DIARRHOEAL DISEASES.DIARRHOEAL DISEASES.
INTRODUCTION.INTRODUCTION.Gastro intestinal complaints are a significant part of paediatrics. Abdominal pains,Gastro intestinal complaints are a significant part of paediatrics. Abdominal pains,
diarrhoea, constipation, emesis and gastro intestinal bleeding are seen frequently.diarrhoea, constipation, emesis and gastro intestinal bleeding are seen frequently.
Diarrhoeal diseases areDiarrhoeal diseases are a major cause of morbidity and mortality in children around thea major cause of morbidity and mortality in children around the
world, accounting for 1.8 million deaths annually in children younger than 5 years, orworld, accounting for 1.8 million deaths annually in children younger than 5 years, or
roughly 17% of all child deaths (Levine, 2006).roughly 17% of all child deaths (Levine, 2006). Diarrhoeal diseases are indicators of poorDiarrhoeal diseases are indicators of poor
water supply and inadequate sanitation, systemic infection and poor weaning methods aswater supply and inadequate sanitation, systemic infection and poor weaning methods as
well as abnormality of the GIT.well as abnormality of the GIT.
In our discussion we are going to look at Diarrhoeal diseases under the followingIn our discussion we are going to look at Diarrhoeal diseases under the following
classifications Bloody diarrhea such as Dysentery and Non-bloody diarrhea such asclassifications Bloody diarrhea such as Dysentery and Non-bloody diarrhea such as
Cholera and Typhoid fever.Cholera and Typhoid fever.
Definitions of diarrhoea.
1. Diarrhoea is abnormally frequent evacuation of watery stools (Novak, 2001).
2. Diarrhoea is an increase in the number of stools or an increase in the fluid content
of the fecal material (Bernstein et al, 2003).
3. Diarrhoea is defined as three or more loose watery stools in a 24 hour
period(CBOH,2002)
Classifications.
Diarrhoea can be classified as inflammatory, non inflammatory, bloody and non bloody;
however in our discussion the focus will be on bloody as well as non bloody diarrhoea.
Blood diarrhoea.
Dysentery is an acute or chronic disease of the large intestine of human beings,
characterized by frequent passage of small, watery stools, often containing blood and
mucus, accompanied by severe abdominal cramps. Ulceration of the walls of the intestine
may occur. Although many severe cases of diarrhoea have been called dysentery, the
word properly refers to a disease caused by a specific amoeba, Entamoeba hystolytica,
virus, or a bacillus that infects the colon (Encarta ® Encyclopedia, 2005).
1
1. Bacillary Dysentery (Shigellosis). 1. Bacillary Dysentery (Shigellosis).
Bacillary dysentery is an acute inflammation of large intestines characterized byBacillary dysentery is an acute inflammation of large intestines characterized by
diarrhoea, blood and mucous in stool.diarrhoea, blood and mucous in stool.
Bacillary dysentery is caused by certain nonmotile bacteria of the genus Shigella (Encarta
® Encyclopedia 2005).
Causes.Causes.
The cause is shigella. Shigella is in 4 strains:The cause is shigella. Shigella is in 4 strains:
1.1. Shigella flexneriShigella flexneri
2.2. Shigella boydiiShigella boydii
3.3. Shigella dysenteriaeShigella dysenteriae
4.4. Shigella sonneiShigella sonnei
Epidemiology.Epidemiology.
This form of dysentery is also most prevalent in unhygienic areas of the tropics, but,
because it is easily spread, sporadic outbreaks are common in all parts of the world. This
dysentery is usually self-limiting and rarely manifests the more severe organ
involvements characteristic of amoebic dysentery (Encarta ® Encyclopedia, 2005).
Shigellosis commonly occurs among confined populations, such as those in nursingShigellosis commonly occurs among confined populations, such as those in nursing
homes (Diseases, 1993). Crowded living conditions.homes (Diseases, 1993). Crowded living conditions.
Pathophysiology.Pathophysiology.
When the bacillus enters the GIT, it invades the large intestines causing inflammation ofWhen the bacillus enters the GIT, it invades the large intestines causing inflammation of
the mucosa.the mucosa.
Ulceration and bleeding of the mucosa result to blood stained and mucoid stool.Ulceration and bleeding of the mucosa result to blood stained and mucoid stool.
In the later stage, pus forms due to infection.In the later stage, pus forms due to infection.
Adjacent lymph nodes may be affected resulting into fever.Adjacent lymph nodes may be affected resulting into fever.
Mode of spread.
Feacal oral.
Bacillary dysentery is spread by contaminated water, milk, and food. Faeces from active
cases as well as those from healthy carriers contain immense numbers of the disease-
2
producing bacteria. Flies carry the bacteria on their feet or in their saliva and faeces, and
deposit them on food; ants are also believed to spread the disease (Encarta ®
Encyclopedia, 2005).
Incubation period.Incubation period.
The incubation period is within a week i.e. one (1) to seven (7) days.The incubation period is within a week i.e. one (1) to seven (7) days.
Signs and symptoms.Signs and symptoms.
The clinical spectrum varies from mild, chronic diarrhoea to an abrupt massive toxic
process with a high mortality. The most common presentation involves;
Sudden onset of sign s and symptoms.Sudden onset of sign s and symptoms.
Abdominal cramps. Abdominal cramps.
Fever.Fever.
Diarrhoea follows, often frequent with small volumes but mixed with blood andDiarrhoea follows, often frequent with small volumes but mixed with blood and
pus.pus.
Urgency(sudden desire to defecate).
Tenesmus (painful straining at stool).Tenesmus (painful straining at stool).
Dehydration is not unusual.Dehydration is not unusual.
Vomiting.Vomiting.
Meningismus and seizures often develop due to presence neuro toxins (Bernstein
and shelov, 2003).
Medical management.
Diagnosis.
It is diagnosed in the lab by examination of stool collected from an infected person and
below are some of the investigations done.
Investigations.Investigations.
History and clinical presentation.
Stool for culture and sensitivity. Stool for culture and sensitivity.
3
Microscopic examination of a fresh stool specimen may reveal mucus, RBCs andMicroscopic examination of a fresh stool specimen may reveal mucus, RBCs and
polymorphonuclear leucocytes;polymorphonuclear leucocytes;
Sigmoidoscopy may reveal typical superficial ulcerations.Sigmoidoscopy may reveal typical superficial ulcerations.
Treatment.Treatment.
In the treatment of bacillary dysentery, proper replacement of fluid is important.
Sulphonamides, tetracycline, and streptomycin were effective in curing acute cases until
drug-resistant strains emerged. Chloramphenical is sometimes used to treat these strains.
Quinolones such as norfloxacin and ciprofloxacin are also effective against Shigella
infection (Encarta ® Encyclopedia 2005).
Recommended antibiotics for shigella: nalidixic acids first line antibiotic.Age or weight. Nalidixic acid tablet ( 250mg)
Give 4 times daily for 5 days.2 to 4 months ( 4 to 6 kg). Quarter tab.4 to 12 months ( 6 to 10 kg). Half tab.12 months to five years ( 10 to 19 kg). One tab.
Second line antibiotic: cotrimoxazole. Trimethoprim + sulphamethoxazole 2 times daily for five days.Age or weight. Adult tab. Paediatric. Syrup.
480mg. 120mg. 240mg/ 5mls.2 to 12 months ( 4 to 10 kg). Half tab. Two tabs. 5mls. 12 months to 5 years (10 to 19 kg). 1 tab. 3 tabs. 7.5mls
Complications.
1. Anaemia due to bleeding.
2. Perforation due to ulceration created by bacteria.
3. Peritonitis as a result of perforation.
4. Renal failure due to dehydration.
5. Meningitis due to the neurotoxins irritation to the brain.
6. Seizures due to irritation by neurotoxins.
7. Rectal prolapse due to Tenesmus.
4
AMOEBIC DYSENTERY-AMOEBIOSIS. AMOEBIC DYSENTERY-AMOEBIOSIS.
This is a chronic enteric infection caused by protozoa known as Entamoeba hystolyticaThis is a chronic enteric infection caused by protozoa known as Entamoeba hystolytica
(Billings and stokes, 1982).(Billings and stokes, 1982).
Amoebiosis is an infection of the large intestines caused by Entamoeba hystolytica a
single celled parasite (Berkow et al, 1997).
Forms.Forms.
Amoeba hystolytica (protozoa) is in 2 forms:Amoeba hystolytica (protozoa) is in 2 forms:
1. Resting or cystic form; (inactive form) the cyst will grow into a vegetative form that is
an adult.
2. Vegetative form ;( active form or trophozoite) these are motile which enter the
intestinal wall and cause ulcers of the small intestines, causes diarrhoea and expels
Trophozoites. Trophozoites.
Mode of transmission.Mode of transmission.
Faecal oral.Faecal oral.
Amoebic dysentery is most commonly spread by water or contaminated, uncooked foodAmoebic dysentery is most commonly spread by water or contaminated, uncooked food
or from carriers. Flies may carry the cysts to spread the amoeba from the faeces ofor from carriers. Flies may carry the cysts to spread the amoeba from the faeces of
infected people to food (Encarta ® Encyclopedia 2005).infected people to food (Encarta ® Encyclopedia 2005).
Epidemiology.Epidemiology.
It’s endemic in many tropical countries, but is attributed to unsanitary conditions than toIt’s endemic in many tropical countries, but is attributed to unsanitary conditions than to
heat. It is the most common type of dysentery in the Philippine Islands, the Malayheat. It is the most common type of dysentery in the Philippine Islands, the Malay
Archipelago, and the Caribbean, but it also occurs in almost all temperate countriesArchipelago, and the Caribbean, but it also occurs in almost all temperate countries
(Encarta ® Encyclopedia 2005).(Encarta ® Encyclopedia 2005).
Pathophysiology.Pathophysiology.
Just like in bacillary dysentery, but the ulcers they form are flux like. Once ingested, theJust like in bacillary dysentery, but the ulcers they form are flux like. Once ingested, the
trophozoite the intestinal wall and intestinal mucosal through the mesenteric artery. Thetrophozoite the intestinal wall and intestinal mucosal through the mesenteric artery. The
trophozoite will reach the liver causing total destruction of the liver thus causingtrophozoite will reach the liver causing total destruction of the liver thus causing
destruction and hepatocellular necrosis and then liver abscess. It also affects the spleendestruction and hepatocellular necrosis and then liver abscess. It also affects the spleen
and lungs as well as brain and other organs as the trophozoite spread through circulation.and lungs as well as brain and other organs as the trophozoite spread through circulation.
5
Signs and symptoms.Signs and symptoms.
Some clients’ remains asymptomatic but are carriers of the protozoan and can transmit
the infection to others if careful hand washing and food handling procedure are not held.
Some of the presentations are as follows;
Onset is gradual; may take 2 weeks or years.Onset is gradual; may take 2 weeks or years.
Abdominal pains that may be on and off on the right lower quadrant of theAbdominal pains that may be on and off on the right lower quadrant of the
abdomen.abdomen.
Nausea and vomiting.
Fowl smelling stools containing pus, blood.
Diarrhoea may alternate with constipationDiarrhoea may alternate with constipation
Tenderness in the affected colon area.Tenderness in the affected colon area.
If there is hepatic Amoebiosis there would be: general body malaise, swingingIf there is hepatic Amoebiosis there would be: general body malaise, swinging
temperature, sweating, and enlarged tender liver.temperature, sweating, and enlarged tender liver.
Inceased flatulence.
Medical management.
Diagnosis.
Amoebiosis is diagnosed in the lab by examination of stool collected from an infected
person and below are some of the investigations done.
Investigations.Investigations.
History taking.History taking.
Clinical picture.
Microscopic examination of stool.Microscopic examination of stool.
Sigmoidoscopy with biopsy/ proctoscpy.Sigmoidoscopy with biopsy/ proctoscpy.
Liver aspiration at sometimes. Aspirate can be pink and chocolate or yellowish.Liver aspiration at sometimes. Aspirate can be pink and chocolate or yellowish.
Blood culture.
Sputum.
Chest x-ray.
Treatment.Treatment.
6
Metronidazole, children; 1-3 years; 200mg orally 8 hourlyMetronidazole, children; 1-3 years; 200mg orally 8 hourly
Tinidazole, children; 50-60mg/kg daily for 3 days.Tinidazole, children; 50-60mg/kg daily for 3 days.
Complications.
1. Wasting due to interference with intestinal absorption.
2. Anaemia.
3. Hepatomagaly due to hepatonecrosis.
4. Liver abscess due to invasion of the liver
5. Spleenomegally due to spleen invasion.
6. Perforation due to trophozoite ulceration of intestinal wall.
7. Appendicitis due to trophozoite invasion of the appendix.
Viral Dysentery.
Viral dysentery is caused by a virus occurring in epidemic and is marked by acute watery
diarrhoea (Novak, 2001).
NON BLOOD DIARRHOEAS.
TYPHOID FEVER.
Typhoid fever is one of the leading preventable global causes of death due to infectious
disease. Typhoid Fever is acute infectious disease caused by the typhoid bacillus
Salmonella typhi. The bacillus is transmitted by milk, water, or solid food contaminated
by faeces of typhoid victims or of carriers, that is, healthy people who harbour typhoid
bacilli without presenting symptoms (Encarta ® Encyclopedia, 2005).
Definition.
It is an acute systemic disease characterized by defined lesions in the payer’s patches,
mesentery, spleen and accompanied by fever, headache and abdominal pains (Rubin and
Farber, 1999).
Paratyphoid fever is clinically similar but mild disease that results from infection with
other species of salmonella including salmonella paratyphi (Rubin and Farber, 1999).
Causes.
7
S.typhi which causes typhoid fever;
Epidemiology.
Humans are the only natural reservoir for salmonella typhi. It is acquired from
convalescent patients or chronic carriers, the later tend to be old women with gallstone or
billiary scarring in whom salmonella typhi colonizes the gall bladder or biliary tree.
Through out history armies and refugees have been susceptible to typhoid fever.
The disease has become rare in countries where there is modern control of sewerage and
water as well as milk supplies.
Mode of transmission.
Feacal – oral.
Pathophysiology.
The earliest pathological disorder is the degeneration of the brush boarder (numerous
micro villi lining the apical surface) of the intestinal epithelium as a result of bacterial
attachment and perforation. Ingestion of contaminated or inadequately processed foods,
especially eggs, chicken, turkey, and duck or discharges of infected persons may be
swallowed through the mouth and organisms reach the intestines and attach themselves to
the payer’s patches causing hypertrophy. In some cases, lymphoid hyperplasia in the
intestines progress to capillary thrombosis causing necrosis of the overlaying mucosa.
They form characteristic ulcers which later cause perforation along the long axis of the
bowel. This GIT ulceration frequently bleeds and occasionally perforates producing
infectious peritonitis (Rubin, 1999). Systemic dissemination of the organisms lead to
focal granuloma in the liver and spleen and other organs and cause bacteraemia. Dying
bacillus releases endotoxins leading to systemic toxemia.
Incubation period.
8
The average incubation period is about 1 to 3 weeks.
Signs and symptoms.
These are divided into the following 3 stages:
Stage 1.
General malaise and fever ( fastigium)
Arthralgias( pain in the joints)
Headache and dry cough.
High fever which is step ladder fashion.
Nausea and vomiting slow bowel movements.
Diarrhoea which is accompanied by pain in the right side of abdomen.
Stage 2- It is known as typhoid stage.
High fever continues 2 to3 days but no chills or rigors.
Rose spots appear on the lower chest and abdomen in around a third of patients.
The pulse becomes low and weak (Bradycadia).
Persistent headache and lips looks grayish.
Delirium may set in.
Marked weight loss.
At this stage it is said that the stool is pea’s soup.
Spleenomegally might be found.
Stage 3.
The fever falls by lysis and this happens after 4 weeks of manifestation.
Anemia is visible.
Stool might be bright red or tarry looking.
Pulse increases.
Pain in the right iliac fossa with rigidity of abdominal wall.
Vomiting.
Medical management.
9
Investigations.
History.
Clinical presentation.
Blood for culture and sensitivity (effective in the first week).
Stool and urine for m/c/s (effective in the 3rd and 4th week).
Rectal swab for microscopy examination.
FBC which will show leucopenia (during 3rd week).
Widal test, an agglutination reaction against somatic and flagella antigens, may
suggest a typhoid fever with a four fold rise in titers.
Differential diagnosis.
Tuberculosis, Appendicitis, Meningitis, Pneumonia.
Treatment.
Antimicrobial chosen depends on organism sensitivity.
Possible choices include first antibiotic effective against the typhoid bacillus,
Chloromycetin,
(Encarta ® Encyclopedia 2005).
Ampicillin, Amoxicillin, Chloramphenical, Ciprofloxacin, Ceftriaxone and for severely
toxic patient, Cotrimoxazole.
Control .
• Compulsory inspection of milk and water supplies, and the pasteurization of milk
in particular, have greatly reduced the incidence of the typhoid bacilli. Of equal
importance in the control of typhoid fever has been the recognition of carriers (who can
then be prevented from handling food), and improvement of sewerage facilities.
• Another important factor in the control of typhoid fever is typhoid inoculation of
people exposed to the disease, such as hospital employees and travellers to areas with
poor sanitary facilities.
CHOLERA.
10
Definitions.
1. This is an acute infectious disease caused by vibrio cholera marked by severe
diarrhoea with extreme fluid and electrolyte depletion, and by vomiting, muscle
cramps and prostration (Novak, 2001).
2. Cholera is severe diarrhoea illness caused by the enterotoxin of vibrio cholerae,
an aerobic, gram negative rod (Rubin and Farber, 1999).
Epidemiology
Found in the tropical countries, which are overcrowding and with poor sanitation such as
India, East, Central and Southern Africa.
Causative organism.
V.cholerae, a motile aerobic rod. The reservoir is man.
There are 4 strains of V.cholerae
- El tor
- Ogawa
- Hikojima
- Inaba
Mode of Transmission.
Feacal - Oral route.
Transmission of V. cholerae is through contaminated water or food or through greetings,
Sea foods. Flies act as vectors of V.cholerae.
Incubation period.
The incubation period for V. cholerae is 4 to 48 hours.
Pathophysiology.
According to Rubin and Farber, (1999) once the vibrio are ingested they transverse the
stomach enter the small intestines and propagate. Although they do not invade the
intestinal mucosa, the vibrios elaborate a potent toxin that induces massive out pouring of
water and electrolytes. Severe diarrhoea (“rice water stool”) leads to dehydration and
hypovolaemic shock.
11
Signs and symptoms
There is acute onset of disease ranging from 4 to 48 hours.
There is abrupt painless, profuse diarrhoea known as rice water stool.
Vomiting (projectile) usually follows diarrhoea.
Dehydration is marked by sunken eyes, loss of skin tugor, pale face, weakness
and muscle cramping.
The extremities may be cold.
Oliguria is present.
Medical management.
Investigation.
History.
Clinical presentation.
Culture of V.cholerae from stool or rectal swab, vomitus indicates cholera.
Fresh Stool for microscopic examination will reveal the vibrio.
Treatment.
Rehydration by rapid IV infusion with large amounts of isotonic Saline/ Ringers
Lactate solution, alternating with isotonic Sodium bicarbonate or Sodium lactate.
After IV infusions have corrected hypovolaemia, patient only needs fluid
infusions sufficient to maintain normal pulse rate and skin tugor or to replace
fluid lost through diarrhoea.
Drugs: Recommended Antibiotics.
12
ANTIBIOTICS CHILDRENTetracycline4 time daily for 3 days
12.5mg/kg
CotrimoxazoleTwice daily for 3 days
30mg/kg
ErythromycinChildren: 3 times daily for 3 days
10mg/kg
Chloramphenical4 times daily for 3 days
50mg/kg
Complications.
Renal failure due dehydration.
Hypovolemic shock.
Cardiac arrest due to potassium depletion.
GASTROENTERITIS.
Gastro enteritis is the general term for a group of conditions that are usually caused by
infections and produce symptoms such as loss of appetite, vomiting, mild to severe
diarrhoea, cramps and discomfort in the abdomen (Berkow, 1999).
This is an inflammation of the mucosa of the stomach and intestines.
More likely to occur in developing countries; also called “traveler's diarrhoea” (Saunders,
1997). It is more frequent in the very young and in older adults.
Acute diarrhoea in children.
Causes.
Most episodes of acute diarrhoea are caused by intestinal infections. The organisms
responsible include the following:
1. Viruses, mostly rotavirus and norovirus.
2. Bacteria which include:
Entero pathogenic E-coli.
13
Entero-toxigenic E-coli.
Campylobacter jejuni.
Shigella.
Salmonella.
Vibrio cholera.
3. Protozoa which includes cryptosporidium and giardia.
4. Chemicals like medications or poison.
5. Radiation injury as in radiotherapy or nuclear accidents.
6. Lactose intolerance, attracting fluids into the intestinal lumen leading to excessive
lose of fluids.
7. Granulomatous process of the bowel wall that causes non infectious type of
diarrhoea.
Predisposing factors.
These are the factors that makes an individual prone to developing diarrhoea, these
include:
Unsafe drinking water, erratic water supply and poor sanitation.
Poor personal and domestic hygiene due to inadequate or lack of water supply.
Non availability and adequacy of isolation facilities.
Un vaccinated children, especially against measles are prone to developing
measles associated diarrhoea.
Over crowding places.
Pathophysiology.
Regardless of the cause of diarrhoea the following are the common mechanisms that
occur:
Secretory diarrhoea: Secretory diarrhoea caused by vibrio cholerae causes secretion
of water and electrolytes (sodium, potassium, chloride and hydrogen bicarbonates)
from the small intestines. The loss of water and electrolytes causes isotonic
dehydration with reduced blood volume, potassium depletion and base deficit
acidosis.
14
Osmotic diarrhoea: There is an excessive osmotic force, excreted by luminal solutes
lead to out put of more than 500mls of stool per day which stops on fasting or
removal of the predisposing factor .e.g. dry foods like groundnuts or lactose milk that
attracts water to it leading to it being lost in form of diarrhoea. Lactose milk leads to
diarrhoea because in some adults there is no lactase, Lenin that digests fats.
Exudates diarrhoea: There is mucosal destruction that leads to output of purulent
and bloody stool, it persist even on fasting. This occurs mainly with bacterial
infections e.g. shigella dysentery.
Malabsorption diarrhoea: There is improper absorption of gut nutrients producing
voluminous, bulky stool with increased Osmolality combined with excess fat in stool
(steatorrhoea).this type usually abates on fasting.
Deranged motility diarrhoea: This mechanism occurs because of the improper gut
neuromuscular function leading to increased motility of intestinal contents, poor
digestion and poor absorption of nutrients. This produces high variable patterns of
increased stool volume.
Signs and symptoms.
Presentation of signs and symptom depends on the cause of diarrhoea
1. There are may be pain, urgency, perineal discomfort and incontinence.
2. Low volume, painful bloody stool as in dysentery.
3. Vomiting, diarrhoea, abdominal cramps and fever.
4. Mucus in stool.
5. Sunken eye ball, irritability, dizziness, poor skin tugor, headache, dry or
cracked mucus membranes, pallor, hypotension, cardiac arrhythmias and
cold clammy skin.
6. Lethargy, apnoea, atria tachycardia and shallow breathing due to
bicarbonate build up secondary to vomiting.
Classification of dehydration.
15
o The World Health Organization (WHO) recommends a simpler system for
use by both physicians and lay health workers, which classifies
dehydration as none, some, or severe (see table below).
Severe dehydration
Two of the following signs:• Lethargic or unconscious • Sunken eyes • Not able to drink or drinking poorly • Skin pinch goes back very slowly
Some dehydration
Two of the following signs:• Restless, irritable • Sunken eyes • Thirsty, drinks eagerly • Skin pinch goes back slowly
No dehydration Not enough of the above signs to classify as some or severe dehydration (no signs of dehydration).
* Adapted from World Health Organization. The treatment of diarrhoea: a manual for physicians and other senior health workers. 4th rev. 2005.
o Table 2. Assessment of Dehydration*
Variable Mild (3-5%) Moderate (6-9%)
Severe (¡Ý10%)
Blood pressure Normal Normal Normal to reduced
Quality of pulses Normal Slightly
diminished Moderately diminished
Heart rate Normal Increased Increased
Skin tugor Normal Decreased Decreased
Fontanelles Normal Sunken Sunken
Mucous membranes Slightly dry Dry Dry
16
Eyes Normal Sunken orbits Deeply sunken orbits
Extremities Normal cap refill
Delayed cap refill Cool, mottled
Mental status Normal Listless Lethargic, comatose
Urine output Slightly decreased <1 mL/kg/h <0.5 mL/kg/h
Thirst Slightly decreased
Moderately increased
Too lethargic to indicate
o*Adapted from Practice parameter: The management of acute gastroenteritis in young children. American Academy of Pediatrics.
Physical assessment.
General survey.
History: The history helps both in differentiating gastroenteritis from other, often more
serious, causes of vomiting and diarrhea in children, and in estimating the degree of
dehydration. In some cases, the history can also aid in determining the type of pathogen
responsible for the gastroenteritis, though only rarely will this effect management.
Diarrhea: Duration of diarrhea, the frequency and amount of stools, the time
since last episode of diarrhea, and the quality of stools. Frequent, watery stools
are more consistent with viral gastroenteritis, while stools with blood or mucous
are indicative of a bacterial pathogen (dysentery). Similarly, a long duration of
diarrhea (>14 d) is more consistent with a parasitic or noninfectious cause of
diarrhea.
Vomiting: Duration of vomiting, the amount and quality of vomitus (i.e. food
contents, blood, bile), and time since the last episode of vomiting. When
symptoms of vomiting predominate, one should consider other diseases such as
gastro esophageal reflux disease (GERD), gastric outlet (e.g. pyloric stenosis) or
intestinal obstruction (e.g. hernia, intussusception), CNS etiologies, diabetic
ketoacidosis, or urinary tract infection.
17
Urine output: Increase or decrease in frequency of urination measured by
number of wet diapers, time since last urination, color and concentration of urine,
and presence of dysuria.
Abdominal pain: Location, quality, radiation, severity, and timing of pain, per
report of parents and/or child. In general, pain that precedes vomiting and diarrhea
is more likely to be due to abdominal pathology other than gastroenteritis.
Signs of infection: Presence of fever, chills, myalgia, rash, rhinorrhea, sore
throat, coughs. These symptoms may indicate evidence of systemic infection or
sepsis.
Appearance and behavior: Weight loss, quality of feeding, amount and
frequency of feeding, level of thirst, level of alertness, increased malaise,
lethargy, or irritability, quality of crying, and presence or absence of tears with
crying.
Antibiotics: History of recent antibiotic use increases the likelihood of
Clostridium difficile colitis.
Travel: History of travel to endemic areas may make prompt consideration of
relatively rare organisms, such as parasitic diseases or cholera.
Physical examinations.
The physical examination should confirm and clarify the assessment of dehydration and
should narrow diagnostic possibilities generated by the history.
General survey: Weight, appearance, level of alertness, lethargy, irritability
HEENT: Presence or absence of tears, dry or moist mucous membranes, sore
throat, sunken eyes, or sunken fontanelle
Cardiovascular: Heart rate, blood pressure, quality of pulses, perfusion,
temperature of skin and distal extremities.
Respiratory: Rate and quality of respirations; the presence of deep, acidotic
breathing increases the likelihood of dehydration.
Abdomen: Abdominal tenderness, guarding, and rebound, bowel sounds.
Abdominal tenderness on examination, with or without guarding, should prompt
consideration of diseases other than viral gastroenteritis.
18
Back: Flank/costovertebral angle (CVA) tenderness increases the likelihood of
pyelonephritis.
Rectal: Quality and color of stool, presence of gross blood or mucous in stool.
Extremities: Capillary refill time, warm or cool extremities.
Skin: Abdominal rash may indicate typhoid fever (infection with Salmonella
typhi) while jaundice might make viral or toxic hepatitis more likely.
Treatment.
Minimal or no dehydration: No immediate treatment is required. Instruction to
caretakers about ORS to be taken at home. Giving instructions regarding signs of
dehydration are recommended.
Plan A. for treating minimal or no dehydration.
Age Amount of ORS to give
after each loose stool.
Amount of ORS to
provide for use at home.
Less than 24 months. 50 – 100 ml. 500ml/ day.
Two up to ten years. 100 – 200 ml. 1000ml / day
Ten years or more. As much as wanted. 2000ml / day.
Source:CBoH,2002.
Mild-to-moderate dehydration: Children should be given 50-100 mL/kg of ORS
over a 2- to 4-hour period to replace their estimated fluid deficit, with additional
ORS given to replace ongoing losses (10 mL/kg body weight for each stool and 2
mL/kg body weight for each episode of emesis). After the initial rehydration
phase, patients may be transitioned to maintenance fluids as described above.
o ORS should be given slowly by the parent using a teaspoon, syringe, or
medicine dropper at the rate of 5 mL every 1-2 minutes. If tolerated by the
patient, the rate of ORS delivery can be increased slowly over time.
o For patients who do not tolerate ORS by mouth due to persistent vomiting
or oral ulcers, nasogastric (NG) feeding is a safe and effective alternative.
Multiple large clinical trials have found NG rehydration to be as
19
efficacious as intravenous rehydration but more cost-effective and with
fewer adverse events.
o Patients with moderate dehydration should be reassessed frequently by the
clinician to ensure adequacy of oral intake and resolution of the various
signs and symptoms of dehydration.
Severe dehydration: This constitutes a medical emergency requiring immediate
resuscitation with intravenous fluids.
o Intravenous access should be obtained, and patients should be
administered repeat boluses of 20 mL/kg lactated Ringer (LR) or normal
saline (NS) until pulse, perfusion, and mental status return to normal. If no
peripheral veins are available, an intraosseous line should be placed.
Serum electrolytes, bicarbonate, urea/Creatinine, and glucose levels
should be sent.
o Once resuscitation is complete and mental status returns to normal,
rehydration should continue with ORS as described above, as it has been
shown to decrease the rate of hyponatremia and hypernatremia when
compared to intravenous rehydration.
Plan B: Treat mild to moderate dehydration.
Approximate amount of ORS solution to give in the first four [4] hours.
age Less than
four
months.
Four to
eleven
months.
Twelve to
twenty
three
months.
Two to
four years.
Five to
Firthteen
years.
Firthteen
years or
older.
Weight: Less than
four
months.
5 – 7.9 kg. 8 – 10.9
kg
11 – 15.9
kg.
16 kg –
29.9 kg.
30 kg or
more.
In ml 200 – 400. 400 – 600. 600 – 800. 800 –
1200.
1200 –
2200.
2200 –
4000.
Source:CBoH,2002.
20
Plan C.Treament for severe dehydration with ringers lactate solution.AGE First give 30mls/kg in: Then give 70mls/kg in:Infants less than one year. One hour Five hours.
Older 30minutes. Two and half hours.
Source : CBoH, 2002.
N.B.In developing countries, clinicians can use WHO ORS or a homemade
solution of 3 g (1 tsp) salt and 18 g (6 tsp) sugar added to 1 L of clean water
(WHO, 2002).
Feeding and nutrition: In general, children with gastroenteritis should be
returned to a normal diet as rapidly as possible. Early feeding reduces illness
duration and improves nutritional outcome.
o Breastfed infants should continue to breastfeed throughout the rehydration
and maintenance phases of acute gastroenteritis.
o Formula fed infants should restart feeding at full strength as soon as the
rehydration phase is complete (ideally in 2-4 h).
o Weaned children should restart their normal fluids and solids as soon as
the rehydration phase is complete. Fatty foods and foods high in simple
sugars should be avoided.
o For most infants, clinical trials have found no benefit of lactose-free
formulas over lactose-containing formulas. Similarly, highly specific diets,
such as the BRAT (bananas, rice, applesauce, and toast) diet, have not
been shown to improve outcomes and may provide suboptimal nutrition
for the patient.
Patient is nursed on a commode bed
21
PROBLEM ANALYSIS USING THE ROPPER LOGAN AND TIERNEY MODELPROBLEM ANALYSIS USING THE ROPPER LOGAN AND TIERNEY MODEL
OF NURSING.OF NURSING.
Maintenance of Safe EnvironmentMaintenance of Safe Environment
•• Potential for aspiration, and injury because of restlessness, child may fall because ofPotential for aspiration, and injury because of restlessness, child may fall because of
abdominal pain.abdominal pain.
• Potential for dehydration because of diarrhoea and vomiting.
• The child may develop hypothermia because of dehydration.
• Potential for circulatory over load during rehydration therapy.
• Potential for spreading infection because of inadequate isolation and preventive
measures.
• Potential for renal failure because of dehydration.
Communication. Communication.
•• Voice changes and difficulties in communicating because of severe pain andVoice changes and difficulties in communicating because of severe pain and
lethargy.lethargy.
•• The may be crying excessively because of pain and restlessness.The may be crying excessively because of pain and restlessness.
• Knowledge deficit to both care taker and patient about the disease process and its
management.
Breathing.Breathing.
•• The patient may be tachypnoeic because of respiratory acidosis.The patient may be tachypnoeic because of respiratory acidosis.
Eating and Drinking. Eating and Drinking.
•• The child may be anorexic because of due severe abdominal pain or the diseaseThe child may be anorexic because of due severe abdominal pain or the disease
process. process.
•• Nausea and vomiting may be present because of gastro intestinal irritation byNausea and vomiting may be present because of gastro intestinal irritation by
organisms or inflammation. organisms or inflammation.
•• There will be altered nutrition deficit because of anorexia, nausea and vomiting.There will be altered nutrition deficit because of anorexia, nausea and vomiting.
• Potential for electrolyte imbalance because of vomiting, limited intake and
diarrhoea.
22
• There will be fluid volume deficit because inadequate fluid intake, nausea, vomiting
and excessive diarrhoea.
Personal Cleansing And Dressing.Personal Cleansing And Dressing.
•• Poor personal hygiene because of excessive diarrhoea and general body weakness.Poor personal hygiene because of excessive diarrhoea and general body weakness.
Elimination. Elimination.
•• Rectal irritation and ulceration because excessive and frequent diarrhoea. Rectal irritation and ulceration because excessive and frequent diarrhoea.
• Potential for oliguria because of dehydration.
Work and Play.Work and Play.
•• Limited activity due to severe pain, diarrhoea and weakness.Limited activity due to severe pain, diarrhoea and weakness.
• There will be activity intolerance because of prostration and muscle cramps.
Expressing Sexuality.Expressing Sexuality.
•• Altered body image because of loss of weight.Altered body image because of loss of weight.
•• Inability to carry out Gender/sex roles because of hospitalizationInability to carry out Gender/sex roles because of hospitalization
Rest and Sleep.Rest and Sleep.
•• Disturbed sleep pattern because of severe abdominal pain, vomiting andDisturbed sleep pattern because of severe abdominal pain, vomiting and
diarrhoea.diarrhoea.
Mobilization.Mobilization.
•• There will be reduced mobility because of fatigue and general body malaiseThere will be reduced mobility because of fatigue and general body malaise
which may predispose the patient to having complications of prolonged bed rest such aswhich may predispose the patient to having complications of prolonged bed rest such as
loss of skin integrity and hypostatic pneumonia. loss of skin integrity and hypostatic pneumonia.
DYING.DYING.
•• The mother / caretaker will emotionally / psychologically affect because of fear ofThe mother / caretaker will emotionally / psychologically affect because of fear of
losing the child. losing the child.
• The parents or care taker may be anxious, apprehensive or worried because of
inadequate knowledge about the prognosis of the child.
NURSING PROBLEMS.NURSING PROBLEMS.
1.1. Fluid volume deficit.Fluid volume deficit.
2. Altered nutrition less than body requirements.
23
3. Abdominal pain.
4.4. Knowledge deficit about the disease.Knowledge deficit about the disease.
5. Impaired skin integrity.
6. Altered sleep pattern.
24
Problem.Problem. NursingNursing
diagnosis.diagnosis.
Goals. Nursing interventions.Nursing interventions. Evaluations.Evaluations.
1. Fluid1. Fluid
volume deficit.volume deficit.
Fluid volume Fluid volume
deficit deficit
related to related to
inadequate inadequate
fluid intake, fluid intake,
vomiting andvomiting and
diarrhoea diarrhoea
manifested manifested
by loss of by loss of
skin tugor, skin tugor,
oliguria and oliguria and
sunken sunken
orbits. orbits.
Patient will havePatient will have
improved fluid volumeimproved fluid volume
within four hours.within four hours.
•• I would assess the level of dehydrationI would assess the level of dehydration
hourly to monitor progress and preventhourly to monitor progress and prevent
circulatory overload.circulatory overload.
• I would administer prescribed fluids
depending on the level of dehydration to prevent
hypovolaemic shock.
• I wound monitor intake and out put to
prevent fluid overload.
Patient hasPatient has
improvedimproved
hydration statushydration status
manifested bymanifested by
normal skin tugornormal skin tugor
and improvedand improved
urine out put. urine out put.
2.Abdominal2.Abdominal
pains.pains.
Abdominal PainAbdominal Pain
related torelated to
irritatedirritated
mucosa,mucosa,
The patient will beThe patient will be
relieved of abdominalrelieved of abdominal
Pain within an hour.Pain within an hour.
•• I assess the nature, duration, location andI assess the nature, duration, location and
severity of pain in order to come up with painseverity of pain in order to come up with pain
relief strategies.relief strategies.
•• Promote bed rest in a quite environment,Promote bed rest in a quite environment,
The patient will beThe patient will be
relieved ofrelieved of
abdominal painabdominal pain
within an hour within an hour
25
3. Impaired skin integrity.
ulceration andulceration and
muscle spasmsmuscle spasms
evidenced byevidenced by
restlessness,restlessness,
crying/ andcrying/ and
verbalization.verbalization.
Impaired skinImpaired skin
integrity relatedintegrity related
to contact withto contact with
diarrhoeal stooldiarrhoeal stool
and inadequateand inadequate
perinealperineal
hygienehygiene
manifested bymanifested by
redness on theredness on the
anal region,anal region,
irritation,irritation,
swelling andswelling and
ulceration.ulceration.
Clint will have normalClint will have normal
skin integrity withinskin integrity within
four days.four days.
minimizing on visitors. minimizing on visitors.
•• Allow the patient to maintain his ownAllow the patient to maintain his own
preferred comfortable position to relievepreferred comfortable position to relieve
abdominal pain.abdominal pain.
•• Provide diversional therapy (toys, T.V.)Provide diversional therapy (toys, T.V.)
so as to divert the patient’s mind from the pain. so as to divert the patient’s mind from the pain.
•• Instruct patient to eat slowly and chewInstruct patient to eat slowly and chew
small pieces of food to prevent abdominalsmall pieces of food to prevent abdominal
discomfort.discomfort.
• Administer the prescribed analgesia for
relief of pain.
• Assess the skin of the perineal area to plan
for appropriate intervention.
• Cleanse area with warm water after each
bowel movement, rinse well and dry with soft
towel to prevent further skin breakdown and
promote comfort.
• Apply ointments such as Zinc oxide,
Vaseline and barrier cream to protect skin and
evidenced by beingevidenced by being
restful. restful.
The patient hasThe patient has
shown signs ofshown signs of
healing of thehealing of the
perineal area byperineal area by
the end of fourthe end of four
days.days.
26
promote healing.
• Use an anaesthetic spray or ointment to
reduce discomfort locally.
4. Altered4. Altered
nutrition lessnutrition less
than bodythan body
requirements.requirements.
AlteredAltered
nutrition lessnutrition less
than bodythan body
requirementsrequirements
related torelated to
inability toinability to
digest nutrients,digest nutrients,
nausea andnausea and
vomitingvomiting
manifested bymanifested by
weakness andweakness and
loss of weight.loss of weight.
Patient will havePatient will have
improved nutritionimproved nutrition
status within one week.status within one week.
• Assess presence of anorexia, nausea and
vomiting as well as precipitating factors in order
to plan for appropriate feeds (NGT, IV.Oral).
• I would serve small frequent meals to
prevent nausea, vomiting and promote absorption
of nutrients.
• I would do oral toilet to promote
salivation and appetite.
• I would monitor my client’s weight daily
to assess progress.
• Administer anti emetics as prescribed one
hour before meals to prevent vomiting during and
after meals.
• I would elevate head of bed at least 35 to
40 degrees during tube feeding and for one hour
after completion of intermittent tube feeding to
The client has
improved nutrition
status as evidenced
by weight gain of
about 1kg by the
end of one week
27
prevent aspiration of feeds and to promote feeds
retention.
5. Altered5. Altered
sleep patterns.sleep patterns.
Altered sleepAltered sleep
pattern relatedpattern related
to abdominalto abdominal
pain, excessivepain, excessive
diarrhoeadiarrhoea
manifested bymanifested by
restlessness andrestlessness and
insomnia.insomnia.
Patient will havePatient will have
normal sleep patternnormal sleep pattern
within 24 hours. within 24 hours.
•• Ascertain the causes of sleep patternAscertain the causes of sleep pattern
disturbance so that appropriate actions could bedisturbance so that appropriate actions could be
taken.taken.
• Monitor sleep pattern in order to develop
the effective interventions.
• Administer prescribed analgesia/ other
drugs to promote rest.
• Ensure the patient is dry all the time to
prevent discomfort.
Patient has normalPatient has normal
sleep patternsleep pattern
evidenced by restevidenced by rest
full sleep within 24full sleep within 24
hours.hours.
28
DISCHARGE PLAN DISCHARGE PLAN
1. Medication.
Teach the parents and care takers the dosage, administration, action, and side
effects of all the drugs in use
Advice the patient/ parents/ care taker to complete the course of treatment even
when the patient is relieved of pain so as to promote effective recovery.
Avoid the use of the over the counter drugs to prevent development of resistance
or over dose.
2. Diet.
Advice the care takes / parents to with breast feeds and prescribed meals at
regular intervals.
1. Avoid sweet fluids when there is diarrhoea to prevent worsening the
condition.
2. Breastfed infants should continue to breastfeed throughout the
rehydration and maintenance phases of acute diarrhoea.
3. Formula fed infants should restart feeding at full strength as soon as the
rehydration phase is complete (ideally in 2-4 h).
4. Weaned children should restart their normal fluids and solids as soon as
the rehydration phase is complete.
5. Fatty foods and foods high in simple sugars should be avoided.
6. Highly specific diets, such as the BRAT (bananas, rice, applesauce, and
toast) diet, may provide nutrition for the patient.
3. IEC.
Improving water supply and sanitation.
Promoting personal and domestic hygiene has beneficial effect in the prevention
of diarrhoea.( treat water before drinking, cover left over foods, warm food before
eating, hand washing after using toilets, hand washing before handling food).
Vaccination against measles prevents measles associated diarrhoea.
Parent and care takers should be advised on the importance or review dates to
monitor progress.
29
Conclusion.
Diarrhoea is one of the most common diseases in most communities with poor hygiene. it
affects individuals, families and communities that do not uphold the preventive and
control measures at all times. Diarrhoea in its severity form is fatal due to dehydration
and electrolyte imbalances leading to high morbidity and mortality rate especially among
children. Therefore accurate monitoring of intake and output is important for successful
replacement of lost fluids. Strict infection control measures should be instituted to
prevent spread of infection and the patient / care taker / parents should be instructed in
importance of proper food handling and preparation to prevent infections such as
salmonellosis, shigellosis, Amoebiosis and cholera. The health personnel and
stakeholders should put concerted efforts in to control and prevention of diarrhoeal
diseases.
References..
Berkow et al Eds, (1997): the Merck manual medical information. Merck and co., new
jersey.
CBoH, ZIHP, USAID, (2002). Integrated Technical Guidelines For Frontline Health
Workers, Lusaka.
Gettrust, V.K. and Brabec, D.P., (1992). Nursing diagnosis in clinic practice. Delmar
publishers, California.
30
Lewis et al, (2004): Medical-Surgical Nursing Care. Mosby Inc, St Louis, Missouri.
Novak, P.D., (2001). Dorland’s pocket medical dictionary. W.B. Saunders Company,
Philadelphia.
Rubin, E. and Farber, L.J., (1999). Pathology. Lippincott Williams and Wilkins,
Baltimore.
WHO, MoH, UNICEF, (2002). Integrated management of childhood illness. Lusaka.
Microsoft ® Encarta ® Encyclopedia 2005 © 1993-2004 Microsoft Corporation. All
rights reserved
31