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).

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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-

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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

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