Understanding and Managing�Acute Diarrhoea in Infants and Young Children
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DEPUTY MINISTER
HEALTH AND FAMILY WELFARE
INDIA
NEW DELHI - 110- 011 |
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FOREWORD
In commending Dr. O.P. Ghai's brief yet exhaustive elucidation of the science and art of managing childhood diarrhoea, I would like to underline the unusual social priority deserved by this fairly simple procedure. Perhaps the principles involved are in a sense so elementary that it takes an effort on the part of the professional to adopt it in practice with a seriousness appropriate to its validity and usefulness.
According to one estimate, there are 1400 million episodes each year of young child diarrhoea and 5 million consequent deaths in the developing countries. While the incidence of diarrhoea is understandable in an environment where safe water is not always available and sanitary practices are a frequent casualty, the recurring massive toll of lives and health, especially of children, is entirely unnecessary. The central scientific message of Dr. Ghai's paper is that the tragedy is preventable at affordable cost by simple methods within the means of the generality of the people. I would add the good news that the preventive effort has begun, successfully and on a social scale, across the developing world, including here in India.
A major condition has to be fulfilled before childhood deaths from diarrhoea become a thing of the past. In one word, it is building of awareness in the minds of the people, including health workers at different levels, about the consequents of diarrhoea to the individual child and to society as a whole, and secondly about the means available and accessible for controlling them.
What are the consequences? These go even beyond the nipping of large numbers of young lives. In collusion with other adverse factors like malnutrition and vaccine-preventable childhood diseases, recurrent
diarrhoea reduces absorption of food as well as of lessons at
school, retards growth, lowers the quality of life, increases the burden on the
health system, puts a strain on the public health budget and acts as a
disincentive to limiting family size. Its overall effect on society-adults as
well as children-is to depress social and economic productivity.
The principle of oral rehydration technology to prevent severe
dehydration and death has been known for a long time. Indeed, it is in one form
or another part of the traditional art of healing in most parts of the world
including India. It is another matter if this practice has gone into disuse,
largely from the impact of certain commercial aspects of latter-day medical
practice. The scientific validation and general acceptance of the oral
rehydration therapy has therefore come as a welcome development of recent times.
So, too, is the parallel understanding of the extent and severity of diarrhoeal
dehydration as a result of investigations over the past few years. The time has
thus come to mount a decisive assault on a hitherto under-rated public health
problem-by transferring the knowledge, skills and confidence to mothers and
families even in remote villages for intervening on their own initiative
whenever diarrhoea occurs.
This educational process of communications has to spread in
ripples starting from the medical scientist, moving through the practising
professional and the front-line health worker, to reach the mother in the
household. It is an encouraging sign of our transitional times that necessary
trend by making professional knowledge intelligible and available to a widening
and increasing concerned audience.
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UNDERSTANDING AND MANAGING ACUTE DIARRHOEA IN INFANTS AND YOUNG CHILDREN
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SYNOPSIS
Acute diarrhoea is a major cause of morbidity and mortality in infants and young children allover the world, more so in the developing countries. Encouragement of breast feeding, better food hygiene, improvement of nutritional status of children and good environmental sanitation are important strategies for lowering the incidence of
diarrhoea. It is equally important to reduce the high rate of diarrhoeal deaths because of loss of fluid and electrolytes from the body. as well as malnutrition and its sequelae
due to repeated attacks of acute diarrhoea. The principal interventions to
achieve these objectives fall into the following categories in descending order
of priority.
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Fluid and Electrolyte Management
Mother should be encouraged to feed the baby with simple home- available
or home-made fluids from the very onset of the illness, in order to
quickly replace the fluids lost in diarrhoeal stools. This prevents
dehydration (loss of water from the body) and maintains circulatory and
renal functions. This should be followed by a clinical back up for more
severe cases, who might require therapy with an oral rehydration
solution with approved constituents. When fluid replacement is started
early, intravenous medication is seldom necessary.
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Nutritional Management
Oral rehydration therapy prevents deaths due to dehydration, but by
itself is not enough to provide long-term health benefits and reduce the overall infant and child mortality. Children with recurrent attacks of diarrhoea become undernourished. Early feeding hastens recovery. Infants should continue to be fed as was done prior to the onset of
diarrhoea, breast-feeding should not be interrupted and refeeding should be started early. During convalescence extra nutrient-rich food should be given to ensure rapid and complete nutritional recovery.
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Treatment of
Causative Agent
A vast majority of diarrhoeal episodes are caused by
viruses or agents which do not require antimicrobial treatment. Antimicrobial
treatment is needed only for dysenteries, cholera and infections with bacteria
and protozoa which invade the mucosa. These account for less than 10 per cent of
cases. Injudicious use of antimicrobial agents causes emergence of resistant
strains of organisms, resident flora of the gut which are protective are
destroyed and toxic complications of some antibiotics are a real and significant
danger.
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Other Drugs
Drugs such as antimotility agents. antisecretory drugs,
binding agents and other time-honoured medications for diarrhoea do not offer
any significant benefits when subjected to scientific scrutiny. In fact, these
could be potentially harmful. Often these divert attention and resources from
the central issues of fluid therapy, nutritional management and specific
treatment when required. Antimotility drugs are potentially dangerous and must
not be used for acute diarrhoea in infants and children below 5 years of age.
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I. INTRODUCTION
Diarrhoea is a common but
potentially serious illness in early childhood. A child suffers, on an average,
10 to 15 episodes of diarrhoea in the first five years of life. Of these, three
to five occur in the first year of life. A child may lose almost as much water
and electrolytes from the body during an episode of diarrhoea as an adult, since
the length and surface area of intestinal mucosa of a child, from where the
diarrhoeal fluids are secreted, are fairly large. Loss of one litre of fluid from
the body of a child weighing 7 Kg is much more hazardous compared with a similar
depletion from an adult of 70 Kg weight. Significant dehydration disturbing the
balance of electrolytes and acid- base status of the body occurs in about 2 to 3
per cent of all cases of diarrhoea. Some of these cases may prove fatal, if
fluids and electrolytes are not replaced to restore normal circulation and body
functions which are impaired in the dehydrated state.
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Diarrhoea has been shown to have significant impact on
nutrition. Most field studies identify diarrhoea as the major determining factor
leading to malnutrition in the developing countries. It IS the child with
multiple episodes of diarrhoea and particularly chronic diarrhoea, who suffers
most severely from protein-energy malnutrition. But even a brief episode of
diarrhoea leads to the loss of I to 2 per cent of body weight per day. Infants
and young children in developing countries are sick for about 10 per cent of the
time (or nearly 30 days per year) with diarrhoeal illness. Thus over the time
even the creeping deficit associated with mild illness can accumulate to become
a major nutritional deficiency. If diarrhoea becomes unusually prolonged or is
recurrent, the child becomes severely malnourished, since he/she also loses
nutrients through stools. The appetite is impaired and food is often withheld
from the child by the mother due to an erroneous belief that starvation rests
the bowel and promotes early recovery from diarrhoea.
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Atrophy of the Intestinal epithelium in cases of
malnutrition causes malabsorption and accentuates malnutrition. A vicious cycle
of diarrhoea-malnutrition-diarrhoea sets in. Since, malnourished children are
more prone to suffer from other infections as well, diarrhoea- malnutrition
symptom complex contributes to the large majority of early childhood deaths
either directly or indirectly. Prevention and proper management of diarrhoea,
therefore, assumes a high priority.
II. WHAT CAUSES DIARRHOEA
Most cases of acute
diarrhoea in young children are due to infections with a wide variety of
organisms. All of these are riot amenable to the presently available
antimicrobial agents. The exact incidence of these microbes may vary from place
to place and at different periods of the year. Broadly speaking, 30 to 40 per
cent of diarrhoeal episodes are caused by viruses, of which rotavirus is the
best example. About 50 per cent are due to bacterial infections of the gut. The
presence of bacteria in the stools by itself is not proof of these being
causative agents. Bacteria cause diarrhoea by two distinct mechanisms viz.
- through the action of toxin and
- direct invasion of the intestinal mucosa.
Cholera vibrio is an important agent causing diarrhoea in some
parts of India and also when normal sanitary arrangements are overstretched
during major religious congregations such as Kumbh melas and during natural
calamities. In young children, 30 to 40 per cent of all cases of diarrhoea can
be attributed to toxin producing strains of Escherichia coli. These as well as
cholera vibrio do not actually invade the intestinal mucosa. There is usually no
evidence of inflammatory response in the gut.. Toxins produced by these
organisms stimulate the enzyme adenyl cyclasein the enterocytes, which
increases the production of cyclic AMP. The latter promotes active losses of
electrolytes and water from the intestinal cells. There are additional
mechanisms of diarrhoea due to cholera vibrio.
In 5 to 10 per cent of all cases of diarrhoea the microbes
such as shigella actually invade the mucosal cells, proliferate there and cause
necrosis. The damaged cells are shed resulting in passage of blood and mucus in
the stools, the clinical syndrome of dysentery. Infection with this organism
needs to be managed with antimicrobial agents.
Cholera vibrio is an important agent causing diarrhoea in some
parts of India and also when normal sanitary arrangements are overstretched
during major religious congregations such as Kumbh melas and during natural
calamities. In young children, 30 to 40 per cent of all cases of diarrhoea can
be attributed to toxin producing strains of Escherichia coli. These as well as
cholera vibrio do not actually invade the intestinal mucosa. There is usually no
evidence of inflammatory response in the gut.. Toxins produced by these
organisms stimulate the enzyme
| RECOGNISED ENTEROPATHOGENS FOR ACUTE DIARRHOEA |
| Viruses |
Bacteria |
Parasites |
Rotavirus
Norwalk Agent
Adenoviruses
Calicivirus
Coronavirus
Astrovirus |
Escherichia coli
- Enterotoxigenic*
- Enteropathogenic*
- Enteroinvasive
- Enterohaemorrhagic*
- Enteroadherent
Vibrio
cholerae*
Shigella*
Campylobacter jejuni
Staphylococcus
aureus*
Clostridium
perfringens*
Clostridium
difficile*
Non-typhoid
salmonella
Yersinia
enterocolitica
Vibrio
parahaemolytica
Aeromonas
hydrophila
Bacillus cereus
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Entamoeba histolytica
Giardia lamblia
Strongyloides stercoralis
Trichuris trichuria
Cryptosporidia |
*These
organisms produce enterotoxins
Table 1 |
Campylobacter jejuni invades the intestinal mucosa and is
isolated in 5 to 10 per cent of diarrhoeal cases.
Non-typhoid salmonella are an infrequent cause of diarrhoea especially in immune-compromised 1
infants. It may cause severe morbidity and may end fatally due to systemic
infection.
Infestations with Entamoeba histolytica and
Giardia lambia result in subacute and chronic illness. Malaria due to
Plasmodium falciparum is often implicated as a cause of acute diarrhoea in tropical
countries. Intestinal helminths are not causes of acute diarrhoea. Their
frequent presence in stools simply reflects high prevalence in the population.
| MECHANISM OF ACTION
OF ENTEROPATHOGENS |
Organisms which adhere
to the mucosa and produce
enterotoxins (secretory diarrhoea,
no inflammation of the gut). |
Enterotoxigenic E. coli
Vibrio cholerae |
Organisms which damage the
brush border and its enzymes
(cause
carbohydrate malabsorption). |
Enteropathogenic E. coli
(some of these are enteroadherent)
Rotavirus |
Organisms that invade the
mucosa and proliferate in the
intestinal epithelium. |
Shigella
Enteroinvasive E. coli |
Organisms which proliferate in
the lamina propria and invade
the mesenteric lymph anodes. |
Non-typhoid salmonella;
Campylobacter jejuni;
Yersinia enterocolitica |
Disordered small intestinal
epithelial renewal. |
Rotavirus |
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Table 2 |
III. HOW DOES DIARRHOEA CAUSE
SIGNIFICANT PHYSIOLOGICAL DISTURBANCES IN THE BODY
Water constitutes about 75
per cent of body weight at birth and approximately 60 per cent of child's body
weight is present in two separate compartments-the extracellular (E.C.F.) and
intracellular (I.C.F.) The extracellular compartment includes circulating blood,
interstitial fluid and secretions. Diarrhoea losses come from ECF and
replacement fluids should be of a similar composition: relatively rich in sodium with low potassium. Kidneys regulate the electrolyte
content of the extracellular compartment by filtering, concentrating, diluting
and reabsorbing fluids and metabolites from the circulation. Functional ability
of the kidney of very young infants is not fully developed as compared with
older children.
Large amounts of water and water-soluble nutritive substances
such as electrolytes, metabolites and vitamins are lost from the body during
diarrhoeal episodes. Loss of water from the body causes a reduction or shrinkage
in the volume of extracellular compartment. In about half of these cases, the
concentration of sodium in the plasma or extracellular compartment remains
nearly normal (about 140 mEq/ L). Since excessive sodium may be lost in the
stools in another 40 to 45 per cent of cases, there is a relative decline in the
serum and ECF sodium level (hyponatremia). Sodium is a major osmotic determinant
of ECF Therefore, the osmolality of ECF falls, causing movement of water from
the extracellular to intracellular compartment. This causes further shrinkage
of the already reduced extracellular compartment volume. Skin turgor or
elasticity is normally maintained by the presence of water and fat in the
tissues. Shrinkage of extracellular water in both hypo and isonatremic types of
dehydration impairs the skin elasticity. The skin appears to be wrinkled like
that of an old man. On pinching, it takes a few seconds for the skin folds to
return to normal.
In about 5 per cent of diarrhoea cases (especially if the
mother has given fluids with more salt) serum sodium levels may be elevated to
more than 150 mEql L. In these patients, the osmotic pressure of ECF is
relatively higher. Therefore, water moves from inside the cells to the
extracellular compartment. This restores the depleted extracellular fluid and
therefore partially masks the loss of skin turgor. The skin may appear soggy or
leathery. The physician is likely to erroneously underestimate a severe case of
hypernatremic dehydration as mild dehydration unless hel she takes into account
the other more important sequelae of dehydration such as circulatory or renal
impairment.
As the extracellular compartment is depleted, the blood
volume is reduced. This results in a weak thready pulse and a fall in blood
pressure. Extremities appear cold. Because of low hydrostatic pressure in the
renal glomeruli, the filtration of urine is reduced. The quantity and frequency
of urination falls. This is ominous because poorly functioning kidneys cannot
regulate the metabolic derangements. Urine flow is a good indicator of the
severity of illness. In severe cases, renal failure may eventually set in.
Diarrhoeal stools contain large amounts of potassium.
Therefore, the serum potassium level invariably falls if diarrhoea persists for
more than a few days. The affected children present with abdominal distension
and hypotonia of muscles. Electrocardiogram shows ST depression and flat T
waves.
Since intestinal secretions are alkaline and considerable
bicarbonate is lost in diarrhoeal stools, acidemia usually accompanies
diarrhoeal dehydration. Patients in such cases remain asymptomatic till the base
excess falls to 12 mMol/ L. As the base excess falls below this level, the
breathing becomes deep and rapid (Kussmaul breathing).
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To sum up, in early and mild cases of diarrhoea, the child may
be thirsty and slightly irritable. As the diarrhoea continues and dehydration
worsens, the child becomes more irritable and develops a pinched look. His/ her
fontanelle, if open, is depressed, the eyes appear sunken, the nose is pinched,
and the tongue and the inner side of cheeks appear dry. Abdomen becomes
distended in hypokalemia. The child passes urine at longer intervals. As
acidosis worsens, the breathing becomes deep and rapid. In extreme cases, the
child appears moribund, pulse appears to be weak and thready, blood pressure
falls and the quantity of urine passed is markedly reduced. Children with severe
dehydration succumb rapidly if they are not promptly treated. |
| CLINICAL
FEATURES OF DEHYDRATION |
| Mild |
Moderate |
Severe |
| Irritable |
Irritable
Weak
pulse
Some
reduction in
urine volume |
Moribund, apathetic
Peripheral circulatory
failure (cold extremities,
warm
body, excessive
blanching,
weak pulse)
Marked reduction in urine volume |
| |
Fontanelle depressed
Eyeballs
sunken
Facies
dry and pinched
Buccal mucosa dry
Lips parched
Loss
of skin turgor
(except
in in hypernatremic variety) |
Fontanelle markedly
depressed
Eyeballs markedly sunken
Facies markedly dry and
pinched
Buccal mucosa
dry
Lips
parched
Loss of skin turgor
(except hypernatremic in which
it may not be variety
prominent) |
| Thirsty |
Thirsty |
Thirsty |
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Table
3 |
IV. CLINICAL APPROACH TO DIAGNOSIS
In rotavirus diarrhoea. vomiting
is an early feature and diarrhoea is more severe. Most patients have mild to
moderate fever. Norwalk virus infection occurs in slightly older infants and
pre-school children.
Stools are large and watery in secretory diarrhoea due to
infection with toxigenic strains of E. coli or cholera vibrio. The
foecal matter appears as curdy deposits. Vomiting is common in cases of cholera.
Fever, abdominal cramps and tenesmus with passing of blood and
mucus in stools indicate dysentery (colitis), due to infection with shigella.
Small amounts of blood in stools may be seen in infections
with salmonella. campylobacter or invasive strains of E. coli. Infection
of the gut with staphylococci, Candida albicans or Clostridium difficilc should
be suspected in severe cases of diarrhoea in very sick infants, who had received
prolonged treatment with broad spectrum antibiotics.
V. LABORATORY APPROACH TO DIAGNOSIS
| The following investigation may be
carried out in order of priority, but these are not absolutely essential for
effective management of the case, which can be done equally well on the clinical
basis. |
- Microscopic examination of stools for pus cells, red blood
cells' and macrophages (cellular exudate) and presence of cysts or vegetative
forms of Entamoeba histolytica or Giardia lamblia.
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Blood investigations such as pH, base excess, electrolytes such
as N+, K+ haemoglobin level, urea and osmolality.
- Record of the pH or reaction of the stools by dipping a strip of pH
indicator paper of blue litmus paper in the stools suspension.
- Culture of stools for enteropathogenic bacteria.
- Tests for the presence of toxins in the organisms cultured from stools
e.g. distension of the isolated rabbit ileal. loop or GM1 ELISA etc.
- Tests for the presence of rotavirus by electron microscopic
examination or by ELISA test.
VI. WHAT IS THE PHYSIOLOGICAL BASIS
FOR MANAGEMENT
In most cases of acute
diarrhoea, electrolytes such as chloride and sodium besides water are actively
secreted from the gut mucosa and thus lost in stools. However, physiologists
observed that while water
and sodium were being lost, nutrients such as glucose, amino acids and
dipeptides continued to be absorbed without difficulty in a majority of cases.
The uptake of glucose and other nutrients by the body is an
enzyme mediated active physiological process. The carrier mechanisms for the transport of glucose and that for sodium across the cell membrane are
interlinked. As glucose is absorbed in the gut, sodium is carried along and also
absorbed, even though it is being actively lost in secretory diarrhoeas due to
the effects of the toxin elaborated by some causative agents such as
enterotoxigenic strains of Escherichia coli and cholera vibrio. If an
iso-osmolar solution of glucose and sodium is given orally, glucose and sodium
are absorbed. Sodium absorption also promotes absorption of water This is the
physiological basis of oral- rehydration therapy, which is a fascinating
advance of modern medicine and has probably saved more lives than any other
treatment modality.
Oral rehydration solution with a concentration of 90 mEq/L of
sodium is ordinarily used for all types of diarrhoea at all ages. There may be a
minimal risk of hypernatremia developing in the neonates and very young infants
with immature kidney functions. However, the risk is very small and it can be
easily eliminated if one part of water is given after two parts of ORS. After
hydration has been achieved, ORS with a lower concentration of sodium (e.g. 60
mEq/L) will suffice for maintenance needs of fluid and electrolytes.
Alternatively the WHO formula can be supplemented with drinks of water or breast
milk. The fear of hypernatremia is often exaggerated. In fact, hypernatremia
should be corrected slowly. A sudden fall of sodium concentration with the
use of very hyponatremic solutions orally may cause sudden changes in movements
of fluids across cell membrane in neurones and precipitate convulsions.
Oral rehydration solution (ORS) should preferably be given
with a teaspoon or consumed in small sips from a cup or tumbler. A child with
profuse vomiting is more likely to retain the fluid if it is consumed
in small sips. Large gulps of fluid stimulate gastrocolic reflex resulting
in a quick passage of motion and often vomiting.
VII. PRINCIPLES OF THERAPY
1. SEVERE CASES
The status of dehydration should be
determined quickly and emergency treatment instituted if necessary.
2. MILD TO MODERATE CASES
- Fluid, electrolyte and acid-base homeostasis should
be preserved and maintained.
- Nutritional status of the patient should be restored as
early as possible. Breast feeding should be continued. Refeeding should be
started early and extra food supplements should be given during convalescence.
- Antimicrobial agents should be sparingly used and only
for specific indications such as dysentery and cholera.
- There is no scientific basis for the use of anti-motility
or binding agents.
- Associated features such as persistent vomiting,
abdominal distension and convulsions should be managed appropriately.
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3. FLUID MANAGEMENT
The key to effective fluid management in childhood
diarrhoea is early replacement of fluid losses, starting with the first sign of
liquid stool. Plenty of fluid should be given to the child early in the illness
to prevent dehydration. As long as renal function is maintained, profound electrolyte and pH disturbances do not occur.
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Initial Management with any Fluid available at Home
The mother should be advised to offer fluids
that are easily available at home in as much quantity as the child can take
orally without vomiting. Thus coconut water, butter-milk, rice kanji with salt,
lemon- sugar-salt beverage (salted-nimbupani-sherbat), weak tea etc. may be
given ad lib either with a teaspoon or in small sips from a tumbler. In
mild cases, diarrhoea and vomiting are generally controlled within a short
period and dehydration does not develop.
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Oral Rehydration Therapy (ORT) with Home-made
Solution
A fairly satisfactory solution for oral
rehydration can be prepared at home by mixing eight level teaspoonfuls of cane
sugar (40 grams of sucrose), one level teaspoonful of table salt (five grams of
NaCl) with or without a lemon squeezed in one litre of potable water. Since 2 g
of sugar releases I g of glucose, 40 g of sucrose is used. Alternatively a 3
finger pinch (upto the first crease) of table salt and closed fistful of cane
sugar are mixed in half a litre of water.
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Some health workers have successfully substituted 20 g
of glucose or 40 g of cane sugar by 50 g of puffed rice powder in the home made
ORS and got equally satisfactory results. It may be possible to replace a part
of puffed rice powder with other cereals or cooked legumes, such as rice and dal
gruel or khichri in areas where it is a culturally preferred mode of diarrhoeal
management. It takes about 5 to 7 minutes of boiling to prepare this. The
preparation must be allowed to cool and dissolved properly before
administration.
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Oral Rehydration Salts (ORS) Solution
If the diarrhoea is prolonged and dehydration becomes evident,
it is desirable to rehydrate the child orally by administering a solution with
the composition approved by the World Health Organization (glucose 20 g; sodium
chloride 3.5 g; trisodium citrate 2.9 g or sodium bicarbonate 2.5 g and
potassium chloride 1.5 g dissolved in one litre of safe drinking water). This
solution provides 90 mEq/L of Na, 20mEq/L of K, 80 mEq of Cl and 30 mEql L of
HCO3. It is administered in small sips or with a teaspoon to prevent vomiting or
rapid passage of stools due to hyperactive gastro-colic reflex. It. should be
given freely till the dehydration is corrected. Broadly speaking a
one-year-old infant needs about 1000 ml of ORS in 24 hours. To compensate
for additional losses with continuing diarrhoea, an extra 100 ml of oral
rehydration solution should be given for each diarrhoeal stool. The quantity
of ORS required for 6 to 12 hours may be prepared at a time to avoid extraneous
contamination of ORS during storage.
4. EMERGENCY TREATMENT
Severe dehydration is a major paediatric emergency, which may
end fatally if not managed early and adequately. A severely dehydrated child
appears drowsy, is apathetic and becomes moribund. As he / she goes
into peripheral circulatory failure, extremities appear cold, though the
body may be warm. The skin blanches for more than a few seconds. Pulse is
weak and fast. The quantity of urine passed is reduced or the child does not
urinate for several hours. Besides these, other clinical features more characteristic of moderate dehydration are also present. These include depressed
anterior fontanelle (if open), sunken eyeballs, dry oral mucosa and poor skin
turgor. They are thirsty and irritable. In children with nutritional wasting
of the subcutaneous tissue, the skin elasticity is impaired even when there is
no dehydration. Therefore, in malnourished children. associated dehydration
should be diagnosed if the little finger of the examiner, passed over the inner
side of the cheek, feels dry.
Less than one per cent of all'
cases of diarrhoea in the community develop severe dehydration and circulatory
or renal insufficiency and need emergency treatment to save their life or
prevent irreversible physiologic damage. Therefore, it is not
necessary to give intravenous fluids in any but the most severe case of
diarrhoea. Besides being expensive and time consuming, intravenous medication may be
potentially hazardous because of the risk of overhydration
and possibility of introducing infection in the veins causing
thrombophlebitis or septicaemia.
If a child develops severe
dehydration and/ or has persistent vomiting with or without marked upper
abdominal distension, it is prudent to start an intravenous drip of Ringer's
lactate solution, given at a rate of 30 ml/ kg/ of body weight in the first
hour. The rate of drip is slowed to 20ml/ kg/hr in the next 2 hours. If the
child does not pass urine within three hours of starting intravenous infusion,
acute renal failure should be suspected. It is important to check all signs to
be sure that the child is fully hydrated before labelling it as acute renal
failure. In cases of acute renal failure, it is not desirable to further push
fluids and specialist's help should be sought for the management of renal
failure. A child who starts passing urine in two hours should receive 40 ml/ kg
of Ringer's lactate solution intravenous in the next two hours as well. Concurrently,
oral rehydration therapy should also be started as described above. The
patient is kept under surveillance and as his condition improves and he starts
taking ORS, the intravenous medication can be discontinued. It should be
possible to remove the I. V. needle in almost all cases within four hours as
rehydration will be completed by then. Thereafter oral rehydration therapy will
suffice for replacing continued losses and maintenance requirements of fluids.
VIII. NUTRITIONAL MANAGEMENT OF
DIARRHOEA
A
considerable quantity of nutrients is lost in diarrhoeal stools. Appetite is
impaired and food is often withheld from the child by the mother because of an
erroneous belief that rest to the bowel promotes early recovery. Some
malabsorption of food occurs during diarrhoea, but it is only partial. Most
nutrients are well absorbed during diarrhoea. Some' hydrolytic (disaccharidases)
enzymes and absorptive mechanisms for glucose and aminoacids may be partially
compromised during viral diarrhoea. Transient carbohydrate malabsorption may
occur. Since carbohydrates may pass unchanged in the lower gut, these raise
intraluminal osmotic pressure and draw water from the gut by osmosis and increase the severity of diarrhoea. Unabsorbed
carbohydrates are also metabolised to short-chain fatty acids by colonic
bacteria and are then absorbed from the colon. These pathological changes are
transient and do not last for more than a few days in most cases. Therefore it
is safe and desirable to continue feeding in acute diarrhoea.
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Since children with diarrhoea develop
protein-energy-malnutrition, the diet should be easily digestible and
nutritionally balanced. Presence of nutrients in the gut promotes absorption of
sodium and water and hastens recovery of the intestinal epithelium because food
in the intestine stimulates rapid cell turn-over and renewal of intestinal
lining. More lives are lost because of unnecessary starvation in diarrhoea.
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Feeding during diarrhoea may be considered under three
heads:
- Exclusively breast-fed infants;
- Fully weaned infants receiving only animal milk;
- Infants who receive both solid and liquid diet whether partially breast-fed or not.
1. Breast-fed babies: The infant should continue to be breast-fed during an
attack of diarrhoea. Breast feeding should be allowed as often as the infant
desires it.
Breast-fed children are less prone to diarrhoea. Since the
human milk has low buffering capacity, stools of breast-fed babies are acidic.
Their E. coli count is low, but that of Lactobacillus bitidus is high. Breast
milk contains viable phagocytes and other protective substances, such as
secretory IgA and specific IgM which protect against most enteropathogens but
possibly not against rotavirus infection. Breast-fed children have better growth
performance.
2. Non-breast-fed infants: There is some controversy about optimal feeding
practices for this group. The general consensus is that the milk should be
diluted with an equal volume of water and fed along with ORS till the diarrhoea
stops. Thereafter, the child should receive regular formula milk. Meanwhile, the
mother should be reassured that although a temporary increase in the frequency
of motions might occur initially, eventual recovery will be faster if the
patient continues to be fed. Some children may have a transient mild
disaccharide malabsorption in the post
diarrhoea period as evidence by low pH of stools (less than 5.5, on two
occasions) and presence of 1/2 per cent or more of reducing substance in the
stools. This usually does not necessitate withdrawal of milk. Most
patients can tolerate half to two-third diluted milk in such post-diarrhoeal,
transient disaccharide malabsorption, which generally lasts 3 to 14 days.
3. Older infants who are receiving
both solid and liquid diet including either breast milk or animal milk: The diet
should contain adequate amount of concentrated foods, so that enough nutrients
are absorbed from a small quantity of food. Milled cereals are preferred
to whole cereals. A well cooked gruel of rice and lentil is usually well
tolerated. Mashed bananas are also good. The diet should be iso-osmolar. These
foods should be started within 4 to 6 hours of starting the treatment. Soft
drinks and fruit juices with high sugar content should preferably be avoided
during diarrhoea. Food should be easily digestible and given in smaller
quantities at shorter intervals. Contrary to popular belief, most children
tolerate small quantities of fats and oils which are rich sources of
energy, and the diarrhoea does not get worse.
4. During convalescence: the dietary
intake should be increased to compensate for losses and to promote rapid
nutritional recovery.
IX. DRUGS
Most
cases of diarrhoea are self-limiting and generally no medication is necessary
except in a few situations. Drug formulations which enjoy very wide
popularity among the physicians include the following:
- Antibiotics and chemotherapeutic
agents.
- Stool binding agents.
- Drugs reducing motility of the
gut.
- Anti-secretory drugs.
Most of these agents
have very limited use. Their role is discussed below.
1. ANTIBIOTICS AND
CHEMOTHERAPEUTIC AGENTS
Since a large
majority of cases of diarrhoea are caused by viruses or toxigenic bacteria and
there is little evidence of inflammation of gut mucosa, it is neither necessary
nor desirable to use antibacterial substances.
Most of these agents
have very limited use. Their role is discussed below.
| ANTIBIOTICS AND CHEMOTHERAPEUTIC
AGENTS FOR DIARRHOEA |
| Organisms |
Antibiotics |
Dosage |
| Shigella |
Ampicillin
Co-trimoxazole
Nalidixic
acid
|
100 mg/kg in a single dose
10 mg TMP plus 50
mg
SMX/kg/day
in 2 divided
doses
for 5 days.
60 mg/ kg/ day in
divided doses
for 7 days. |
| Vibrio
cholerae |
Tetracycline
Doxycycline |
25 mg/kg/day in divided
doses for 7 days (Do not use
in
children below 8 years)
5mg/ kg in a single dose
(may
be used in younger children) |
Enteroinvasive E. coli
Campylobact
er jejuni |
As for Shigella
Self-limiting
Antibiotics not necessary |
Erythromycin, doxycycline,
furazolidone, chloramphenicol or
aminoglycosides may be
used |
| Non-typhoid Salmonella |
Ampicillin |
100 mg/kg/day in divided doses for 10 days |
Entamoeba
histolytica
Giardia
lamblia |
Invasive amoebiasis
Metronidazole
Luminal
amoebicides
Diloxanide furoate (Furamide)
Paramomycin
Metronidazole |
35 to 50 mg/kg in 3 divided
doses for 4 days
20 mg/ kg/ day in 3 divided
doses for 10 days
25 to 30 mg/ kg/ day in 3 divided
doses for 5 to 10 days
20 mg/ kg/ day in divided
doses for 3 days. |
|
Table
4 |
Antibiotics do not shorten the duration of illness
except in cases of cholera. Their indiscriminate use leads to emergence of
resistant strains of harmful bacteria and eliminates resident flora which
protect the gut. Further more, all drugs are potentially toxic and hazardous.
Antimicrobials should be used only for infectious agents such as shigella,
cholera vibrio, Entamoeba histolytica and Giardia. They may be prescribed for
very small and sick newborn infants infected with enteropathogenic strains of E.
coli.
2. BINDING AGENTS
Formulations based on pectin, kaolin or bismuth salts are
popular among both physicians and the laity. So far there is little scientific
evidence that these are useful. These agents do not reduce excessive losses of
fluids and electrolytes, even though the stools appear more solid and the mother
is psychologically reassured.
3. ANTI-MOTILITY AGENTS
Synthetic analogues of opiates such as diphenoxylate
hydrochloride (Lomotil) and loperamide (Imodium) reduce peristalsis or gut
motility. Reduction of gut motility may not abort an attack. On the other hand, it
may give more time for the harmful bacteria to multipl) in the gut. Therefore,
the course of illness is often prolonged following their use. These drugs also
cause distension of abdomen and other undesirable side effects of opiates. These
are best avoided in infants. These are rarely used in older children. These
may be given judiciously in some cases of chronic diarrhoea and severe tenesmus
or cramps.
4. ANTI-SECRETORY AGENTS
Several drugs are currently being evaluated for their anti-secretory
properties in the hope that these may reduce the magnitude and duration of
diarrhoea and obviate the need for hydration therapy. Such drugs should be safe,
inexpensive, capable of oral use and effective against most causes of diarrhoea.
Aspirin, chlorpromazine, beta-adrenergic blockers etc. have been evaluated but
are not recommended.
X. SYMPTOMATIC TREATMENT
1. VOMITING
An occasional vomit in a child need not be treated. In such cases the children
can easily tolerate sips of cold water or oral rehydration solution. If vomiting is persistent, it may be better to
delay feeding for a few hours, while at the same time giving clear fluids with a
teaspoon or in small sips. One or more doses of metoclopramide 0.1 to 0.2 mg/ kg
or phenothiazine (0.5 mg/ kg) may be given in cases of severe vomiting, but
should preferably be avoided since these can cause oculogyric spasms.
2. ABDOMINAL DISTENSION
If bowel sounds are present and the abdominal distension
is mild, no specific treatment is necessary. Paralytic ileus due to hypokalemia,
necrotising enterocolitis or septicaemia should be suspected if intestinal
sounds are absent and distension is gross. In these cases, oral intake should be
withheld for some time. Potassium chloride (30-40mEq/ L) should be administered
intravenously with parenteral fluids, if urine is being passed (15 per cent KCI
solution provides 2 mEq/ ml). The affected child should be screened carefully
for any occu;t infection. Intermittent nasogastric suction gives symptomatic
relief.
3. CONVULSIONS
Convulsions associated with diarrhoea may either be due to
hypo- or hypernatremia, meningitis, encephalitis, hypocalcemia following
bicarbonate therapy for acidosis, cerebral venous thrombosis, or may simply be
seizures precipitated by fever. One should also be alert to the possibility of
Reye's syndrome, if the preceding vomiting is severe and if there is significant
sensorial depression. If hypo-or hypernatremia can be excluded, lumbar puncture
must be done. The treatment of convulsions depends on the cause. Symptomatic
control of seizures can be achieved either with diazepam (0.2 mg/ kg/ dose I.
V., max. 5 mg), phenobarbitone (5 to 10 mg/ kg dose I.M.), paralydehyde (0.1 ml/
kg/ dose I. M. max. 5 ml) or phenytoin (10 mg/ kg/ initially I. V. slowly
followed by 5 mg/ kg/ day).
XI. PROTRACTED DIARRHOEA
In about 5 per cent of acute
diarrhoea cases in the community, illness may last more than 2 or 3 weeks
because of persistent colonisation of upper small intestines by microbes,
dietary allergies especially in very young infants and carbohydrate intolerance
because of intestinal damage resulting in low levels of disaccharidases. Infants
and children with decreased host immunity such as after an attack of measles, or
delayed repair of intestinal damage because of associated protein-energy
malnutrition are more prone to protracted diarrhoea. Younger infants who are
weaned very early develop intolerance to food proteins such as cow's milk or even soya milk. Poor personal hygiene
and environmental or food contamination may lead to recurrent intestinal
infections before the infant recovers from a previous episode. Protozoal
infections with Giardia lamblia or Entamoeba histolytica and inadequate
treatment of acute diarrhoea are other important causes.
Causes of persistent Diarrhoea

In these children, attention should be focused on adequate nutrition
intake and selective, judicious use of antimicrobials. Low lactose diets may
help when there is carbohydrate intolerance. If the child is given half-diluted
milk for a few days with a phased increase in the concentration of milk given in
the next week, most cases of protracted diarrhoea improve. Prevention and
management of protracted diarrhoea primarily involves encouragement of breast
feeding and good nutritional management of acute diarrhoea.
Mechanism of persistent Diarrhoea

XII. PREVENTION OF DIARRHOEA
AND MALNUTRITION
Prevention of diarrhoea and
its nutritional consequences should receive major emphasis In health education.
Since breast milk offers distinct advantages and protection from diarrhoea
illness, its continuation should be vigorously encouraged and its importance in
promoting growth and development of the infant should be stressed. Exclusive
breast feeding may not be adequate to sustain growth beyond the first 5 to 6
months of life. Therefore supplementary feeding with energy-rich food mixtures
containing adequate amounts of nutrients such as balanced amounts of proteins,
fats, iron and vitamins should be introduced by 4 to 5 months of age without
stopping breast feeding. Cultural practices such as 'Ann-prashan' ceremony, in
which solid supplements are introduced in the diet at 5 or 6 months of
life, should be promoted and reinforced. Complementary feeding should be
protected from contamination during preparation, storage or at the time of
administration.
Mother should be properly guided to avoid this risk, by
concrete recommendations such as use of clean containers, avoiding exposure of
food to dust, flies or cockroaches. Proper washing of hands before preparation
or administration of food to the baby should be stressed. Water given to the
child or used for preparing feeds should be clean, potable, preferably boiled.
Vegetables and fruit should be washed and peeled before these are fed to the
child. Improvement of environmental sanitation, good water supply, adequate
sewage disposal system and protection of food from exposure to bacterial
contamination are effective long-term strategies for control of all infectious
illnesses including diarrhoea. These measures should be sustained and adequate
to achieve the desired goals.
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