Paediatrics & Child Health

Lecture 11
Gastro-Intestinal Tract Disorders
Dr. J.K Choge; PhD
Course: Paediatrics and Child Health
Course Code: BCM 218
Semester: One
Academic Year: 2015/2016
Class: 2nd Year (Up-grading)
University of Kabianga
 Infectious Diseases
Definitions of ‘Diarrhoea’ - 1
1. ‘Diarrhoea’ is an increase in frequency, fluidity or
volume of bowel movements relative to the usual
habit of each individual*
2. ‘Diarrhoea’ is the condition of having at least three
loose or liquid bowel movements each day*

• Diarrhoea often lasts for a few days and can result

in dehydration due to fluid loss
 Infectious Diseases
Classifications of ‘Diarrhoea’ * - 2
1.Acute/Chronic Diarrhoea
2.Inflammatory/Non-inflammatory Diarrhoea
 Acute diarrhoea: Less than two weeks
 Chronic diarrhoea: Persistent for > 2 weeks
 Inflammatory diarrhoea: Involves
inflammation
 Non-inflammatory diarrhoea: No
inflammation
 Infectious Diseases
Epidemiological Aspects of ‘Diarrhoea’ * - 3
• Prevalence of different enteropathogens
varies with the:
 (1) Age of the affected individual
 (2) Environmental factors
 (3) How the diarrhoea is acquired
 (4) Classification (if acute or chronic)
 (5) State of the host’s immunity
 Infectious Diseases
Epidemiological Aspects of ‘Diarrhoea’ - 4
Feature Developed Countries Developing Countries
Episodes per annum <1 3 - 10
Seasonality Winter None
Severe Dehydration Rare Frequent
Nutritional sequelae Rare Usual
Measles-associated Non-existent 15 – 63%
Epidemic Rare Frequent
Polymicrobial Unusual > 20%
Case fatality rate < 0.01% 0.6%
 Infectious Diseases
Aetiology of Diarrhoea - 5
• In Kenya, different studies have achieved between 60% and
65% isolation rates. The organisms isolated mainly included:
1. Enteral (G.I.T) infections
 Viral: Rota virus (human)
 Bacterial: Escherichia coli (EPEC/ETEC); C. jejuni, Shigella,
Salmonella, Vibrio cholerae
 Parasitic: Ent. Histolytica, Giardia lamblia
 Fungal: Candida albicans (especially neonates)
 Infectious Diseases
Aetiology of Diarrhoea - 6
2. Parenteral (outside G.I.T) Childhood Infections:
 Malaria
 Respiratory tract infections*
 Urinary tract infections
 Stress*

3. Non-infective Causes of Diarrhoea (< 33% of cases):

 Anatomical defects: Malrotations, Hirsprung’s disease
 Malabsorption: Disaccharidase deficiency; Pancreatic insuffienciency
 Endocrinopathies: Thyrotoxicosis; Diabetes mellitus, Addison’s disease;
Adrenogenital syndrome
 Neoplasms: Neuroblastomas, phaeochromocytomas, lymphomas, carcinoid,
vasoactive intestinal peptide-producing tumours;
 Others: AIDS; Protein-losing enteropathy, Ulcerative colitis, granulomatous colitis,
acrodermatitis enteropathica
 Infectious Diseases
Aetiology of Diarrhoea - 7
Microorganism Inflammatory Non-inflammatory
Viruses Nil Rotavirus, Adenovirus
40/41, Astrovirus,
Norovirus, Other
Bacteria E.coli (EIEC, EHEC); C. E.coli (ETEC. EPEC), V.
jejuni, Shigella spp., cholerae, Compylobacter
Salmonella spp., others spp. Salmonella spp; others
Protozoa Entamoeba histolytica Cryptosporidium hominis,
Balantidium coli Giardia intestinalis/lamblia,
Cyclospora cayetanensis, I.
belli, B. hominis,
Enterocytozoon bieneusi
(Microsporidia)
 Infectious Diseases
Aetiology of Enteropathogenic Travellers’ Diarrhoea - 8
Pathogen Prevalence (%)
Enterotoxigenic E. coli (ETEC) 30 - 80
Compylobacter jejuni c. 20
Shigella species 5 - 15
Salmonella species 3 – 15
Giardia lamblia 0 -3
Cryptosporidium species ?
Entamoeba histolytica 0–3
Rotavirus 10
Astrovirus 1
Norovirus 1
Unknown 10 -15
 Infectious Diseases
Patho-physiology of Diarrhoea – 9
• Diarrhoea is as a result of interference with two
main functions of the intestinal mucosal cells:
 (i) Absorptive function/Defect
 (ii) Secretory function/Defect

• Also important are pathophysiological causes

of increased stool liquidity mechanisms (next
slide)
 Infectious Diseases
Patho-physiology of Diarrhoea – 10
• Pathophysiology of diarrhoea may also be seen in terms
of the following disturbances:
1. G.I.T Disturbances: pathophysiological causes of
increased stool liquidity mechanisms:*
 (a) Osmotic diarrhoea,
 (b) Secretory diarrhoea,
 (c) Increased bowel motility diarrhoea,
 (d) Decreased surface area diarrhoea,
 (e) Mucosal invasion diarrhoea
2. Fluid and Electrolyte disturbances*
 Infectious Diseases
Patho-physiology of Diarrhoea – 11
 G.I.T Disturbances:
• Osmotic diarrhoea:
 Occurs when excess non-absorbable solutes are
present in the bowel and they retain water in the
lumen
 Osmotic diarrhoea stops during fasting
 Examples: It occurs with indigestion, G.I.T
transport defects, ingestion of non-absorbable
solutes*, in lactose and other sugar intolerances*
 Infectious Diseases
Patho-physiology of Diarrhoea – 12
 G.I.T Disturbances:
• Secretory Diarrhoea:
 Occurs when the large and small intestines
secrete rather than absorb electrolytes and
water
 It is basically a problem of reduced absorption
and increased secretion
 Persists even after fasting
 Examples: Cholera, Toxigenic E.coli
 Infectious Diseases
Patho-physiology of Diarrhoea – 13
 G.I.T Disturbances:
• Increased bowel motility(altered intestinal
transit) Diarrhoea:
 Occurs due to reduced transit time when
food passes the bowel more quickly
 Examples: diarrhoea due to irritable bowel
syndrome; thyrotoxicosis; infections
 Infectious Diseases
Patho-physiology of Diarrhoea – 14
 G.I.T Disturbances:
• Decreased surface area diarrhoea:
 Is whereby there is reduced functional
capacity with malabsorption
 Examples: Short bowel syndrome, sprue,
coeliac disease, Rota virus enteritis, giardiasis
 Infectious Diseases
Patho-physiology of Diarrhoea – 15
 G.I.T Disturbances:
• Mucosal Invasion Diarrhoea:
 Occurs when bacteria invade bowel mucosal lining*
 Results in inflammation with decreased caloric
absorption and
 Also results in increased bowel motility and bloody
diarrhoea with WBCs during microscopy
 Examples: Salmonella spp., Shigella spp., Ameoba
spp., Yersinia, Compylobacter jejuni
 Infectious Diseases
Patho-physiology of Diarrhoea – 16
 Fluid and Electrolyte Disturbances:
• In order to understand the fluid and electrolyte
disturbances in diarrhoeal diseases in children,
it is necessary to understand the fluid
requirements of a healthy child

• A normally functioning body requires a certain

amount of fluid in the daily diet
 Infectious Diseases
Patho-physiology of Diarrhoea – 17
 Fluid and Electrolyte Disturbances:
 Oral Daily Fluid Requirements for a healthy child *:

• Prematures:
 200ml/kg/day (gradually increased during 1st wk of life)

• Children up to 10Kg:
 150 ml/kg/day (maximum of 1000ml/day)

• Bigger children (>10Kg):

 100 ml/kg/day (maximum of 2000ml/day)
 Infectious Diseases
Patho-physiology of Diarrhoea – 18
 Fluid and Electrolyte Disturbances:
Fluid and Electrolyte Balance in Diarrhoeal Diseases*:

•There is a major difference in fluid turnover in children and in adults

•Children are particularly dependent on a proper fluid balance; their

normal daily fluid turnover* per kilogram body weight is about five
times as much as in adults

•Fluid turnover can be measured by checking the amount of fluid

that is taken into the body (intake) and the amount of fluid that
leaves the body (output)
 Infectious Diseases
Patho-physiology of Diarrhoea – 19
 Fluid and Electrolyte Disturbances:
 Compensation Mechanisms in Dehydration*:
•Consequences of Diarrhoeal losses:
Water and electrolytes (mainly sodium, potassium, chloride, bicarbonate)
are lost
1. Electrolyte imbalance
2. Dehydration
3. Shock and Cellular Damage (Cardiac Arrest, Convulsions)*

•The body tries to get rid of excess acid products by forced respiration
(acidotic respiration)*

•The ‘3-D’ sequence is: Diarrhoea Dehydration Death

•Appropriate Oral Rehydration is therefore vital in preventing this sequence!
 Patho-physiology of Diarrhoea
ABSORPTIVE FUNCTION/DEFECT - 20
Three mechanisms of water and electrolyte
absorption have been identified at mucosal
level:
 (i) Coupled absorption of sodium and glucose*:
plays the major role; hence ORS formulation*
 (ii) Coupled absorption of sodium and chloride:
easily inhibited by rising levels of intracellular
cyclic AMP
 (iii) Passive diffusion: plays minor role
Patho-physiology of
Diarrhoea
ABSORPTIVE FUNCTION - 21
Secondary active transport
•In secondary active transport, also
known as coupled transport or co-
transport, energy is used to transport
molecules across a membrane
•In contrast to primary active transport,
there is no direct coupling of ATP instead
it relies upon the electrochemical
potential difference created by pumping
ions in/out of the cell
•Permitting one ion or molecule to move
down an electrochemical gradient, but
possibly against the concentration
gradient where it is more concentrated
to that where it is less concentrated
increases entropy and can serve as a
source of energy or metabolism(e.g. in
ATP synthase)
•Cotransporters can be classified as
symporters and antiporters depending
on whether the substances move in the
same or opposite directions
Patho-physiology of
Diarrhoea
ABSORPTIVE FUNCTION - 22
SYMPORT
•Symport uses the downhill movement of
one solute species from high to low
concentration to move another molecule
uphill from low concentration to high
concentration (against its electrochemical
gradient)
•Both molecules are transported in the
same direction
•An example is the glucose symporter
SGLT1, which co-transports one glucose (or
galactose) molecule into the cell for every
two sodium ions it imports into the cell
•This symporter is located in the small
intestines, trachea, heart, brain, testis, and
prostate
•It is also located in the S3 segment of the
proximal tubule in each nephron in the
kidneys
• Its mechanism is exploited in glucose
rehydration therapy and defects in SGLT1
prevent effective reabsorption of glucose,
causing familial renal glucosuria
Patho-physiology of
Diarrhoea
ABSORPTIVE FUNCTION - 23
Antiport
•In an antiport two species of ion or
other solutes are pumped in opposite
directions across a membrane

•One of these species is allowed to

flow from high to low concentration
which yields the entropic energy to
drive the transport of the other solute
from a low concentration region to a
high one

• An example is the sodium-calcium

exchanger or antiporter, which allows
three sodium ions into the cell to
transport one calcium out
 Patho-physiology of Diarrhoea
2. SECRETORY FUNCTION/DEFECT - 24
• Normal secretion occurs within the crypts of Liberkuhn

• At cellular level, secretion involves intracellular messengers (e.g. cyclic

AMP, calcium) and extracellular stimuli (e.g. prostaglandins, acetylcholine,
serotonin) that can increase crypt cell apical membrane permeability to
chloride

• This allows the chloride to be secreted, coupled with sodium and water
• Secretory diarrhoea may result from:
 (i) Osmotic secretion
 (ii) Hydrostatic pressure on laminae, capillaries and lymphatics
 Active secretion mediated by toxins, bile salts, long-chain fatty acids,
prostaglandins, e.t.c
 Infectious Diseases
Effects of Acute Childhood Diarrhoea - 25

• Two major effects of acute childhood

diarrhoea are: -
 (i) Dehydration, which may be fatal
 (ii) Protein Energy Malnutrition (P.E.M), in
case of prolonged morbidity
• These effects occur in 80% of children aged
between 2 and 5 years
• 90 – 95% of all forms of diarrhoea are acute
 Infectious Diseases
Clinical Features of Diarrhoea - 26
Clinical Inflammatory Non-inflammatory
Features
Symptoms Nausea, vomiting, abdominal Abdominal pain, tenesmus, fever
pain, with or without fever
Stool Voluminous, watery Frequent, small volume, blood-
stained, pus cells mucoid
Site Proximal small intestine Distal ileum, colon
Mechanism Osmotic or secretory Invasion of enterocytes to mucosal
cell death and inflammatory
response
 Infectious Diseases
Complications of Acute Diarrhoea - 27
• Haematological: • CVS:
 Dehydration

 Shock
Electrolyte imbalance
 D.I.C  Localized thrombosis
• CNS:  Septicaemia
 Convulsions;

 Pulmonary oedema (fluid
Cerebral palsy
• G.I.T: overload)
 Malabsorption; • R/S:
 Rectal prolapse  Pneumonia
 P.E.M
• Renal:
 Microinfarction (from D.I.C)
 Pre-renal: Acute Renal Failure • Others:
 Renal: Renal parenchyma and tubular  Local ulcers (injection sites)
damage from D.I.C
 Infectious Diseases
Assessing Degree of Dehydration* - 28
Clinical Features Mild Dehydration Moderate /Some Severe Dehydration
Dehydration
About 10% of cases About 80% of cases About 10% of cases
General Thirsty, alert, Thirsty, restless, Drowsy, limp, cold
appearance restless lethargic, irritable cyanotic extremities
(infant/young child) ; comatose
General Thirsty, alert Thirsty, alert, Usually conscious,
appearance postural apprehensive, cold,
(Older child) hypotension cyanotic, sweaty
extremities,
wrinkled skin of
fingers/toes,
muscle cramps,
giddiness on
standing
 Infectious Diseases
Assessing Degree of Dehydration* - 29
Clinical Features Mild Dehydration Moderate /Some Severe Dehydration
Dehydration
Vital signs:
•Radial pulse •Normal rate & •Rapid •Rapid, feeble or
volume absent
•Respiration •Normal •Deep, may be •Deep and rapid
rapid
•Systolic BP •Normal •Normal or low •Low or
unrecordable
Anterior fontanelle Normal Sunken Very sunken
Tears Present Absent Absent
 Infectious Diseases
Assessing Degree of Dehydration* - 30
Clinical Features Mild Dehydration Moderate /Some Severe Dehydration
Dehydration
Eyes Normal Sunken Deeply sunken
Skin turgor Normal Slow retraction Very slow retraction
Urine flow Normal Reduced and dark Absent several hrs;
(bladder empty)
% Body weight lost 4 – 5% (≤ 5%) 6 – 9% (5 – 10 %) 10+ % (11 -15%)
Estimated fluid 40 – 50 mls/kg 60 -90 mls/kg 100 – 110 mls/kg
deficit
 Infectious Diseases
Clinical Signs of Sodium Derangements* - 31
Clinical Isonatraemia Hyponatraemia Hypernatraemia
Features
About 50% of cases About 48% of cases About 2% of cases
•Thirst •Rare • Rare •Marked thirst
•Convulsions •None •May occur •May occur
•Anorexia, •May be normal •Common
vomiting
•General •Fair •Shocked; •Irritable; Restless
condition Comatose •Mentally retarded

Fluid loss Proportionate water Sodium > Water Water > Sodium
and sodium loss loss loss
ECF volume Markedly decreased Severely decreased Decreased
ICF volume Maintained Increased Decreased
(cells swollen)
 Infectious Diseases
Clinical Signs of Sodium Derangements* - 32
Clinical Features Isonatraemia Hyponatraemia Hypernatraemia
Skin temperature Cold Cold Cold or Hot
Skin turgor Poor Very poor Doughy (rubbery)
Skin feel Dry Clammy Doughy /Thick
Eye ball Sunken and soft Sunken and soft Sunken
Mental state Lethargic Coma Hyper-irritable
Blood pressure Low Very low Moderately low
 Infectious Diseases
Management of Dehydration* - 33
1. Fluid and Electrolyte Replacement:
Resuscitation stage; Maintenance stage
2. Dietary Management*
3. Management of Dehydration with extreme
electrolyte derangements: Hypernatraemia;
Hyponatraemia
4. Drug therapy*
5. Preventive Management
 Management of Dehydration
Fluid/Electrolyte Therapy in Resuscitation Phase - 34
Degree of Age Group Type of Fluid Volume given Duration of
Dehydration per kg/b.wt Therapy
(ml/kg) (Hrs)
Mild All ORS 50mls/kg Within 3-4 hrs
Moderate All ORS 100mls/kg Within 4 hrs
(some)
Severe Infants I-V HSD 70mls/kg Within 3 hrs*
Older children I-V HSD 100ml/kg Within 4 hrs
initially as fast
as possible till
pulse is
palpable
 Management of Dehydration
Fluid/Electrolyte Therapy in Maintenance Phase - 35
Severity of Diarrhoea* Route/Type of Fluid Amount
Mild Diarrhoea Mouth/ORS Daily needs of 120-
(one stool/24hrs or < 150mls/kg/24hrs plus
12motions/24hrs) 10mls/kg/stool passed
Severe Diarrhoea Mouth/ORS 120-150ml/kg/24hrs (i.e.
(over one stool every daily needs) plus
2hrs or > 12 20mls/kg/stool passed
motions/24hrs)
 Infectious Diseases
Principles of Diarrhoea Management - 36
1. Evaluate the patient: History; Physical examination*
2. Prevention of Dehydration: if it hasn’t already occurred
3. Correct fluid/electrolyte deficits: if clinical dehydration is
present
4. Maintain adequate fluid, electrolyte and nutritional
balance: during and after diarrhoea episodes
5. Manage inter-current problems/Complications: infections,
other complications
6. Health Education: aimed at prevention of further attacks
 References
• Anjaiah, B. (2009). Clinical Paediatrics. 4 th edition. Paras Publishing.
• Gordon, C. C & Alimuddin, I . Z. 2009. Manson’s Tropical Diseases.
22nd Edition. Saunders Elsevier Publishers.
• Kliegman, R.M, et al., (editors). (2011). Nelson Textbook of
Pediatrics. 19th edition. Elsevier Saunders Publishers.
• Lichtman, M.A., et al (editors). (2006). Williams Hematology. 7 th
edition. McGraw-Hill Medical Publishers.
• Newell, S.J. and Darling, J.C. (2008). Lecture notes: Paediatrics. 8 th
edition. Blackwell Publishing.
• Seear, M. (2000). A Manual of Tropical Pediatrics. Cambridge Low-
price editions. Cambridge University Press.
• www. wikipedia website: the free encyclopedia