduces to 10-15; skin elastisity and turgor moderately reduced also.Subcutaneous fat on abdomen 0.8-1 sm.

Сlinical symptoms of malnutrition II stage – 20-30% weight loss.
State of moderate severity; pallorness, dryiness of the skin; psychomotorical development is reduced; muskle hypotonia, Decreasing of appetite, vomiting; coefficient weight / length low than 56; proportion index changes; the index degree of nourishment of Chulitskaya reduces to 0-10; polyhypovitaminosis, anemia, hypo and dysproteinemia; signs of rickets; frequent intercurrent infections with poor symptoms. Decreases immunologic reactivity.

Сlinical symptoms of malnutrition III stage – more than 30% weight loss.
General state of the patient is grave, severe emaciation, cachexia, subcutaneous fat is absent, menthal retardation, somnolents, athrophy of the muscles, temperature of the body is low, regurgitation, vomiting, frequent stools, weight loss more than 30%, lenght loss – more than 4 sm, the index degree of nourishement of Chulitskaya is negative, skin elastisity and turgor are absent, skin and mucus are very dry, great abdomen, breathing is difficult. Heart beats are quiet, bradycardia, immunologic reactivity paralyses, all systems and organs are impaired – anemia, rickets, bacterial infections.

Malnutrition III st.


Malnutrition III st.

Malnutrition III st.

Malnourished children are clearly more susceptible to infection. The consequent interaction of infection with malnutrition is one of the major factors of the increased morbidity and mortality. Many authors demonstrated that nutritional deficiency was associated with 60,9% of the death from infectious diseases. Diarrhea and measles were the diseases with the greatest morbidity and mortality in which malnutrition was the main factor. The mechanism by which infection leads to a malnourished child include a) anorexia; b) replacement of solid foods with a low-energy, low-protein diet; c) decreased nutrient absorption resulting from diarrhea and intestinal parasites; d) increased urinary losses of nitrogen, potassium, magnesium, zinc, phosphate, sulfur and vitamins A, C, B2. Increased urinary nitrogen excretion results from an increased mobilisation of amino asids from peripheral muscle for gluconeogenesis in the liver with a deamination and exretion of nitrogen in the form of the urea. Without an increased dietary intake, to compensate for losses, a kwashiorcor-like syndrome results. Despite the mobilisation of aminoasids from peripheral muscle, there is also the decrease in whole blood amino acids after the exposure to an infectious agent. An increased synthesis of acute-phase reactants, including haptoglobin, C-reactive protein, a-antitrypsin, a2-macroglobulin, also occurs.
<!–
Diagnosis
I.Damage of growth and development of the child
II. peripheral blood : leukocytosis with a prepoderanse ofneutrophils electrolyte losses acidosis, hyponatremia, hypoalbuminemia polyhipovitaminoses, anemia, low level of ferments, low level of T-, B-lymphocytes and immunoglobulines .
III. Stool examination for blood, leukocytes, pH, fat, reducing sugars or parasites;
IV.Culture of stool, urine and blood.
Children with protein–energy malnutrition may have either hypochromic microcytic or normochromic normocytic anemia, which is the result of defective hemoglobine synthesis. Infection also affects the endocrine system. Changes in hormone levels occur simultaneously with infection and precede the changes in amino acids.
During diarrhea, it is significant loss of potassium and magnesium in the stools, leadind to a decrease in serum electrolytes. There is also urinary loss of electrolytes as a result of increased muscle breakdown. Iron absorption and methabolism are also affected by infection. Infections such as malaria and typhoid may cause increased hemolysis and resultant acute hemolytic anemia.
Treatment
Nutritional Management
FEEDING
1 PERIOD – period of making toleranse to food
MALNUTRITION OF 1 STAGE
1 DAY – 1/2 – 2/3 of day volume of food
2 DAY – 2/3 – 3/4 of day volume of food
3 DAY – full volume of food
MALNUTRITION OF 2 STAGE
1 week – 1/2 of day volume of food
2 week – 2/3 of day volume of food
3 week – full volume of food
MALNUTRITION OF 3 STAGE
1 week – 1/3 of day volume of food
2 week – 1/2 of day volume of food
3 week – ¾ of day volume of food
4 week – full volume of food
PARENTERAL FEEDING
AMINOASIDS
POLIAMIN, ALVESIN, LEVAMIL
PROTEIN GIDROLIZATES
INFEZOL – 20/ ml/kg in 10% glucose (1:1) temperature 20°-30° C with 1 IU
insuline to 5 gr. of glucose – 5-8-10 drops/minute – 5-8 days
MEDICAMENTAL THERAPY
FERMENTS
FESTAL, PANCREATIN, DIGESTIN
2. BACTERIAL DRUGS
HILAC, BIFIDUM – BACTERIN, BIFI-FORMA, LINECS
3. STIMULATOR THERAPY
APILAC, METILURACIL, PENTOKSID
4. VITAMINS
AEVIT, B,C, P
5. HORMONE THERAPY
NEROBOL – 0,1 MG/KG/DAY
RETABOLIL – 1 MG/KG/DAY
6. SYMTOMATIC TREATMENT
FERUM-LEK – 1 MG/KG/DAY INTRAMUSCULAR
PER OS – 5 MG/KG/DAY ACTIFERIN (DROPS)
7. ANTIOCSIDANT THERAPY
TOCOFEROL ACETATI – 3-5 MG/KG/DAY
Assessment of feeding problems. The caretakers of all infants ages 1 week to 2 months are asked questions about whether there is any difficulty feeding; whether the child is breastfed, and if so, how many times a day; and whether the infant usually receives any other foods or drinks, and if so, how often. An assessment of breastfeeding is then recommended in the algorithm if the infant has any difficulty feeding, is feeding less than six times a day, has a low weight-for-age, or is taking any other food or drinks, but has no indications for urgent referral to hospital.
The part of the nutrition algorithm concerned with assessment of the feeding of older children contains three sections: usual breastfeeding practices, usual consumption of other foods and fluids, and any modifications of these feeding practices during the current illness. The questions on breastfeeding refer to the frequency of daytime breastfeeding and any occurrence of nighttime breastfeeding. The questions on other foods and fluids solicit information on the kinds of items, their frequency of administration, and the use of feeding bottles; for low weight-for-age children, information is also sought about the portion size, who feeds the child, and the methods of feeding.
Nutrition counseling. The feeding recommendations encompassed within the algorithm are divided into five age categories: birth to 4 months of age, 4-6 months, 6-12 months, 12-24 months, and older than 24 months. Exclusive breastfeeding at least six times daily is suggested for the youngest age group, and introduction of complementary foods is recommended for those 4 to 6 months, depending on the presence of specific indicators of apparent need. These indicators included poor weight gain (not defined), hungry appearance after breastfeeding, and demonstration of interest in semisolid foods. During the next age period, continued breastfeeding on demand is recommended, along with at least three to five adequate servings daily, depending on breastfeeding status, of locally available foods rich iutrients and energy. The recommendations specify the appropriate order of feeding: first, breast milk; then semisolids; and finally other fluids.
During the period from 12-24 months, continued breastfeeding is recommended, as well as five adequate servings of family foods or other recommended foods. The suggested order of serving semisolids and breastmilk is reversed from that stated for the preceding age group. For the oldest age group (>24 months), three servings daily of family foods and two nutritious snacks are recommended. A footnote providing examples of the kinds of foods that might be offered for the periods from 6 to 24 months suggests an energy-rich food (possibly a thick cereal with added oil), meat, fish, eggs or pulses, and fruits and vegetables.
Comments on Infant Feeding Assessment
It will be necessary to develop appropriate age-specific feeding recommendations (considering issues of food availability, cultural beliefs, and prevailing nutritional problems) for each country or subregion within the country before successful implementation of the nutritional treatment algorithm will be possible at new locales. The IMCI proposes to do this within the local adaptation activities. Once these recommendations are developed, the assessment of child feeding within the context of the SCI visit can be simplified to examine the extent to which the locale-specific recommendations are already being used for an individual child, and to reinforce recommended practices.
Infants found to have low weight-for-age between 1 week and 2 months of age will be targeted for a feeding assessment. Low weight-for-age during the first few weeks after birth, however, may be caused primarily by low birth weight. A substantial proportion of infants may therefore be assessed unnecessarily for breastfeeding problems, a possibility that will need to be investigated. A 1-week-old infant who weighs less than at birth may have feeding problems, whereas a small infant who has gained weight probably does not. Thus, weight in relation to birthweight may be a better indicator of feeding problems during this period; information on birth weight, however, is often unavailable.
As stated, breastfeeding will not be assessed for infants who have fed in the previous hour, regardless of identified low weight or feeding problems. If the infant has not fed for at least an hour, there is to be 4-minute period when breastfeeding is observed. Assessment of attachment probably needs to be done within a few days after birth–if it is not adequate at this time, the infant will be at serious risk of malnutrition and dehydration. Even making the assessment at 1 week postpartum may be too late. The assessment would require careful training of personnel because it is not easy to do well.
Comments on Assessment of Feeding in Children Age 2 Months to
2 Years
The questions about breastfeeding will, appropriately, provide information on whether the child is currently breastfed during the day and at night. It is not certain, however, whether all mothers will be able to report their frequency of nursing. Because the feeding recommendations specify that the child should be fed as often as he or she wants, it would be desirable to obtain information on the signals used to initiate a feed (mother’s preference or child’s demand). Finally, mothers should be asked whether they are aware of any problems with breastfeeding.
The questions on other foods may need to be reformulated in each locale. If, for example, there are common local preparations that are suitable for young children, mothers might be questioned specifically about their knowledge and use of these foods. It is not clear how information on serving size will be obtained, especially when the children do not receive their own servings and when there are multiple caregivers. Each of these questions must be developed during the locale-specific adaptation phase. Because the committee was unconvinced of the importance of the order of feeding breast milk and semisolids, the lack of questions pertaining to serving order was not viewed as problematic.
Comments on Feeding Recommendations
The committee felt that several aspects of the feeding recommendations are unnecessarily complicated. In particular, it should be possible to reduce the number of age groups presented, and it may be possible to eliminate the recommendations regarding the order of individual foods served. At the same time, much more effort should be devoted to defining what is meant by a “good daily diet” in a given setting. This will require adaptation of the algorithm in each country, and a process must be developed to prepare country-specific recommendations based on the general guidelines.
The emphasis on local adaptation of the Food Box is strongly endorsed by the CIN. In some countries, existing governmental and nongovernmental nutrition programs have already acquired valuable information on child feeding practices, feeding problems, and feasible solutions to some of these problems that could be incorporated into the modified feeding recommendations. Nevertheless, the CIN believes that the available information needed to serve as the basis for feeding recommendations will be poor in many countries and regions. It is unrealistic to expect that resources would necessarily be available to fill these information gaps. Therefore, the CIN strongly suggests that the mechanisms for generating this information, and the resources to do so, be clearly identified and developed prior to full in-country implementation of the SCI.
Little information is available on the relationships between dietary intake and functional outcomes in children beyond two years of age. A number of studies suggest, however, that the growth velocity of children of this age in developing countries approximates that of children in more affluent nations (Allen, 1993). Therefore, specific feeding recommendations may no longer be necessary for children of this age range in developing countries when local data suggest adequate growth and nutritional status. The committee agrees that the suggested provision of two nutritious snacks in addition to three meals of family foods a day seems acceptable and is unlikely to produce any harm. Only recommendations that are important for child nutrition and health should be articulated, however, to avoid any unnecessary expenditure of health worker time for counseling oonessential matters. In addition, it may be better to give intensive age-specific advice to mothers of children in the age group when growth faltering tends to occur, rather than attempt to target those with anthropometric deficits. It will be important to be able to tap into resources for feeding advice and support already operating in a community, or to develop them. This may be especially possible in, for example, Latin America (as compared to many parts of
It appears that the component of the algorithm that will be most difficult to implement will be the country-specific recommendations for special foods for infants during the period from 6 to 12 months. The committee recommends that general guidelines be prepared first regarding ideal characteristics of the special foods and a process to allow translation of these guidelines into specific recommendations in a given setting. In particular, quantitative guidelines are needed on the recommended energy density, feeding frequency, and nutrient content of special foods for this age group. The committee was not provided with information on these issues and felt that a great deal of additional thought will need to be devoted to them. The current recommendations on the kinds of foods that comprise a good daily diet are too vague to be very useful in planning adequate diets. In many instances there may be several ways to increase the quantity or quality of complementary foods that are equally adequate from a nutritional viewpoint, but not equally feasible or acceptable from the viewpoint of the family. In order to increase the likelihood that families will be able to follow the feeding recommendations given during the counseling session, it is critical that the recommendations be sound from both a biomedical and a social science perspective.
The optimal age for introduction of complementary foods is controversial. While some recent evidence suggests that these foods may not be necessary before 6 months of age (Cohen et al., 1994), more information is needed on this question, especially for populations with large numbers of low-birth-weight infants or undernourished mothers. If these recent observations are confirmed, separate feeding recommendations for infants from 4 to 6 months of age may become superfluous.
Although it is recognized that individual children may require complementary foods at different ages, the committee recommends, from an operational perspective, that the age at which additional foods should be introduced be stated. Moreover, the currently proposed indicators of apparent need for complementary foods were of great concern to the committee for two reasons. First, the definition of inadequate weight gaieeds to be specified. This is a major challenge, especially given the current debate about the appropriate reference data to use for breastfed infants. Second, the appearance of hunger after breastfeeding may easily be misinterpreted. It is conceivable that infants who are uncomfortable after a feed for any of a number of possible reasons will be assumed–erroneously–to be receiving an inadequate amount of breastmilk. Thus, if advice on introduction of complementary foods is to be individualized, better indicators must be developed.
The committee was not aware of sufficiently compelling scientific evidence to warrant specification of the order of breastmilk, foods, and other liquids in the course of a single feeding episode. These recommendations, as currently stated, may be especially difficult to communicate to caregivers because of the different suggested orders of breastfeeds and semisolids before and after the age of 12 months. Unless additional evidence is forthcoming, the committee recommends that the advice be simplified to the following: other foods and liquids should be offered at least three times a day, after or between breastfeeds. The committee was uncertain about the specific age at which children could consume customary family foods in place of specially prepared infant foods. This may vary in individual countries, depending on the types of family foods available and prevailing cultural beliefs. Until further information is available, the recommended transition at 12 months seems reasonable.
Milk should be mentioned in the footnote that describes a good daily diet. The recommendation to add oil to thick cereals should be made with caution, because this practice can easily dilute the concentration of protein and micronutrients in the food, and consequently the amounts of these nutrients consumed by the infant. This is an area of current research that needs to be encouraged.
The CIN feels that it is important in both the training protocols and the adaptation manuals to explicitly recognize the role of family members other than the mother in transmitting and implementing feeding advice. It is not always the mother who brings the child into the health facility. The caretaker accompanying the child will depend on such factors as the work patterns of the mother, cultural norms concerning travel outside the village and interaction with authorities; and perceived severity of the child’s condition (both at the initial visit and at follow-up visits). While it may be convenient (as is currently the case) to frame the algorithm in terms of the mother/child dyad, the CIN recommends considering substituting “mother/caretaker” for “mother” in the IMCI charts.
In addition to asking the mother/caretaker about current feeding practices and whether or not the child’s feeding has changed during the illness, the committee also recommends that she be asked what she perceives as the main problem (if any) in feeding this child. Not only would such a question draw the attention of the health worker to constrained resources (such as time, food, and money) where they are as much or more of a barrier to optimal feeding as lack of information about correct feeding practices, but it would also convey to the mother/caretaker that her analysis of the feeding problem is considered valuable. In some cases, when the health worker understands what the mother/caretaker views as the most important feeding problem, together they can come up with a practical solution. In addition, however, a considerable body of research and programmatic experience suggests that when mothers are made to feel that their viewpoint is respected and considered valuable by health workers, they are more likely to follow the advice being given and to return for future visits to the health facility.
One component of the nutrition algorithm is to advise the mother/caretaker of infants or children diagnosed as having moderate malnutrition or feeding problems to return with the child in 14 days. A further follow-up visit after another 14 days is recommended if the child is not judged by the health worker to be doing well nutritionally at the first follow-up visit. The CIN feels that the practicality or feasibility of follow-up visits needs to be carefully assessed in terms of the distance from where families live to the primary level health facility; competing demands on the family member’s time (particularly the time of the mother); and the benefits or additional services that the mother might expect to receive on behalf of herself or the sick child at the time of the follow-up visit. The committee recognizes that the issue of the practicality of follow-up visits extends beyond the nutrition components of the algorithm, but because follow-up visits after 14 days are an important component of the nutrition advice given to the mother, the CIN wishes to raise the issue for consideration. In many settings over half of all children under 5 years of age are likely to be classified as malnourished or anemic (ACC/SCN, 1992), so it is probable that many follow-up visit recommendations will be triggered, thus making their practicality an appropriate concern.
The CIN would like to offer two suggestions concerning the issue of practicality of follow-up visits. The first is that further information should be obtained concerning the proportion of recommended follow-up visits that actually occur, as well as any factors that are strongly associated with an increased or decreased likelihood of the sick child being brought in for a follow-up visit. There are several potential sources of such information. One is systematic evaluation of the past experience of first-level health facilities with follow-up visits for sick children. Another source of information would be stand-alone research on follow-up visits. A third source would be careful evaluation of the follow-up visit element of the IMCI as it is implemented in the field to test if the health worker can go to the family rather than expecting the mother or another family member to bring the child back to the facility. In addition, where something of value to the family will be obtained at the follow-up visit (for example, the growth monitoring programs are linked to take-home food rations), the visit is more likely to occur. Anthropological research concerning child survival interventions leads to the conclusion that if the mother/caretaker expects only to receive further advice, and perhaps to be evaluated negatively on the progress that her child is making, the likelihood of a follow-up visit is significantly diminished (Coreil et al., 1994).
Treatment of Anemia
While iron deficiency is the primary cause of anemia, it is generally accepted that another important cause of anemia, especially during pregnancy, is folate deficiency. For this reason, combined iron-folate supplements are available from WHO. The IMCI recommends not using supplements containing folate in malarious areas because of competition with antimalarials. Also, the effectiveness of folate supplements for reducing anemia in adult women has been shown in several countries to be negligible. Consideration should be given to the potential benefits for children of combining other nutrients in iron supplements rather than, or in addition to, folate. For example, retinol (Mejia and Chew, 1988; Muhilal et al., 1988; Suharno et al., 1993) and riboflavin (Powers et al., 1985) supplements have produced significant improvements in anemia compared with iron alone.
Treatment of Vitamin A Deficiency
It has long been recognized by WHO that the appearance of xerophthalmia in a population indicates a high prevalence of vitamin A deficiency, which may provoke the need to provide vitamin A to all children seen in the clinic and/or country-level programmatic interventions.
The algorithms suggest that vitamin A be given to all children with measles, with “severe malnutrition or severe anemia,” or “malnutrition or anemia.” The committee felt that these recommendations were appropriate.
Under the algorithms for Identifying Treatment of the child with malnutrition or anemia, the recommendation is to “Make sure child is receiving foods containing Vitamin A.” This recommendatioeeds to be reexamined, and perhaps altered to refer more specifically to animal products high in vitamin A (retinol). Plant foods do not contain preformed vitamin A, and absorption of carotenoids (pro-vitamin A) may be poor in the many regions of the world where fat intakes are low. Increasing intake of plant sources of the pro-vitamin may therefore be less effective unless some oil is added to the local diet. The addition of oil, however, needs to be done with caution, as described under our comments on appropriate complementary foods for infants.
The nutrition algorithm is divided into three broad components: assessment, classification, and treatment (see Appendix D for the algorithm). The nutrition assessment component, “Classify Nutritional Status,” relies on relatively simple measurements for the identification of malnutrition and anemia. It assumes that a scale is available for weighing the child, but not a lengthboard to measure height or length or equipment for measuring hemoglobin or hematocrit. The identification of malnutrition and anemia is based on the presence or absence of following: visible severe wasting, pallor, clouding of the cornea, foamy patches on the whites of the eyes, or edema of both feet. The child is also weighed, and weight-for-age is classified as “low” or “not low.” Based on these symptoms, the child (age 2 months to 5 years) is classified in one of the three groups described in the following sections.
May be prescribed dietary support: yogurt, provision ofaproteine hydrolysate formula, increasing fluid intake, administration of broad-spectrum antibiotics in the case of infections, central venous hyperalimentation. The nutritional support must provide adequate calories to meet metabolic needs.Vitamines, ferments, anabolic hormones are also may be given. Treatment consists of feeding adequate amounts of both calories and protein in a form accepted and tolerated by the infant and measures to combat intercurrent infection. Although the mortality rate is high, the response of the infants and young children who do recover is gratifyingly rapid. Nitrogen is retained with great efficiency, and “catch-up” growth readily occurs. The ratio of protein to calories in the diet need be no different from that iormal diets; 10 to 15% of calories should come from protein. Prevention of infant malnutrition is one of the largest challenges faced by child health workers in the world. Diarrhea frequently accompanies severe malnutrition.
Prognosis: is excellent with early treatment.
Assessment of the temperature. A doctor evaluates the skin temperature by symmetrically feeling each part of the body and comparing the upper areas with the lower ones. Any distinct difference in temperature is noted. Although not a common anomaly, one of the key signs for coarctation of the aorta is warm upper extremities and cool lower ones. A doctor also observes the skin temperature of the dressed child. Young children produce heat rapidly, and they quickly become overheated if dressed too warmly. Many parents do not realize this and fail to change the amount of clothing to accommodate climactic variations.

Assessment of the temperature
Assessment of the texture of the skin. A doctor palpates the skin in symmetric spots of the body and in the extremities particularly on the palms and soles and notes their moisture and temperature. Normally the skin of young children is smooth, soft and slightly dry to the touch, not oily or clammy.
Assessment of the skin elasticity. It is best determined by grasping the skin on the external surface of the palms or flexor surface of an elbow between a thumb and index finger, pulling it taut, and quickly releasing it. Elastic tissue immediately assumes its normal position without residual marks or creases. In children with poor skin elasticity and turgor the skin remains suspended or tented for a few seconds before slow falling back.
Assessment of the skin turgor. It is determined by tension of the soft tissues of the shoulder or the femur with fingers. Normally the doctor must feel flexibility or elasticity of the tissues.
The skin turgor and its elasticity are the best estimates of an adequate hydration and nutrition.
While evaluating turgor, the nurse also inspects for signs of edema, normally evident as swelling or puffiness. Periorbital edema is a sign of several systemic disorders, such as kidney diseases, but may normally be seen in children who have been crying or sleeping or who have allergies. Edema should be evaluated for change according to position, its specific location, and response to pressure. For example, in pitting edema, pressing a finger into the edematous area will cause a temporary indentation.
Assessment of the skinfold thickness
It is examined by grasping the fold of the skin and subcutaneous fat on the abdomen, under the scapula, the shoulder blade and thigh between a thumb and an index finger.
Normally the skinfold thickness is 1.5-

Assessment of the skin fold