Diarrhoea

ACUTE DIARRHOEA

Enriqueta Román Riechmann MD

Definition

Diarrhoea is a change in the individual bowel habit resulting in more frequent and/or looser stools. It expresses an acute gastrointestinal inflammation (acute gastroenteritis). In childhood, gastrointestinal infection is the most common cause of acute diarrhoea worldwide¹^, ².

Aetiology

In industrialized countries the most clinically significant agents in infant acute diarrhoea are viruses (Table 3.1), mainly group A rotavirus (3.1A, B). Other viruses involved are human calicivirus (norovirus and sapovirus, formerly known as Norwalk and Sapporo virus), astrovirus and enteric adenovirus (types 40 and 41), with some common features (Table 3.2)³.

3.1 A: Electron microscopy of rotavirus particles from an infant with acute diarrhoea (courtesy Centers for Disease Prevention and Control, Atlanta, GA, USA); B: schematic of the complete rotavirus particle with structural proteins in the different shells.

Most common bacteria are Campylobacter spp. and Salmonella spp., followed by Shigella, Yersinia and Escherichia coli. The major parasitic infections are Giardia and Cryptosporidium².

Epidemiology

Viral gastroenteritis is the second most common disease in developed countries. The sporadic form affects all children in the first 5 years of life. Viruses are transmitted fundamentally by the faecal-oral route. There is faecal
excretion of viral particles in the days prior to clinical symptoms and continuing through to its resolution. Rotavirus is a seasonal infection and in temperate climates infections peak during the winter months³. In bacterial enteric infection transmission can be through contaminated water or foodstuffs.

Table 3.1 Main agents of infectious acute diarrhoea

*Viruses*
•	Group A rotavirus
•	Enteric adenovirus
•	Astrovirus
•	Human calicivirus
–	Norovirus
–	Sapovirus
*Parasites*
Giardia lamblia
Cryptosporidium parvum
*Bacteria*
•	Salmonella
–	S. typhi and paratyphi
–	Nontyphoidal Salmonella
		S. enteritidis
		S. typhimurium
•	Shigella
–	Shigella sonnei
•	Campylobacter
–	C. jejuni
•	Yersinia
–	Y. enterocolítica
•	Escherichia coli
–	Enteropathogenic E. coli
–	Enterotoxigenic E. coli
–	Enteroinvasive E. coli
–	Enterohaemorrhagic E. coli
–	Diffusely adherent E. coli
–	Enteroaggregative E. coli
•	Aeromonas

3.2 Pathogenesis of viral diarrhoea: rotavirus infects selectively mature enterocytes on the tips of small intestine villi, leading to their destruction and villi atrophy. (Courtesy Faculty of Biological Sciences, University of Barcelona, Barcelona, Spain.)

Table 3.2 Main features of viral agents

•	RNA viruses (except adenovirus)
•	Nonlipoproteic envelope
•	Seasonal distribution
•	Asymptomatic infection ↔ severe disease
•	Frequent coinfections
•	Endemic, sporadic cases/epidemic, outbreaks
•	Faecal-oral transmission

Pathophysiology

Diarrhoea occurs when the volume of water and electrolytes present in the colon exceeds its capacity for absorption. This can be mainly due to an increase in the secretion and/or a decrease in the absorption level of the small intestine.

Decreased intestinal absorption occurs as a result of intestinal damage or inflammation (3.2). Viruses causing diarrhoea infect selectively mature enterocytes, causing cell lysis and producing a decrease in disaccharidase activity and in mechanisms for active sodium and water absorption. The consequence is a malabsorptive or osmotic diarrhoea. Diarrhoea caused by bacterial infection is most frequently secretory. Bacteria can activate one of the intracellular pathways leading to intestinal secretion through enterotoxins.

Clinical features

Acute diarrhoea is a self-limiting process. Viral diarrhoea is typically acute in onset, watery-like, and the faeces do not contain mucus, blood, or white cells. Diarrhoea can lead to dehydration, acidosis, and electrolyte imbalance. Vomiting appears at the beginning of the process. The most common age is 6-24 months and rotavirus infection is associated with a more severe disease³.

In the secretory and osmotic diarrhoeas, faeces are watery and profuse. The invasive diarrhoea is frequently characterized by mucus and macroscopic blood. Nevertheless, viral gastroenteritis cannot be distinguished from that caused by bacteria through clinical history or physical examination, although some characteristics may suggest bacterial diarrhoea (Table 3.3).

Table 3.3 Clinical features suggestive of bacterial diarrhoea

Children older than 3 years
Acute onset
No vomiting
Hyperthermia
Bloody diarrhoea
Increase in CRP
Faecal white cells

Table 3.4 Assessment of dehydration degree (adapted from ESPGHAN 2001and CDC report 2003)⁶^, ⁷

Symptom	Minimal or no dehydration	Mild to moderate dehydration	Severe dehydration
Body weight loss	<3%	3-9%	>9%
General condition	Well, alert	Restless, irritable	Lethargic or unconscious: floppy
Eyes	Normal	Slightly sunken	Deeply sunken
Tears	Present	Absent	Absent
Mouth and tongue	Moist	Dry	Very dry
Thirst	Drinks normally, not thirsty	Thirsty, eager to drink	Drinks poorly, unable to drink
Skin fold	Instant recoil	Recoil in <2 seconds	Recoil in >2 seconds
Fontanelle	Normal	Sunken	Sunken
Heart rate	Normal	Normal to increased	Tachycardia, bradycardia in most severe cases
Quality of pulses	Normal	Normal or slightly decreased	Moderately decreased
Extremities	Normal capillary refill	Delayed capillary refill	Cool, mottled
Urine output	Slightly decreased	<1 ml/kg/h	<1 ml/kg/h

Assessment

In most cases, a complete clinical history and a careful physical examination is all that is necessary⁴^,⁵^,⁶. These should rule out any life-threatening cause such as intussusception, surgical abdomen, and haemolityc-uraemic syndrome⁷. The severity of dehydration is assessed in terms of weight loss as a percentage of total body weight. An assessment of dehydration degree can be made by diverse scales of clinical signs and symptoms (Table 3.4, 3.3).

Supplementary laboratory studies are usually unnecessary. There are some recommendations on which patients should have blood tests (serum electrolytes, urea/creatinine, bicarbonate) (Table 3.5) and on which patients should have faecal laboratory study (Table 3.6), as aetiology is irrelevant for clinical management. Tests for specific pathogens
include stool cultures for bacteria and detection of faecal viral antigen by enzyme immunoassay (EIA), agglutination with latex particles, or immunochromatography.

3.3 Signs of dehydration.

Table 3.5 Recommendations on blood tests (adapted from AAP 1996)⁵^, ⁸

•	Severe dehydration
•	Moderate dehydration where clinical signs might indicate hypernatraemia
•	Moderate dehydrated patients whose histories or physical findings are inconsistent with straightforward diarrhoeal episodes
•	History of excessive hypertonic or hypotonic fluid ingestion

Table 3.6 Recommendations for faecal laboratory study

•	Immunocompromised
•	Blood in the stool
•	Uncertain diagnosis
•	Severe or prolonged diarrhoea
•	Hospitalization
•	Recent travel abroad

3.4 Diagram to show the processes involved in cotransport of organic solutes and sodium and secondary water absorption.

Treatment

There is no specific treatment for acute gastroenteritis. The main objective is to treat the dehydration and to lead to nutritional recovery. Treatment includes two phases, rehydration with quick replacement of fluid deficit, followed by maintenance in which rapid realimentation and maintenance fluids are indicated.

Rehydration

The molecular process for cotransport of glucose and sodium was the basis for oral rehydration therapy (ORT) development (3.4). ORT is recommended globally for the management of acute diarrhoea²^, ⁶^,⁷^,⁸.

The World Health Organization (WHO), the American Academy of Pediatrics (AAP), and the European Society of Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) recommend the use of ORT in the treatment of gastroenteritis with mild to moderate dehydration (Table 3.7). Oral rehydration solution (ORS) is more physiological, cost-effective and has fewer adverse effects that intravenous therapy. Intravenous fluids should be reserved for patients with severe dehydration.

Table 3.7 Oral rehydration solution composition

	Sodium (mmol/l)	Potassium (mmol/l)	Chloride (mmol/l)	Base (mmol/l)	Glucose (mmol/l)	Osmolarity (mOsm/l)
WHO (1975)	90	20	80	30^Bic	110	310
ESPGHAN (1992)	60	20	60	10^Cit	74-111	200-250
WHO (2002)	75	20	65	10^Cit	75	245
^Bic Bicarbonate; ^Cit Citrate