Acute diarrhoea

Published on 13/02/2015 by admin

Filed under Gastroenterology and Hepatology

Last modified 13/02/2015

Print this page

This article have been viewed 1755 times

13 Acute diarrhoea

V. Duncombe, John Almeida

Case

A 70-year-old man presents with crampy, left-sided abdominal pain and bloody diarrhoea for 7 days. The patient has a background history of ischaemic heart disease and peripheral vascular disease. He also has bronchiectasis requiring regular courses of antibiotics.

Examination reveals an afebrile man whose is tachycardic and hypotensive. He has evidence of left flank tenderness but no masses or distension, and bowel sounds are normal. Rectal examination reveals bright red blood on the glove. There are carotid bruits and evidence of peripheral vascular disease; otherwise the examination is unremarkable.

He is anaemic with a haemoglobin of 90 (normal is 120–140) and a neutrophilia. His ESR and CRP are also both elevated. Stool examination shows red cells, but no white cells. A C. difficile toxin is positive, while blood cultures are negative. A flexible sigmoidoscopy is performed; this notes diffuse inflammation from the rectum to the splenic flexure with normal mucosa above it. Pseudomembranes are present. He is treated with metronidazole and hydration and then makes an excellent recovery.

This patient has pseudomembraneous colitis from Clostridium difficile, which is an important cause of diarrhoea in the context of recent antibiotic therapy. Ischaemic colitis would be a consideration in the setting of vascular disease and acute onset of bloody diarrhoea with pain, but was not found here.

Introduction

Diarrhoea remains a common problem around the world in both developing and industrialised countries. It is usually mild and self-limiting, but may develop into an overwhelming life-threatening illness. It is arbitrarily defined as acute if it is of less than 2 weeks duration.

Definition

Diarrhoea is defined as a change in bowel habit with an increase in stool frequency or fluidity or both. It is the change from normal for that individual that is significant, with a normal range being from one bowel motion every 3 days to three times daily.

Normal physiology

In the non-fasting state, approximately 9 L of fluid pass into the small intestine, of which only 1–2 L pass into the colon and 100 mL is present in the stool. The colon has an absorptive capacity of 3–5 L a day, and an ileal flow of greater than this will result in diarrhoea.

Water is absorbed passively in both the small and large intestines because of an osmotic gradient created by active sodium transport. The co-transport of glucose with sodium in the small intestine has been well-documented. Both sodium and glucose must be bound to the carrier before transport can occur. Active transport is promoted by a sodium (Na⁺) gradient created by a Na/K ATP-ase in the basolateral membrane (K = potassium). Co-transport of other sugars and amino acids in the small intestine is also recognised. Advantage can be taken of these co-transport systems by using oral rehydration solutions containing both sodium and glucose to enhance water absorption in the patient with diarrhoea.

Pathophysiology

The pathophysiological mechanisms resulting in acute or chronic diarrhoea can be divided into several major groups: osmotic, secretory, exudative and abnormal motility (see Box 13.1).

Box 13.1 Pathophysiological mechanisms in diarrhoea

Osmotic (non-absorbable solute)

• Carbohydrate malabsorption

• Magnesium salts

• Malabsorption syndromes

• Post surgical, e.g. gastrojejunostomy

Secretory (impaired electrolyte transport)

• Bacterial endotoxins

• Laxatives (non-osmotic)

• Bile salts (e.g. terminal ileal resection or disease)

• Fatty acids

• Hormone-producing tumours (e.g. gastrinoma, vasoactive intestinal polypeptide)

Motility (increased transit)

• Laxative abuse

• Diabetic diarrhoea

• Thyrotoxicosis

• Irritable bowel syndrome

Osmotic diarrhoea results when a non-absorbable solute accumulates within the small intestine. The osmolality of the small intestine is adjusted to that of plasma by water influx across the small bowel and watery diarrhoea results. Examples of osmotic diarrhoea include carbohydrate malabsorption (such as lactase deficiency) and ingestion of magnesium salts. Osmotic diarrhoea ceases when the poorly absorbed solute is removed from the diet.

Secretory diarrhoea results from reduced ion absorption or increased intestinal ion secretion. Bacterial toxins are a common cause and, of these, cholera toxin has been the most intensively studied. Non-osmotic laxatives, bile salts and short-chain fatty acids are other agents than can damage electrolyte transport and result in watery diarrhoea. Hormonal secretion from tumours can also cause secretory diarrhoea (e.g. gastrin and vasoactive intestinal polypeptide).

The third main pathophysiological cause of diarrhoea is inflammatory damage to intestinal mucosal cells: exudative diarrhoea. When the large bowel is involved, blood is commonly present in the stool. Apart from invasive organisms, mucosal damage may result from inflammatory bowel disease, gluten-sensitive enteropathy and irradiation damage.

The fourth major cause is increased transit in the small bowel or colon: abnormal intestinal motility. Increased transit may occur with thyrotoxicosis (due to excess thyroid hormone), diabetes mellitus or in the irritable bowel syndrome (Ch 7).

It is common for a single agent to cause diarrhoea by more than one pathophysiological mechanism. For example, malabsorbed carbohydrates are fermented in the colon to short-chain fatty acids, which impair colonic absorption of water and electrolytes. Similarly, invasive enteric bacterial may also secrete toxins resulting in secretory diarrhoea.

Some generalisations can be made about clinical syndromes arising from different pathophysiological causes of diarrhoea. Osmotic diarrhoea will usually stop when the poorly absorbed solute is omitted from the diet. Secretory diarrhoea will usually continue during fasting and the stools are of large volume (more than 1 L). Invasive organisms will cause inflammation, which often results in blood in the stool. However, considerable overlap exists, such as when secretory diarrhoea results from laxatives. This may cease during fasting if the laxative is also omitted. Similarly, diarrhoea due to invasive organisms may begin as watery diarrhoea when the inflammation is mild.

Clinical Approach to Acute Diarrhoea

The causes of diarrhoea vary depending on the type of practice, but in all settings gastrointestinal infections are a common cause of acute diarrhoea (Box 13.2). It is clinically useful to divide acute causes of diarrhoea into clinical syndromes, watery (non-inflammatory) diarrhoea, blood (inflammatory) diarrhoea, food poisoning, diarrhoea in the traveller, diarrhoea associated with recent antibiotics or other drug use and diarrhoea in the HIV-positive (Fig 13.1) or male homosexual patient. Overlap may occur between the categories. Of course, an illness may begin as watery diarrhoea, only to progress to bloody diarrhoea later.

Box 13.2 Features favouring medically important diarrhoea

• Severe prolonged diarrhoea

• High fever/systemic toxicity

• Severe abdominal pain

• Blood in the stool

• Signs of volume depletion

• Immunocompromised host

Figure 13.1 Practical approach to HIV-associated diarrhoea.

The clinical approach to those with acute diarrhoea should focus initially on:

• separating minor from severe illness;

• selecting patients who need further investigation; and

• instituting specific therapy, where appropriate.

History

A careful history is important in evaluating patients with acute diarrhoea and in separating minor from severe illness. Features that suggest the diarrhoea may not be self-limiting include severe diarrhoea, blood in the stool, severe abdominal pain or a high fever (Box 13.2).

Ask about the duration of symptoms as well as severity. An abrupt onset of diarrhoea, which then gradually improves, suggests an infective process. Systemic features with infectious diarrhoea include fever, myalgia, malaise, nausea and vomiting. The onset of diarrhoea with food poisoning is often severe but short-lived. With prolonged watery diarrhoea, volume depletion is more likely to develop, especially when there is associated vomiting. Large volume, watery diarrhoea may be of small bowel origin. The presence of blood in the stool is usually due to an intestinal inflammatory process (see Box 13.3).

The setting in which diarrhoea occurs also provides clues as to the diagnosis. Recent travel or consumption of food eaten from fast-food outlets suggests infective diarrhoea or food poisoning, especially if other people who ate at the same time and place are affected. A drug history is important with particular attention to antibiotics (Clostridium difficile infection), over-the-counter and herbal preparations. A dietary history including dairy products (lactose intolerance) and sorbitol ingestion may be helpful.

Chronic illnesses may first present with acute diarrhoea. Recent blood diarrhoea, for example, may be the initial onset of inflammatory bowel disease.

Physical examination

The physical examination will help assess the effects of the diarrhoeal illness and may provide clues as to its cause.

Effects may include volume depletion (dry mouth and orthostatic hypertension) and signs of toxicity (high fever, tachycardia and shock).

The abdominal examination may reveal tenderness (inflammatory bowel disease or diverticulitis) a mass or visceromegaly (e.g. colon cancer deposits in the liver). The stool should be examined and the presence of blood noted. A rectal examination is mandatory and may document faecal impaction (overflow diarrhoea in the elderly) or a tumour.

Investigations

The history and physical examination will help differentiate those with minor diarrhoea from those with a more severe illness.

Those with minor resolving diarrhoea need no investigations and no specific therapy beyond maintenance of hydration. Those with features outlined in Box 13.2, where a definitive diagnosis is likely to alter management and outcome, should usually be further investigated. Those diagnostic tests should be targeted, where possible, towards a specific diagnosis according to clues from the history and physical examination.

Blood screen

A full blood count may document anaemia secondary to underlying disease or neutrophilia in bacterial infections. Atypical lymphocytes may be noted in viral illnesses. The creatinine and urea may be elevated in severe diarrhoea with volume depletion.

Stool examination

The presence of red or white cells helps to differentiate inflammatory from non-inflammatory causes of diarrhoea, although the specificity and sensitivity are variable.

Stool cultures are often useful in patients with severe or prolonged acute diarrhoea to help target those who may respond to specific antibiotic therapy.

Specific testing for various pathogens should be requested where appropriate. If the epidemiological settings suggest the possibility of C. difficile infection, a specific request for that pathogen as well as C. difficile toxin should be made. Viral cultures may need to be considered in immunocompromised patients.

Sigmoidoscopy and colonoscopy

Sigmoidoscopy and biopsy will help establish the presence or absence of colitis and histology may help differentiate between infectious colitis and an initial attack of inflammatory bowel disease. However, the two can sometimes be difficult to differentiate on histology alone.

A colonoscopy is usually not needed in the work-up of acute diarrhoea. The presence of bleeding with a normal sigmoidoscopy or the suspicion of ischaemic colitis are situations in which colonoscopy may need to be considered.

Therapy

Acute diarrhoea illnesses range from minor, self-limiting episodes of diarrhoea to devastating illnesses with overwhelming sepsis and profound dehydration. Therapy will need to be tailored depending on the severity of the illness, the nature of the underlying aetiology and the competence of the host’s defence mechanism.

Hospitalisation is usually necessary for those with sepsis or severe dehydration, and should be considered for those who have an impaired immune response.

Hydration

Maintenance of adequate hydration is the only treatment necessary for most episodes of acute diarrhoea. In the presence of nausea, this may require the frequent intake of small amounts of fluid orally. Soups and fruit juice will usually supply the sodium, potassium and glucose necessary for adequate fluid absorption. Oral rehydration solutions are available commercially or can be prescribed, and are used for mild-to-moderate dehydration. Oral rehydration solutions play an important role in developing countries where gastrointestinal infections are common and medical facilities are limited. Intravenous fluids are indicated for severe dehydration.

Diet

The tradition of limiting food during intakes of diarrhoea carries the disadvantage of restricting caloric intake during a catabolic event. Restriction of milk and milk products is usually indicated as secondary lactase deficiency may be present. Products containing sorbitol, including some fruit juices, will exacerbate diarrhoea and are best avoided. Anorexia is obviously a factor during diarrhoeal illnesses, but the maintenance of caloric intake should be encouraged.

Antidiarrhoeal agents

Agents such as loperamide and diphenoxylate are widely used for the symptomatic relief of diarrhoea. They are usually effective and have few side effects. However, they should be avoided in patients with colitis in view of the potential to cause toxic megacolon. They should also be avoided in young children as they are usually infective and may prolong intestinal recovered.

Antibiotics

Antibiotics should be avoided in the routine treatment of acute diarrhoea. They are usually ineffective in reducing the duration of the illnesses and in some cases may prolong excretion of the pathogen. They also have significant side effects and indiscriminate use will increase drug resistance. There are a limited number of situations where antibiotics may be helpful. Box 13.4 outlines the indication for antibiotics and these are discussed in more detail under disease headings.

Conditions Causing Food-borne Illnesses

Food-borne illnesses are caused by the consumption of contaminated food and result in significant worldwide morbidity and mortality. They can be caused by the consumption of bacteria or bacterial toxins, viruses, parasites or chemicals.

Clinical syndromes resulting from such diverse aetiological agents vary, but nausea, vomiting, diarrhoea and abdominal pain are common to most. Neurological, hepatic and renal syndromes may also occur. The rapid onset of symptoms (within 6 hours) suggests ingestion of a preformed toxin. A longer incubation period is associated with bacterial or viral agents.

Some of the common causes of food-borne illnesses are discussed below under aetiological headings.

Bacterial food-borne illnesses

Common causes of food-borne illnesses include Salmonella and Campylobacter species and E. coli—these are discussed later in this chapter. Other major bacterial causes of food-borne illnesses are discussed below.

Clostridium perfringens

C. perfringens is a common food-borne pathogen with an incubation period of 8–24 hours. The illness usually results from the ingestion of meat or poultry and results in watery diarrhoea and crampy abdominal pain. The symptoms are short-lived and usually last 24 hours. Symptomatic therapy with attention to hydration is usually all that is necessary.

C. perfringens may also cause a severe and often fatal illness—enteritis necroticans or ‘pigbel’—which is seen only in underdeveloped tropical countries. Abdominal pain and bloating, vomiting and diarrhoea with shock occur, usually after a feast.

Stool and food can be tested for toxin in special laboratories.

Staphylococcus aureus

Staphylococcal food poisoning results in profuse vomiting, followed by crampy abdominal pain and diarrhoea. These symptoms result from staphylococcal toxins and occur 1–6 hours after the ingestion of contaminated food. Symptomatic therapy only is necessary, with recovery occurring within 24–48 hours, although occasional deaths have been reported.

Diagnosis is clinical, but food and vomitus can be tested for toxin.

Bacillus cereus

Food poisoning with B. cereus is associated with two distinct syndromes: a vomiting syndrome and a diarrhoeal syndrome. Ingestion of a preformed toxin will result in vomiting similar to that of S. aureus lasting about 12 hours. Fried rice has been implicated as the vehicle in the majority of cases. The diarrhoeal illness occurs 6–14 hours after the ingestion of contaminated food and results from the production of an enterotoxin. Diarrhoea, crampy abdominal pain and, less commonly, vomiting last for 20–36 hours.

Vibrio parahaemolyticus

V. parahaemolyticus is associated with seafood and causes food poisoning outbreaks after the ingestion of shellfish or raw fish. It causes explosive watery diarrhoea with an incubation period of 12–24 hours. The diarrhoea may be associated with nausea, vomiting and fever and occurs in about 25% of patients. Occasionally, a dysenteric syndrome may result with blood diarrhoea. A specific request must be made to the laboratory for culturing the organism. Symptoms are generally short-lived and require no specific therapy.

Clostridium botulinum

C. botulinum produces a heat-labile neurotoxin and outbreaks of food-borne botulism have been reported from ingestion of home-preserved foods that have been improperly prepared.

Symptoms usually begin within 12–24 hours and consist of bilateral cranial neuropathy with symmetrical descending paralysis. The diagnosis is made by demonstrating the toxin in serum, stool or food ingested.

Respiratory support may be necessary and an anti-toxin that can prevent further paralysis is available. Full recovery may take months.

Non-bacterial food-borne illnesses

Buy Membership for Gastroenterology and Hepatology Category to continue reading. Learn more here

Related

Clinical Gastroenterology