Module 2 - Diseases and Malfunctions, Course 1: Overactivity of the Intestinal Tract

INTRODUCTION

Gastrointestinal hypermotility or overactivity of the intestinal tract represents a large percentage of the problems which confront the primary care practitioner in our society. The problems range from relatively mild, self-limiting to potentially life-threatening episodes.

Although the causative agent can be identified in some cases (e.g. bacterial gastroenteritis), most are due to nonspecific viral agents and/or psychogenic factors. The fact that psychologic stress is almost certainly a major factor in many of these cases makes the clinician's work much more difficult. Sometimes reassurance by the clinician is the most potent medication. The principle of primum non nocere certainly must be applied here--i.e., First, do no harm!

The treatment of G.I. hypermotility is largely that of treating symptoms rather than causes. This is an extremely important class of diseases--one which is encountered frequently, requires a keen application of problem-solving ability and which is not likely to become rare in the foreseeable future.

2.1 Overactivity of the Intestinal Tract

On completion of this minicourse you will be able to:

  1. Identify and describe the signs, symptoms, natural history and etiology of:
    1. acute gastroenteritis
      1. viral
      2. bacterial
      3. parasitic
      4. enterotoxic
    2. gastroenteritis secondary to food allergy
    3. ulcerative colitis and regional enteritis
    4. functional bowel disease
  2. Identify and describe the laboratory and x-ray investigations useful in the diagnosis of the entities listed in Objective 1.
  3. Describe the usefulness and hazards of the following classes of drugs in the treatment of gastrointestinal disease:
    1. antidiarrheal medication
    2. antibiotics
  4. Construct a treatment plan for a patient with hyperactivity of the intestinal tract which includes both parmacologic and nonpharmacologic approaches.
  5. Construct a differential diagnosis and treatment plan for a patient with hyperactivity of the intestinal tract, given signs, symptoms, Fray and laboratory data.

MINICOURSE 2.1 SECTION 1

OBJ. 1. Identify and describe the signs, symptoms, natural history and etiology of:

  1. acute gastroenteritis
    1. viral
    2. bacterial
    3. parasitic
    4. enterotoxic
  2. gastroenteritis secondary to food allergy
  3. ulcerative colitis and regional enteritis
  4. functional bowel disease

Types and Causes of G.I. Tract Hypermotility

Acute Gastroenteritis

Acute disturbances of intestinal function are common and usually manifest themselves as diarrhea. The most common cause of diarrhea in this country is an acute infectious non-bacterial gastroenteritis that usually is self-limiting and usually is viral in etiology. Its frequency is second only to that of the common cold as a cause of illness in the U. S. The greatest danger ensuing from this illness is dehydration. The younger the patient, the greater the potential danger of dehydration secondary to the loss of fluids per vomiting and/or diarrhea.

Diarrhea may be defined as frequent passage of unformed or liquid stools. Under normal conditions the large intestine resorbs liquids and electrolytes added to the stream of intestinal contents along the gastrointestinal tract. If the small intestine is performing its function normally, the fecal matter arriving at the large intestine is liquid. If stools contain 80% or more of water after passage through the large colon, they are liquid in form. The normal formed stool is usually 60-70% water by weight.

The increase in water content of diarrheas stools can be due to impaired water absorption by the intestinal mucosa or increased secretion of water by the intestinal mucosa. The mucosa of the colon has a high potential for water and sodium absorption.

Diarrhea may be enteric (small intestine) or colonic in terms of site of origin. Enteric diarrhea is characterized by large stool volume containing undigested food and is caused by impairment of digestion. Colonic diarrhea is caused by inflammation in the colon. By the time fecal matter reaches the colon the process of digestion has already been completed and the stools are smaller, do not possess undigested food components but can have evidence of inflammation, such as blood and inflammatory cells.

Acute gastroenteritis is a clinical syndrome and not a specific disease per se. The most common cause of this syndrome in the U. S. is probably viral and whereas a number of viruses that are able to replicate in the intestinal tract have been identified, the microorganisms that are responsible for the endemic as well epidemic attacks of this syndrome have eluded precise identification. Having undergone an attack of acute viral gastroenteritis can produce some immunity against reinfection with the same agent, but there are probably a large number of viruses that can produce this clinical picture and there is little heterologous immunity between the various viral agents (i.e., little or no cross immunity).

1 a-l Acute Viral Gastroenteritis

Acute viral gastroenteritis is marked by relatively sudden onset of nausea and vomiting followed by explosive diarrhea with or without abdominal cramps. Muscle aches and pains (myalgia), loss of appetite (anorexia) often accompany the vomiting and diarrhea. Fever may or may not be present and when present, is usually low grade. The vomiting and diarrhea usually subside spontaneously within 48 hours in adults. (The syndrome can last longer in young children.) The diarrhea stool in acute viral gastroenteritis consists of water and stool remnants. Blood, pus, and mucus are usually absent. The pathologic lesion in acute viral gastroenterities is located in the small intestine.

1 a-2 Acute Bacterial Gastroenteritis

Gastrointestinal infections secondary to Salmonella are probably the most common bacterial gastroenteritides in the U. S. Salmonella gastrointestinal infections, in the vast majority of cases, are transmitted from animals to man and occasionally from man to man. The high incidence of salmonella infections in those domestic animals used as a source of food for man (e.g. chickens), and the presently available bulk processing methods for food and food products can result in the availability of foods for human consumption that possess a high incidence of contamination with salmonella. Every variety of animal has the potential for infection, including pet baby chicks and pet turtles. Most nonhuman isolations of salmonellae are from domesticated fowl.

The incidence of asymptomatic carriers of salmonella in the general population is about 0.2%, but the most important reservoir is domestic and wild animal species, varying from less than 1% to more than 40%. The greatest single source of human infection in the U. S. is the vast reservoir of salmonella in lower animals. For reasons that are not yet clear, professional food handlers as a group have a fairly large percentage of carriers of this bacteria.

Salmonella gastroenteritis is usually brief, self-limiting and generally mild. There is a sudden onset of colicky abdominal pain and loose watery stools which occasionally contain mucus and/or blood. Nausea and vomiting can occur, but are usually of short duration and not severe. Patients usually have some abdominal tenderness on palpation and fever of 38-39 degrees C is common. There is usually hyperactive peristalsis. The symptoms usually subside promptly and uneventfully in 2-5 days.

The stools of a patient with salmonella gastroenteritis are usually loose, slimy, green and smell like rotten eggs. If the infection is more severe, a disruption of the intestinal mucosa can occur with necrosis and ulceration. When this degree of infection is present there can be blood and pus in the stool. Salmonella primarily affects the small intestine, producing edema and inflammation.

Shigellosis, frequently referred to as bacillary dysentery, is another cause of acute bacterial gastroenteritis. The natural disease is limited to man and the asymptomatic carrier or convalescent shigella patient are the only recognized reservoirs. The spread occurs from man to man primarily when organisms from infected feces (deposited on hand or inanimate objects) are ingested. In the U. S. common source outbreaks usually involve food which has been contaminated by careless food handlers.

The major clinical features of shigella gastroenteritis are diarrhea, abdominal pain and fever. The first symptom is typically colicky abdominal pain followed shortly by diarrhea and high fever. Nausea, vomiting, headache and myalgia can be present. The lower abdomen can be tender on palpation and the bowel sounds are hyperactive. As with salmonella gastroenteritis there is a significant group of patients who have mild diarrhea or are asymptomatic. The stools are watery, relatively odorless, contain mucus shreds, are green in color, and in 20-30% of patients contain varying amounts of gross blood.

The major pathologic feature is the presence of mucosal inflammation which involves the entire colon and can extend into the terminal ileum. Changes are most pronounced in the rectum and sigmoid and consist of diffuse swelling and petechial hemorrhages in mild cases. A fibrinous exudate often develops and necrosis of the mucosa can occur which leads to shallow ulcers which bleed readily, thus accounting for the blood in the stool often seen in this disease.

OBJECTIVE 1 Questions

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1. What is presumably the most common cause of acute gastroenteritis in the U. S.? How common is this disease relative to other diseases?

2. What is the great potential danger ensuing from acute gastroenteritis of the type described in Question 1?

3. How much water is there in a formed stool? In a diarrhea stool?

4. Name two mechanisms that could explain the increase in water content of diarrhea stools.

5. Name the clinical features if acute infectious nonbacterial gastroenteritis.

6. Describe the typical contents of the stool in acute nonbacterial gastroenteritis.

7. What are the two most common bacterial gastroenteritides in the U. S.?

8. How are salmonella infections transmitted?

9. Name the greatest single source of human salmonella infections in the U .S .

10. Describe the clinical features of acute salmonella gastroenteritis including a description of the stool.

11. What is the distinction pathologically between salmonella gastroenteritis and Shigella gastroenteritis in terms of the intestinal area involved?

12. How does the gross appearance of the diarrheal stools differ in patients with shigellosis from those with salmonellosis?

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l a-3 Acute Parasitic Gastroenteritis

Among the many parasites isolated from patients in this country, the two most important clinically in terms of gastroenteritis are Giardia lamblia and Entamoeba histolytica. Giardiasis is acquired through the ingestion of cysts of the parasites which are passed in human feces and usually spread through the imbibing of contaminated water and only rarely in food. The disease can also be transmitted by hand to mouth transfer of cysts from the feces of an infected individual.

Many infected patients are asymptomatic, but the most consistent clinical presentation in symptomatic patients is anorexia, nausea, a sensation of gastric fullness and watery diarrhea. In a significant number of patients the diarrhea becomes chronic on an intermittent or continuous basis resulting in weight loss, abdominal distention, flatulence, pale bulky malodorous stools and malabsorption. Giardiasis is a disease of the small intestine; mucosal invasion is the cause.

Amebiasis is a disease of the large intestine caused by an invasion of Entamoeba histolytica into the submuco6a. The infection may be entirely asymptomatic, or chronic, or presenting with mild abdominal discomfort and diarrhea alternating with constipation, or the presentation may be in the form of acute diarrhea. The acute form, referred to as acute amebic dysentery, is characterized by diarrhea with profuse blood and mucus and small amounts of pus. Tenesmus (cramping pains in the left lower quadrant with straining and ineffectual evacuation of the colon) and abdominal pain are common findings in the acute form. (Note: Tenesmus is also characteristic of ulcerative colitis, which must be ruled out.) There may be tenderness over the caecum, ascending colon and sigmoid.

Cases of amebic dysentery are usually sporadic, but epidemics (sometimes waterborne) do occur. Outbreaks of this disease are usually not explosive as are those produced by pathogenic intestinal bacteria such as Shigella. The cyst of the ameba is the infective form. Man passes cysts in his stools and transmission occurs by the ingestion of food or water contaminated by human fecal matter.

1 a-4 Acute Enterotoxic Gastroenteritis

Bacterial enterotoxemia, commonly referred to as food poisoning, is considered by some authorities to be a relative medical emergency, as the consequences can be lethal. Enterotoxins, which cause the most common types of food poisoning cases reported in the U. S., often occur after social events, such as picnics, where food is prepared in advance in an effort to serve a substantial number of people. Bacterial enterotoxins are substances produced by the bacteria. Thus, the toxins are responsible for the signs and symptoms of the disease. Unlike bacterial gastroenteritis, mucosal invasion is n the cause.

One of the most common forms of food poisoning is due to the enterotoxin produced by staphylococci. The symptoms are quite acute and begin approximately within 4-6 hours of the ingestion of food contaminated by the staphylococci. The clinical features consist of sudden intense nausea followed by explosive vomiting and intense abdominal cramping. Diarrhea also occurs but is less intense than the episodes of repeated vomiting. Anorexia occurs. The diagnosis can be based on the short duration of symptoms, the lack of fever and the epidemic involvement of the disease. This is a disorder of the small bowel.

The foods that seem to be involved quite often in this disease are custards, mayonnaise, cream filled pastries, milk products and whipped cream.

Another relatively common cause of food poisoning is the enterotoxin produced by a bacterium known as Clostridium perfringens. This type of bacterial enterotoxemia typically involves the ingestion of food that has been prepared and cooked 24 or more hours before consumption and allowed to cool slowly at room temperature and then served either cold or warm. Clostridial enterotoxins are most commonly found in meat products, usually from beef or turkey products.

The usual clinical picture is as follows: clostridium perfringens food poisoning begins 8 to 24 hours after ingestion of the contaminated food and consists of abdominal pain, abdominal cramps and profuse diarrhea. The diarrhea may be followed by tenesmus. Anorexia is likely to occur. Nausea is an occasional symptom but vomiting is not common, unlike staphylococcal food poisoning.

There are other types of food poisoning, of course, but the two mentioned in this minicourse are both relatively common. In both instances the disease is usually benign and self-limited, but can be extremely serious and even lethal in elderly patients or patients with cardiovascular disease, as the enterotoxemia can be severe enough to result in hypotension.

l-b Food Allergy

Allergies to food can cause hyperactivity of the gastrointestinal tract, but are often difficult to document because proper objective tests are lacking. Skin testing, useful in the detection of certain inhalant allergy syndromes (e.g. hay fever, bronchial asthma) are of little or no value in the specific etiologic diagnosis of food allergies.

Gastrointestinal symptoms caused by food allergies include diarrhea, abdominal distention, abdominal pain, vomiting, and flatulence. The symptoms may range from mild cases where nausea, diarrhea, and abdominal discomfort are present, to severe cases marked by forceful vomiting, severe abdominal colic, bloody and mucoid diarrhea and dehydration. Prolonged episodes of gastrointestinal food intolerance can lead to malnutrition.

Milk is the most common food allergen, but other common food allergens include wheat, apple, egg, tomato, foods in the pea family, corn, citrus fruit and chocolate. Some patients can ingest a food allergen once a week or so and experience no symptoms, other patients can react to the ingestion of even a small amount of the offending allergen.

Because objective tests for the specific diagnosis of food allergens are lacking, one must rely on the patient's history and food diaries to identify offending foods.

l-c Ulcerative Colitis

Ulcerative colitis is a diffuse acute and chronic inflammatory disease of unknown origin which involves a part or all of the colon. The disease may arise suddenly or insidiously and the patients involved may experience spontaneous remission or relapses. Ulcerative colitis can occur at any age, but occurs most frequently in young adults. The incidence is slightly higher in women and in northern climates and in urban areas. The disease is more common in the better educated groups and there is a positive family history in 5-10% of the patients.

The major clinical manifestations of ulcerative colitis include diarrhea, rectal bleeding, abdominal pain, fever and weight loss. Other clinical features that may occur are tenesmus with small "squirts" of bloody mucus, nocturnal defecation and stool incontinence. The bloody mucus "squirts" are distinctive for this disease, although this condition also occurs during acute amebic dysentery. Ulcerative colitis is primarily an inflammatory disease of the mucosa of the colon and affects the rectum and left side of the colon most severely.

The course of the disease varies from very mild where the patient complains of slight blood-staining of the stool without any systemic symptoms to the severe fulminating variety which if not interrupted may be fatal. The average patient with ulcerative colitis experiences increasing diarrhea until 5-10 liquid stools are passed each day and there is an associated loss of appetite, loss of weight, abdominal cramps, weakness and anemia. Examination of the stools reveals the presence of mucus, pus, and blood with little fecal matter. The diagnosis of ulcerative colitis should be entertained where there is sudden onset of persistent diarrhea and the stool contains mucus, pus and blood with little fecal matter.

Regional Enteritis

Regional enteritis is an inflammatory disease of the intestinal tract that is referred to in the literature by a variety of names such as regional ileitis, transmural colitis, granulomatous colitis and Crohn's disease. Like ulcerative colitis, the cause is unknown. Although this disease occurs most commonly in the terminal ileum, it occurs often in the colon and can produce identical lesions from the stomach to the anus.

This disease is approximately one-third as common as ulcerative colitis and although it can affect any age group the peak incidence is between 15 and 35 years of age. The sexes are affected equally. The patients commonly have urban backgrounds, are better educated and have a slightly higher economic status than the average person.

The most common clinical presentation of regional enteritis consists of diarrhea, colicky abdominal pain and weight loss. As with ulcerative colitis, the symptoms vary. Some patients present clinically with the systemic features of fever of unknown origin. Careful data collection of such patients will often reveal some abdominal discomfort, some loose stools, tenesmus, mild anorexia and a complaint of abdominal discomfort which increases after eating. Other patients with this disease present more acutely with sudden development of right lower quadrant pain and tenderness and fever plus either diarrhea or constipation.

In patients with the more chronic form of the disease there is evidence of perianal disease such as pertrectal or ischiorectal fistulae (a fistula is an abnormal passage between two organs or passage between internal organ to body surface), strictures of the bowel, and malnutrition. A "doughy" mass is often palpable in the ileocaecal area (i.e. in the right lower quadrant) that is actually aggregated loops of small bowel.

Ulcerative colitis and regional enteritis are the two most important nonspecific chronic GI inflammatory disorders - both can produce the prominent symptoms of diarrhea, abdominal cramps and fever. Thus, the patient's history of these complaints cannot always help you to distinguish them. Some of the clinical findings that can help you to differentially diagnose the two conditions are as follows:

  1. Rectal involvement occurs in nearly all patients with ulcerative colitis, but in only 20% of those with regional enteritis.
  2. In ulcerative colitis the inflammation generally is superficial, involving the mucosa and submucosa only. In regional enteritis (granulomatous colitis) the inflammation involves all the layers.
  3. Cancer of the colon is relatively common in patients with ulcerative colitis and uncommon in granulomatous colitis.
  4. Gross blood in the stools is extremely common in ulcerative colitis. In regional enteritis rectal bleeding occurs in a minority of the patients and is usually mild and intermittent. The absence of gross blood in the stool in a patient with chronic diarrhea should suggest a diagnosis other than ulcerative colitis.
  5. Perianal fistulae and internal fistulae are uncommon in ulcerative colitis and quite common in granulomatous colitis.
  6. Strictures of the bowel are common in granulomatous colitis and rare in ulcerative colitis.
  7. Ulcerative colitis more commonly affects the rectum and left side of the colon more severely, affecting the entire bowel circumference and producing continuous lesions. Grarulomatous colitis, on the other hand, commonly affects the right side of the colon, sometimes affecting one wall of the intestine, leaving the opposite intestinal wall normal and producing patchy lesions in such a way that diseased segments of the bowel alternate with normal segments (skip lesions).

l-d Functional Gastrointestinal Disease

Functional gastrointestinal disease encompasses a variety of complaints in which no gross organic lesions can be found and the clinical manifestations are probably the result of altered physiological mechanisms. These disorders comprise an estimated 3050% of all the gastrointestinal illnesses that a primary care physician is confronted with. There is at present a rather sharp Limitation in the knowledge of the exact pathophysiology of functional gastrointestinal complaints.

The complaints referable to the G.I. tract offered by patients with this problem range from anorexia, eructation (belching), nausea, a variety of epigastric sensations such as burning (pyrosis), fullness, "gas" pressure and post-prandial feeling of fullness to constipation, abdominal distress and diarrhea. Such complaints are thus referable to both upper and lower G.I. tracts.

The symptoms are varied, but functional disorders of the upper G.I. tract have features in common. These clinical manifestations such as anorexia, nausea, and sense of fullness are vague as defined by the patient when a history is elicited. Although the patient expresses many complaints, he nevertheless presents a healthy appearance and has expressed the same complaints or similar complaints for many years. Physical examination can reveal abdominal tenderness which is quite variable in location. In children functional abdominal complaints are the overwhelming major cause of chronic and recurrent abdominal pain and are usually referable to the periumbilical area due to the embryologic development of the nerve supply to the intestines.

The functional lower abdominal disorders are classified and discussed in the literature on the basis of their more obvious clinical manifestations or their suspected but unproved etiologies. The most prominent of these lower G.I. disorders is the irritable bowel syndrome (IBS) also known as spastic colitis or mucous colitis. This syndrome is characterized by diarrhea, constipation or both alternatively, and feelings of "abdominal distress" which can occur in such varied presentations as postprandial fullness, dull nondescript discomfort in the left lower quadrant of the abdomen or severe cramping abdominal pain. The cramping abdominal pain may be generalized in both lower quadrants or on occasion be localized in the right or left upper or lower quadrants giving rise to difficulties for the examiner in terms of differential diagnosis of other more potentially serious diseases. The pain is usually crampy in character and may last from minutes to hours. Relief of pain with stooling is not universally observed, but when present, is fairly characteristic. All the above complaints are usually of a chronic nature.

There are some historical markers that are not characteristic of IBS. The description of any of these abnormalities should prompt an aggressive evaluation for alternative explanations for the patient's complaint. Such features include: 1) the recent onset of symptoms in an elderly patient; 2) pain unassociated with a change in bowel habits; 3) nocturnal awakening with symptoms; 4) fever, bloody stools, weight loss, and other manifestations of something more than a motility disorder.

Constipation is another frequent complaint of patients with functional G.I. disease and is characterized by the passage of small mucous-covered scybala (plural of scybalum - hard dried mass of fecal matter). Alternating diarrhea and constipation is common with this syndrome. Some patients have continuous or intermittent diarrhea as the only complaint. Such diarrhea can persist for months or years and yet is rarely associated with weight loss.

Other associated gastrointestinal symptoms are passage of excessive gas and mucus per rectum, abdominal rumbling and gurgling, belching, and vomiting (not common). Many patients with functional G.I. complaints have other symptoms of a presumably functional nature such as weakness, nervousness, palpitation, headache and insomnia. Physical examination of patients with lower abdominal disease of a functional nature can reveal tenderness over such areas as the sigmoid colon, or distention of the caecum, but usually the physical examination is otherwise within normal limits.

Functional gastrointestinal abnormalities may be regarded as aberrations of the secretory activities or motor activities (or both) of a gastrointestinal segment. In functional upper G.I. complaints, for instance, it is probable that abnormal gastric tone and incoordination of the gastroduodenal emptying mechanism are responsible for increased intramural tension which in turn causes gastrointestinal distress in the absence of morphologic change.

It is generally agreed that the symptoms of irritable bowel syndrome (IBS) can be attributed to colonic motility abnormalities. Thirty years of colonic motility research has failed to consistently back up this assumption. Another whole theory is that the etiology of IBS is psychogenic or emotional. Clinically this theory is substantiated by the observation that the symptoms often occur during times of stress or anxiety and are often relieved by only reassurance from a single compassionate health provider. The results of recent studies comparing IBS patients and normal individuals in their reaction to stress and these same two groups response to psychotherapy vs. normal management seem to give us this message. Psychological factors are not the root cause of gut dysmotility, but rather modify behavior of the organ. This can occur whether the gut is normal or not. In the case of a malfunctioning intestine, emotional or psychological events will often exaggerate the underlying malfunction.

Another possibility is that these patients may have a low visceral pain threshhold. They may be aware of or more sensitive to contractions and fecal movement than non-IBS individuals.

Functional gastrointestinal complaints are common, vague, varied in presentation, often perplexing in differential diagnosis and as yet have no explanation that can be proven. It is a great problem of immense scope and is responsible for a good deal of the primary health care practitioner's time and energy. The physician extender must take interest in this common problem and not treat these patients as "malingerers," "crocks," "turkeys," etc. These patients suffer even though the cause of their suffering is not readily demonstrable.

OBJECTIVE 1 Questions

13. Name the two most common parasites in the U.S. in terms of gastroenteritis.

14. What part of the intestine is involved in giardiasis and how is the disease usually acquired?

15. What part of the intestine is involved in amebiasis and how is the disease acquired?

16. By what common name is bacterial enterotoxemia known and what are the two most common causes in this country?

17. Contrast the clinical features of these two enterotoxemias.

18. Contrast the pathophysiological difference between bacterial gastroenteritis and bacterial enterotoxemias.

19. What is the most common food allergen and what are some common symptoms produced by food allergens in terms of the gastrointestinal system?

20. Describe the "typical" patient with ulcerative colitis in terms of risk factors.

21. Describe the major clinical manifestations of ulcerative colitis.

22. Name some of the synonyms by which regional enteritis are referred to in the literature.

23. What are some of the common clinical features of regional enteritis?

24. What is meant by the term functional gastrointestinal disease?

25. Contrast ulcerative colitis and granulomatous colitis clinically. Click here to go to the Answer Page

Section 2
OBJ. 2. Identify and describe the laboratory and x-ray investigations useful in the diagnosis of the entities listed in Objective 1.

Laboratory Approaches to G.I. Overactivity

2 a-l Acute Viral Gastroenteritis

The microorganisms that cause acute infectious nonbacterial gastroenteritis are probably viruses that replicate within the human gastrointestinal tract. These agents have not yet been cultivated in vitro nor have they been fully characterized. This illness has been transmitted experimentally in man by bacteria-free stool filtrates obtained from patients infected with acute gastroenteritis.

The stool in viral gastroenteritis never contains any recognizable exudate. It is free of inflammatory cells, blood or fibrin. Culture of the stool is usually non-productive. In individual cases of gastroenteritis isolation of a specific virus on stool culture does not necessarily mean that the agent has caused the illness since a considerable percentage of asymptomatic individuals will grow out the same virus from their stools.

Thus, while a number of viruses possessing the ability to replicate in the intestinal tract have been identified, the microorganisms responsible for the endemic and epidemic (often seasonal) bouts of gastroenteritis have so far eluded identification. In addition, viral culture is time consuming and relatively expensive. By the time the viral agent is identified in an individual patient, the patient is usually over the illness.

The CBC of a patient with acute nonbacterial gastroenteritis is usually normal. X-rays are also of no value in the diagnosis of this disease.

2 a-2 Acute Bacterial Gastroenteritis

The major diagnostic tool in the diagnosis of Salmonella gastroenteritis, after a complete history and physical are obtained, are stool cultures for the purpose of identifying the causative bacterial pathogen. If a stool sample is not readily available, a rectal swab may be obtained and the contents cultured. Stool cultures usually become negative for the Salmonella organism within one week to a month, but on occasion some patients, even though asymptomatic, can excrete the organism for months - so called asymptomatic carriers. The organism can often be cultured from the suspected contaminated food.

Agglutination tests with acute convalescent sera from patients with Salmonella are not very helpful in the diagnosis.

The peripheral white blood count in patients with salmonella gastroenteritis is usually normal. Bacteremia can occur with the disease and all patients suspected of having blood stream invasion by salmonella should have blood cultures. Blood cultures are usually normal when the salmonella only involves the gastrointestinal tract. X-rays are of no help in the diagnosis of this disease.

The definitive diagnosis of gastrointestinal infections due to shigella depend on isolation of the organism from stool cultures or rectal swab. Shigella organisms survive for only a short time in the stool and, therefore, fresh stool specimens are required for culture. Agglutinating antibodies can be detected in a majority of the patients with this disease, but serologic tests are generally of little or no value in the diagnosis of shigellosis. The peripheral blood leukocytes are usually within normal limits. Anemia is uncommon as are positive blood cultures. X-rays are of no value in the diagnosis of this disease.

Although not specific, demonstration of leukocytes in a smear of the patient's stool or of mucus obtained on rectal swab gives an indication of bacterial etiology to the gastroenteritis as opposed to viral gastroenteritis where leukocytes are generally not found in the stool.

A rapid method of distinguishing the presence or absence of a bacterial etiology in patients with gastroenteritis involves the demonstration of leukocytes in a smear of a patient's stool or of mucus obtained from a rectal swab. The presence of leukocytes on such a smear gives an indication of a bacterial etiology of the gastroenteritis. Gastrointestinal infections due to presumed viral etiologies are not associated with inflammatory cells in the stool. Enterotoxemias (food poisoning) such as those due to Staphylococcus aureus or Clostridium perfringens are not characterized by inflammation of the bowel and, therefore, white blood cells are not found in the stool. Invasive bacterial infections of the bowel such as salmonellosis and shigellosis are associated with leukocytes in the stool. These infections produce an increase of polymorphonuclear leukocytes in the stool.

Stools from patients with shigellosis are characterized by large numbers of WBCs in the stool (greater than 50 per high power field), more than 80X of which are polymorphonuclear leukocytes (sometimes band forms are present). In patients with salmonellosis the total white blood count on stool examination is lower than in shigellosis and there is a greater proportion of mononuclear cells (approximately 25z). Patients with inflammatory diseases of the bowel due to noninfectious causes, e.g. ulcerative colitis and regional enteritis, also have an increase in polymorphonuclear leukocytes in their stools, but often have esoinophils among the fecal leukocytes.

This test is rapid and simple and merely requires one to place a small amount of mucus obtained from a rectal swab (or stool) on a glass slide and add methylene blue stain. Wait two to three minutes and examine the slide under low power to note the presence of white blood cells and then under high power to do a differential white cell count. (In searching for eosinophils, Wright's stain is needed.)

2 a-3 Acute Parasitic Gastroenteritis

The diagnosis of giardiasis is sometimes made by identifying the characteristic cysts or trophozoites in a stool specimen. A cyst is a non-motile stage of the parasite which is protected by a wall. It is in this stage that the parasite is readily transmitted to a new host. A trophozoite is the motile stage of the parasite which feeds, multiplies and maintains the parasitic colony in the host.

Several daily stool specimens should be obtained and this serial stool examination may increase the Jikelihood of finding the organism. However, giardia lamblia is not found by stool examination in 50% of symptomatic patients. Diagnosis can also be made by finding cysts or trophozoites in the duodenal fluid. The organism can also be found in the biopsied duodenal mucosa. Probably one of the most reliabJe methods involves examination of fluid aspirated from the duodenum. The most reliable method of diagnosis in giardiasis involves examination of a smear of the biopsied duodenal mucosa stained by Giemsa solution. This latter method should only be utilized if simpler methods fail to yield the organism and the diagnosis is still suspected.

Intestinal amebiasis should be considered immediately when patients present with colonic complains, especially bloody diarrhea, so that appropriate specimens can be obtained before any procedures are performed or medications are given that might alter diagnosis.

Peripheral blood counts and x-rays are of no help in the diagnosis of giardiasis.

The diagnosis of gastroenteritis due to Entamoeba histolytica is best established by identification of the tropozates or cysts of the ameba in the patient's stool. The stools are best examined fresh. Serial samples of stool should be analyzed to increase the likelihood of finding the organism. If stool samples are negative for ameba and the diagnosis is still suspected, one can resort to sigmoidoscopy which permits direct aspiration of the material from areas of inflammation or ulceration. Rectal swabs using cotton strands should not be used because the strands in the specimen can obscure the amebae.

Serologic tests are positive in a great majority of patients with acute amebic dysentery, but because significant antibody titers can persist for months or years after complete cure, this method is of more value in excluding the diagnosis of amebiasis than in confirming it.

The total white blood counts in patients with acute amebic dysentery may be normal or moderately elevated. X-rays are not of much help in diagnosing the average patient with acute amebic dysentery.

2 a-4 Acute Enterotoxic Gastroenteritis

The diagnosis of food poisoning due to staphylococci generally depends on a careful history of food intake and epidemiologic investigation. The diagnosis is based on such features as a short incubation period, short duration of symptoms, lack of fever and the epidemic nature of the syndrome. The exact etiology can only be established if samples of the ingested contaminated food can be shown to contain large numbers of enterotoxin producing staphylococci. This disease should be distinguished from staphylococcal enterocolitis. In the latter disease, there is actually a proliferation of viable staphylococci in the intestine. CBCs, stool cultures and x-rays are of no help in the diagnosis of staphylococcal food poisoning.

The diagnosis of Clostridium perfringens food poisoning also depends on history of food intake and epidemiologic investigation. The disease is usually so benign and self-limiting that laboratory investigations are usually not performed. However, exact etiologic diagnosis depends on the identification of the enterotoxin in samples of the contaminated food. Other laboratory tests and x-rays are of no value in diagnosis.

2-b Food Allergy

The laboratory findings in gastrointestinal symptoms due to food allergies are meager. Eosinophils in the stool mucus can be present but this is not diagnostic; blood eosinophilia can also be present. Extracts of food can be used for skin testing, but it is preferable to diagnose food allergies by history and by elimination diets. Skin testing for food hypersensitivity is generally of little or no value as these tests are not very accurate. Patients can have a positive skin test to a food that causes them no difficulty and vice versa.

OBJECTIVE 2 Questions

1. What is the value of obtaining a stool culture on a patient with acute nonbacterial gastroenteritis? What are the usual CBC results in such patients?

2. What is the major diagnostic tool in the diagnosis of bacterial gastroenteritis?

3. Discuss the value of fecal leukocyte examination in the diagnosis of acute bacterial gastroenteritis.

4. Discuss methods of diagnosing giardiasis. What is the most reliable method?

5. What is the best practical method of diagnosing gastroenteritis due to Entamoeba histolytica?

6. Describe a method for the exact etiological diagnosis of a bacterial enterotoxemia.

7. What is the value of skin testing patients with suspected food allergy?

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2-c Ulcerative Colitis and Regional Enteritis

The most important tools in the diagnosis of ulcerative colitis, after a thorough history and physical examination, are sigmoidoscopy and barium enema. The sigmoidoscopy is probably the most important procedure in the diagnosis of this disease. Ninetyfive percent of patients with ulcerative colitis have involvement of the rectum. The typical sigmoidoscope findings are loss of the normal mucosal vascular pattern, edema and ulceration of the mucosa, friability of the mucosa upon swabbing, a purulent mucosal exudate which, when swabbed, reveals a bare, bleeding mucosa and strictures inside or above the anal canal. Proctosigmoidoscopic biopsy allows confirmation of the inflammatory process.

The barium enema is a very important part of the diagnostic work-up of patients with ulcerative colitis. This study can reveal straightening and shortening of the rectosigwoid and sigmoid area with a very symmetrical involvement of the bowel wall with small ulcerations, a loss of the normal haustral markings and a "lead pipe" appearance of the descending colon. click on the skull to see a barium study
The most significant diagnostic features on barium enema are the continuous involvement, the symmetrical abnormal appearance of the bowel wall and the visualization of inflammatory polyps when they are present. Lesions are mainly in the left colon. Colonoscopy may be used to provide more direct evidence of proximal colon involvement.

The laboratory findings in patients with ulcerative colitis are nonspecific. It is common for patients with this disease to have an anemia which is due to a combination of iron deficiency and chronic inflammation. Leukocytosis with an increase of polymorphonuclear leukocytes is frequent. There is often hypoalbuminemia and an elevated sedimentation rate.

Barium x-ray studies are the major diagnostic tool in the diagnosis of granulomatous colitis (regional enteritis). In this disease barium studies reveal "skip" areas rather than continuous involvement, fistulae, strictures of the bowel wall, coarse mucosal ulcerations and usually noninvolvement of the rectum. One of the characteristic x-ray findings is known as the "cobblestone" appearance; this is due to the fact that in granulomatous colitis the mucosa between intersecting linear and transverse ulcers resembles cobblestones when visualized on x-ray. In this disease the x-ray abnormalities are often on the right side of the colon.

Proctosigmoidoscopy can be of help in diagnosis in some patients in granulomatous colitis. The finding of normal rectal mucosa increases the probability of granulomatous colitis. A proctosigmoidoscopic biopsy can be of help also. If granulomatous tissue is obtained on biopsy, it allows the unequivocal diagnosis of granulomatous colitis. Colonoscopy is very helpful to establish the presence of proximal colon involvement.

Laboratory investigation of patients with regional enteritis will often reveal the extent of the disease. Thus, the inflammation can produce leukocytosis and an elevated sedimentation rate; the blood loss secondary to the ulcerations can cause iron deficienev anemia; the continual leak of albumin from the blood leads to hypoalbuminemia. None of these tests are diagnostic for the disease, however.

2-d Functional Bowel Disease

Functional bowel disease, such as the "irritable bowel syndrome" can be frustrating diagnostically. Most of the time the diagnosis can be made from the history and phvsical examination. The diagnosis should probably be made on the clinical presentation, but to arrive at an accurate and final diagnosis on initial encounter is not realistic. Time is necessary for the patient and clinician to establish a trusting relationship. This is important so as to allow for expression of social and other aspects of the patient's Wife which may be causing stress or anxiety to adversely affect their gut.

Initially a CBC, SMAC and urinalysis should be obtained. In young patients (under 40) , the major diagnostic consideration is inflammatory bowel disease. If the physical examination, sigmoidoscoDv. and laboratory tests are all normal, it is verv unlikely that a serious underlying condition exists, so it is reasonable to postpone anv additional work-up at this point. Adequate follow-up should be provided. In the presence of anemia, hemocult positive stools, or signs and symptoms of systemic disease, then a more aggressive evaluation is appropriate. The older patient (over 40! is at greater risk for harboring an occult neoplasm. At least one air contrast barium enema is called for. A fo]low-up procedure is reouired if a significant abnormality exists or if there is a strong familv history of colonic career. Repeat examination is also needed if the patient's symptoms chance significantlv regardless of the normalev of the initial examination. Also, Just as with the vounger patient, the presence of abnormal lab tests dictate the need for more in-depth evaluation.

It is important to remember that the examining clinician is usuallv dealing with ill-defined symptoms that could arise from any source. It is quite possible to overlook, or miss outright, serious underlving problems. Keep the lines of communication open with the patient and be Prepared to improvise additional diagnostic maneuvers as needed.

Questions:

8. Discuss the two tools most useful in the diagnosis of ulcerative colitis (outside of the history and physical examination) and discuss the typical findings of each.

9. What are the typical barium enema findings in a patient with granulomatous colitis?

10. What laboratory and/or x-ray studies are diagnostic of functional bowel disease?

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MINICOURSE 2.1 SECTION 3

OBJ. 3. Describe the usefulness and hazards of the following classes of drugs in the treatment of gastrointestinal disease:

a. antidiarrheal medication

b. antibiotics

The Pharmacology of G.I. Hvpermotility

The treatment of diarrhea is predominantly based on removal of the causative factors or agents, along with the proper replacement of fluids and electrolytes. Also, certain compounds can be administered which either decrease gastric motility or absorb excess water in the bowel. Both of these actions tend to decrease the loss of water and electrolytes associated with diarrhea. One should remember, however, that pharmacologic management of diarrhea gives only symptomatic relief and does not remove the causative agent. In addition, patients that use these compounds without reporting it to the physician are complicating efforts for detecting and correcting the underlying cause.

The opiate drugs, such as paregoric (camphorated tincture of opium), codeine sulfate and diphenoxylate (Lomotil) have been used for symptomatic relief of diarrhea. These drugs do decrease gastrointestinal motility and, therefore, allow more time for reabsorption of water from the fecal material. However, one must remember that, as with all the other effects of opiates, a tolerance to the antidiarrhea action occurs with a resulting decrease in effectiveness. In addition, the opiates may produce acute pancreatitis.

The antispasmodic drugs (anticholinergic agents) have also been used in the treatment of diarrhea. As with the opiates, these drugs act to increase the duration of time that the feces spends in the bowel, thus allowing an increased reabsorption of water. This action tends to firm the stools and, therefore, combats the diarrhea.

Certain hydrophilic substances have been used in the therapy of diarrhea. The most notable of the hydrophilic substances is psyllium seed. This preparation tends to absorb the excess water in the bowel and form a gelatinous mass. There is little hazard associated with the use of these agents. However, their relative effectiveness is questionable.

Finally, some drugs are designed to decrease the irritation which causes G.I. hypermotility and diarrhea. Bismuth, calcium and magnesium sulfate are felt to have demulcent activity (remove irritation). Absorbants, such as activated charcoal, actually absorb irritants and excess mucous secretion.

Antibiotics

Antibiotic drugs are rarely used in the treatment of gastrointestinal infections. They have at least two effects on the gastrointestinal system: they may alter the bacterial flora and/or have a direct toxic effect.

Alterations in the pathogenic bacterial flora are desirable in the therapy of gastrointestinal infections. However, antibiotics can alter normal bacterial flora when given orally for a desired effect at an extra-G.I. location. Alterations in the normal gastrointestinal bacteria content can cause a wide variety of problems including diarrhea and inefficient absorption of nutrients.

Some antibiotics can be given that are not well absorbed orally. This type of agent is used to specifically treat infections localized within the G.I. tract. Drugs such as neomycin (gram + or -), kanamycin (gram + or -) and certain sulfonamides have been used for this purpose.

EXERCISE 3 OBJECTIVE 3 Questions

1. State the mechanism by which each of the following drugs acts as an antidiarrhetic:

  1. Diphenoxylate
  2. Psyllium seed
  3. Magnesium salts
  4. Atropine (anticholinergic)

2. What are the possible detrimental effects on the gastrointestinal tract associated with the use of antibiotics?

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MINICOURSE 2.1 Section 4

OBJ. 4. Construct a treatment plan for a patient with hyperactivity of the intestinal tract which includes both pharmacologic and nonpharmacologic approaches.

Treatment Plans for Hypermotility

4 a-l Acute Viral Gastroenteritis

The treatment of patients with hyperactivity obviously depends on the etiologic diagnosis, the age of the patient, the extent of the illness, the presence of complications and the presence of concomitant diseases. It is also fairly obvious that the exact etiologic diagnosis of a particular hypermotility state of the intestine as manifested by diarrhea is sometimes difficult to obtain.

When confronted by a patient with diarrhea, one needs to gather preliminary data in an effort to properly diagnose and thus manage the patient's disease. Realizing that, far and away, acute nonspecific gastroenteritis, usually viral in origin, is the most common cause of acute diarrhea. One needs to know: What types of illness are present in the community to which this patient has been exposed? Are others in the family ill? What about coworkers? Has the patient traveled recently? Where? Are the diarrheal stools alike in terms of color, frequency, amount, presence or absence of associated symptoms such as vomiting, fever, weakness, and abdominal pain? Is there any history of attempted self-medication?

The essence of treatment for patients with acute viral gastroenteritis is to: 1) allow the mucosa of the bowel to regenerate, i.e. put the intestine to "rest"; and 2) replacement of lost water and electrolytes to prevent dehydration. Most cases of acute diarrhea are self-limiting and fluid, electrolyte loss and renal impairment is minimal in such cases and can be managed simply. It must be mentioned that children dehydrate much quicker than adults. Children dehydrate more quickly because of their greater proportion of water to body weight, their high ratio of body surface area to mass and the consequent greater proportion of insensible water loss, and their more rapid turnover of body fluids and higher metabolic rate.

Vomiting often accompanies acute nonspecific gastroenteritis and is usually self-limiting, but if vomiting becomes persistent, its presence increases the potential for dehydration and precludes the oral treatment of diarrhea. Suggested remedies for emesis include the administration of ice chips, Coca- Cola syrup, or Emetrol or the administration in more recalcitrant cases of antiemesis per rectum or parenterally.

Antibiotics should not be administered to patients with acute nonspecific viral gastroenteritis as they are not indicated in viral illness and can actually be harmful by altering fecal flora and irritating the intestinal mucosa.

The most commonly used medications for diarrhea are those containing kaolin or opiates. Kaolin, pectin and activated altapulgite preparations are designed to thicken the intestinal contents by absorbing water giving bulk to the stools and diminishing diarrhea. These preparations have never been proved to be effective, however, in reducing the amount of stool water loss or improving the symptoms or shortening the course of the disease.

Opiates act directly and rapidly on the smooth muscle of the colon and small intestine. These medications decrease peristalsis, inhibit propulsive movements and increase segmentation and tone (spasm) and, therefore, allow much time for intestinal water absorption which in turn should produce fewer stools. Such medications, it must be pointed out, have potential danger, especially in the pediatric age group. Antidiarrheal medication such as opiate or opiate-like drugs can produce, via inhibition of peristalsis, fluid retention within the bowel great enough to mask depletion of extracellular fluid and electrolytes. These drugs, therefore, do not necessarily decrease the loss of fluid from the gut but can sequester the fluid in distended loops of bowel. There is no evidence that reduced peristalsis diminishes the loss of fluid and electrolytes into the lumen of an inflamed intestine. These drugs can thus obscure the seriousness of the problem by decreasing the number of stools and preventing weight loss.

Once vomiting ceases, most patients can be treated orally with clear liquids such as 7-Up, weak tea, ginger ale, apple or grape juice. Following this regimen, a gradual increase in the diet can be offered over several days. If the vomiting and/or diarrhea become intractable, intravenous fluids should be administered.

4 a-2 Acute Bacterial Gastroenteritis

The treatment of Salmonella gastroenteritis involves isolation of the patient, adequate fluid administration either orally or parenterally and specific treatment of extraintestinal foci if necessary. Most patients with salmonella gastroenteritis have a relatively benign, self-limited course and do not require antibiotic therapy even though this is a bacterial disease. Thus, antimicrobial agents should not be given to patients with mild to moderate gastroenteritis due to salmonella. There is little evidence that antibacterial drugs exert a statistically beneficial effect upon salmonella gastroenteritis in man. These drugs usually do not shorten the duration of the illness and the length of time that the microorganisms persist in the intestinal tract is unaffected. There is also evidence that giving antibiotics to patients with mild to moderate salmonella gastroenteritis can actually prolong the carrier state.

Exceptions to the idea of not giving antibiotics to such patients include patients with impaired cellular immunity, patients with sickle cell anemia and infants less than one year of age. The patients in the groups named above have an increased risk of acquiring systemic salmonella infections.

For patients with severe salmonella gastroenteritis or those patients presenting with enteric fever ~~ usually with positive blood cultures or positive bone marrow cultures) The recommended treatment is fluorogurnoles, ceftrioxone, trimethoprin/ sulfamethoxazole. (If the bacteria is not resistant, ampicillin is an alternative drug.)

Opiates should not be administered to patients with salmonella gastroenteritis. It is now believed that diarrhea, especially in patients with bacterial gastroenteritis, can be a mechanism whereby the body rids itself of pathogenic organisms. Propulsive motility patterns of the intestine represent an important defense mechanism whereby the intestine can reduce multiplication of or penetration by potentially pathogenic bacteria. As noted previously in this minicourse, opiates decrease intestinal peristalsis. Thus, the body normally attempts to decrease the time of contact between invasive bacteria and intestinal mucosal cells by increased intestinal motility, i.e. diarrhea. Thus, drugs retarding gut motility can be harmful to patients infected with invasive bacterial intestinal pathogens. Therefore, drugs that reduce intestinal motility (such as belladonna or opium alkaloids) should be avoided.

Patients with gastroenteritis caused by shigella require general therapeutic measures, primarily the maintenance of fluid and electrolyte balance. Patients with shigellosis should be isolated until three negative stool cultures on consecutive days are obtained.

For most patients, shigellosis is a self-limited disease. Usually by the time the stool cultures return, the patient is symptomatically improved. Any antimicrobial therapy that is offered, then, is an attempt to secure a bacterial cure rather than a clinical cure, and the symptoms of most patients will not be clinically improved by the antibiotics. Antimicrobial therapy can reduce the excretion of bacteria in the stool and reverse the pathologic process in the bowel. Patients who are more severely ill should receive antimicrobial therapy which will probably decrease the diarrhea, fever and excretion of the pathogen.

Ampicillin can be used if the organism is sensitive. In areas where ampicillin-resistant shigella strains are prevalent, trimethoprimsulfamethoxazole appears to be effective. Bacteriologic cure rates with the use of antibiotics can be high as 80-90% after only 48 hours of therapy. Unlike salmonella patients, ampicillin does not seem to prolong the carrier state.

Exceptions to the idea of not giving antibiotics to the usual patient with mild to moderate shigellosis includes newborns, young infants and patients of any age with another complicating illness. There is some disagreement at this time regarding which patients with shigellosis should receive antibiotic therapy. Some authorities say all should be treated in an effort to control the disease epidemiologically; other authorities say treat the severe cases or those at high risk, such as young infants.

As explained previously in the section on salmonella gastroenteritis, drugs retarding gut motility, such as belladonna or opiate alkaloids, should probably not be given to patients with shigellosis.

4 a-3 Acute Parasitic Gastroenteritis

The general treatment of patients with giardiasis primarily involves maintenance of fluid and electrolyte balance by the administration of fluids, orally or parenterally, depending on the degree of vomiting, diarrhea and dehydration.

For some patients giardiasis is a self-limited disease; in others, drug therapy is necessary to eliminate the parasite. Both metronidazole and quinacrine are effective in eradication of the parasite. Quinacrine is a somewhat more objectionable drug as it stains the skin and sclera yellow in most patients and causes dermatitis in approximately 1% of patients. For these reasons, metronidazole is considered by some authorities to be the drug of choice.

As in all diseases producing fluid loss from vomiting and/ or diarrhea, one of the prime responsibilities of the health care practitioner treating patients with amebic dysentery is to maintain proper fluid and electrolyte balance.

All patients infected with Entamoeba histolytica should probably be treated irrespective of symptoms. It is apparent that some strains of E. histolytica are not pathogenic, i.e., are not tissue invaders, but as yet there is no effective way of differentiating the pathogenic strains from the nonpathogenic strains. Another recommended reason for treating all patients with E. histolytica in the stool is that extraintestinal involvement, especially the amebic liver abscess, can occur without prior symptomatic involvement of the intestine.

Currently the most useful drug for patients with amebic dysentery is metronidazole. Severe ulcerative amebic colitis often responds dramatically to emetine. Ultimately emetine is not curative of the bowel infection and, therefore, tetracycline for 10 days followed by di-iodohydroxyquin for three weeks is recommended.

Patients with asymptomatic or mild infections with amebae should be treated with di-iodohydroxyquin for three weeks. There is an 80% probability of cure from a single course of such treatment.

4 a-4 Acute Enterotoxic Gastroenteritis

The treatment of staphylococcal enterotoxemia (staphylococcal food poisoning) and clostridium perfringens food poisoning is mainly supportive and consists of restoration of fluid and electrolyte balance and symptomatic treatment of the vomiting and diarrhea. In the usual case oral replacement of fluid losses can be instituted. Severe cases require intravenous fluids to offset the dehydration and shock that may ensue.

Nausea and vomiting can be treated with measures mentioned in the section on acute viral gastroenteritis. Persistent diarrhea can be treated by intravenous fluids and by the judicious use of antidiarrhea medicine. Antibiotics are of no value in this condition as the disease is not caused by bacterial invasion of the intestinal wall but rather by enterotoxins. In most cases enterotoxic food poisoning is a benign self-limited condition.

4-b Food Allergy

The treatment of overactivity of the intestinal tract secondary to food allergies consists of an elimination diet. Attempt to determine by dietary history which food or foods are likely causes of the symptomatology. Most patients, upon careful questioning, are apt to report what foods make them feel worse. If only one food is suspected, eliminate it from the diet for two to three weeks to observe if the symptoms disappear. If several foods are suspected, remove all of them and after two or three weeks return one of them. If no symptoms develop, return the others one at a time 3-5 days apart. When milk or comparable milk substitute is withdrawn from the diet as a suspected food allergen for more than two months in older children, provide daily requirements of milk or substitute. Food allergies are often a matter of degree, i.e. symptoms can depend on how much is consumed how often.

4-c Ulcerative Colitis and Regional Enteritis

The therapeutic aims of the treatment of chronic ulcerative colitis are to relieve symptoms, to correct nutritional deficiencies, restore blood volume and attempt to control complications. The management differs according to the degree and form of the disease that is present. The disease can be divided into two categories--insidious disease or fulminating disease. Because the exact etiology of ulcerative colitis is unknown, all treatment is supportive and empirical.

The insidious form of the disease is usually mild and involves primarily the distal segments of the rectum and large intestine. When ulcerative colitis only involves this area of the bowel, bleeding is the major problem. Salicylazosulfapyridine (Azulfidine) should be given until bleeding ceases. Topical steroid medications such as hydrocortisone suppositories or hydrocortisone retention enemas can hasten the healing.

The patient should be placed on a regimen of good eating habits and should avoid anxiety, tension and overexertion. In this stage of the disease the diet is not critical but the patient should avoid consuming foods with unusually high content of roughage.

The severe form of the disease presents the patient and health care provider with multiple problems. It must be recalled that inflammation is a fundamental factor in this disease. As the disease progresses, bowel destruction occurs, resulting in secondary dysfunctions, especially nutritional and metabolic disturbances. The most impressive disturbance is depletion of protein which occurs as a result of inadequate food intake, increased protein catabolism during febrile episodes and losses of nitrogen, fluids and blood and inflammatory exudate from the intestine. The diet should be nonirritating and low-residue with an adequate supply of calories, proteins, vitamins and minerals. Patients with the severe form of ulcerative colitis require rest and nursing care (short hospital stay is advised). Azulfidine, general supportative measures and blood transfusions as needed.

Patients with the fulminating form of ulcerative colitis are very sick indeed. The destructive nature of this inflammatory bowel disease may have caused marked denudation of the colonic mucosa. Such patients usually present with marked tachycardia, fever and diaphoresis and have many bloody discharges from the rectum. These seriously ill patients appear wasted. The erythrocyte sedimentation rate is elevated and the prothrombin time is reduced (probably as a result of hepatic dysfunction and/or insufficient vitamin K).

These desperately ill patients should be hospitalized. Fluid and electrolyte balance should be accomplished by intravenous infusions. As soon as the fever recedes, rectal bleeding decreases and the patient's general condition stabilizes, liquids and azulfidine by mouth can be given. Following this regimen with further improvement, a low residue diet can be offered. Blood transfusions should be given if indicated. Steroids can be given systemically to patients with fulminating disease who fail to respond to the above measures. Steroid dosage should be reduced as soon as possible.

There are patients with ulcerative colitis who do require surgery. When surgery is indicated the procedure of choice is a total colectomy and ileostomy. The major indications for surgical treatment of this disease are massive intestinal bleeding, toxic megacolon, perforation of the bowel, intractable disease and a long history of symptomatic disease. Because there is a high risk of ulcerative colitis patients acquiring carcinoma of the colon, it has been suggested that colectomy be advised for patients who have had the disease longer than 10 years.

A recent addition to the therapeutic arsenal of drugs available for the treatment of ulcerative colitis are immunosuppressive agents such as azathioprine. This medication can be given as an adjunct when steroids fail or when the side effects of steroids become prominent.

The treatment of patients with Crohn's disease (granulomatous colitis, regional enteritis) is very similar to the treatment of patients with ulcerative colitis. They are both chronic diseases of unknown cause and therapeutic management must be comprehensive. Both diseases require supportive care with adequate explanation to the patient of the problems facing him and the available therapeutic regimens. For many patients the activity of the disease decreases after several years.

Medical therapy of this disease has as its objective the suppression of bowel inflammation. Initially, one would give azulfidine to the patient. Azulfidine, according to some authorities, is of no proven value. It is still offered, however, as initial therapy in the hope that it will delay use of hazardous systemic steroid drugs. The diet should be bland. Efforts should be made to maintain electrolyte balance and anemia should be corrected if present. If steroids fail, then an immunosuppressive agent such as azathioprine can be tried.

Surgical treatment of Crohn's disease should be considered in patients with such complications as uncontrollable hemorrhage, intestinal perforation, intestinal obstruction, or chronic fistula.

4-d Functional Bowel Gastroenteritis

The most effective treatment of functional gastrointestinal disease is an empathetic explanation to the patient of the benign nature of his complaint. Many patients with this disorder have an inordinate fear of cancer and the patient needs to be presented with evidence to the contrary.

Treatment of the IBS remains difficult. First of all, it is important to be sure that some serious condition does not underlie the patient's complaints. This is very assuring to the patient and is often sufficient to allow them to live comfortably with their active gut. However, it is also important for the care giver to spend sufficient time with the patient to satisfactorily explain concepts regarding the production of symptoms, and outline simple treatment measures. Avoidance of laxatives, maintaining a high bulk diet, and a trial on a lactose-reduced diet are appropriate, recognizing that all patients will not respond positively to these measures. Drugs that alter gut motility are indicated in some patients for short- term symptomatic relief. There seems to be little reason to offer tranquilizers and mood elevators. Finally, do not neglect to provide periodic follow-up.

EXERCISE 4 OBJECTIVE 4 - Questions

1. What are the essentials required for the treatment of acute viral gastroenteritis?

2. Discuss the role of antibiotics in: a) acute viral gastroenteritis; b) acute salmonella gastroenteritis; c) acute shigellosis; and d) acute bacterial enterotoxemia.

3. Discuss the use of opiate and opiate-like drugs in the treatment of gastroenteritis generally and in the treatment of bacterial gastroenteritis specifically.

4. Name an antiparasitic drug that could be used in patients with gastroenteritis due to Giardiasis as well as in patients with gastroenteritis due to Entamoeba histolytica.

5. What are the most important therapeutic aspects of the treatment of bacterial enterotoxemia?

6. Name the essential ingredients in the treatment of gastrointestinal disease due to a food allergen.

7. If a patient has the insidious form of ulcerative colitis manifested by bloody diarrhea, what medications could you give to hasten the healing of the intestinal mucosa and thus put a halt to the rectal bleeding?

8. Name some indications for surgical intervention in patients with ulcerative colitis and name the procedure usually performed.

9. What is probably one of the most effective treatment modalities that can be offered to a patient with functional gastrointestinal disease?

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MINICOURSE 2.1 SECTION 5

OBJ. 5. Construct a differential diagnosis and treatment plan for a patient with hyperactivity of the intestinal tract, given signs, symptoms, x-ray and laboratory data.

Case Studies

  1. Ms. Tootsie Trotter, a first grade teacher, suddenly became nauseated during the afternoon session of her reading class. Tootsie figured that she could not be pregnant as she was not sexually active and thus ruled this possibility out as a cause of her nausea. She ran to the ladies' comfort station and promptly vomited twice. She went back to the class and finished out the afternoon even though she still had nausea and pains in her arm and leg muscles.

    On the way home, Ms. Trotter experienced cramping abdominal pain and a powerful urge to defecate. She immediately parked her car and went into the nearest ladies' room (located in a gas station) whereby she experienced a tremendous bout of watery diarrhea. The abdominal cramps persisted and our teacher became worried. She drove to the nearest hospital emergency room and sought medical aid, stopping first in the hospital's ladies' room whereby more watery diarrhea came forth.

    Tootsie was greeted by a friendly physician assistant who listened to her history empathetically. He was able to determine that several children in her class and one other teacher in the school had similar symptoms. Physical examination revealed a young woman with a temperature of 100 orally, and no evidence of dehydration. The rest of the examination was within normal limits including her abdomen which was soft with very slight generalized tenderness upon palpation. Vital signs were BP 110/65 and pulse 76 and regular.

    The stool on gross examination (you guessed; Tootsie had to defecate again - during the examination - this time she was given a specimen cup for stool collection) was composed primarily of water and stool remnants and presented no evidence of blood of mucus. Microscopic examination of the stool for leukocytes, using methylene blue stain, revealed no WBC in the sample. Her peripheral white blood count was within normal limits.

    Ms. Trotter was sent home on a clear liquid diet and was told not to self-medicate herself. She was told that she probably was suffering from acute viral gastroenteritis otherwise known as "stomach flu." She was told to report to her family physician if she did not improve. Tootsie was better in 48 hours and returned to her classes, happy that she had had chicken pox as a child as there now was a varicella epidemic in the school.

  2. Herbert Fitzmaurice and Maurice Fitzherbert were college athletes of some renown who went to Mexico City to compete in some pre-Olympic Games track competition - both were sprinters. During their four-day stay in Mexico, they broke training several times and sampled the local tacos, enchiladas, and frijoles.

    On the way home, Herbert became ill and had several bouts of diarrhea during the plane ride. He was happy that he was a short distance runner of some skill as this expertise came in handy as he ran to the men's room during his attacks. Our patient was nauseated but did not vomit and experienced colicky abdominal pains. No one else on the plane seemed to be ill. Herbert noticed that his stools were slimy and green and smelled like rotten eggs. His stools appeared to be slightly blood streaked and contained a small amount of mucous.

    The flight was a relatively short one, but by the time the plane landed Herbert was feeling miserable. His colleague Maurice called a cab and took Herbert to the college student health service. There Herbert was interviewed and examined by a physician assistant who found that the had a 101 temperature orally, a pulse of 96 and regular and a BP of 120/75. The patient appeared mildly dehydrated and had a mildly tender abdomen upon palpation. His abdomen was soft, however. Auscultation of the abdomen revealed evidence of hyperperistalsis. The rest of the physical examination was within normal limits. An examination of some mucus from Herbert's rectum, obtained by rectal swab, revealed many WBCs (after staining with methylene blue). The total leukocyte count on his stools were 35 per high Power field of which 72% were polymorphonuclear leukocytes. Stool cultures were obtained, a CBC was taken, and Herbert was admitted to the college infirmary with a provisional diagnosis of acute bacterial gastroenteritis.

    Herbert's condition rapidly improved in the next 24 hours at which time the laboratory reported that his stool culture was growing out salmonella. His CBC was perfectly normal as were his blood electrolytes. No antibiotic therapy was offered as the patient was getting better spontaneously. Herbert went home (much improved) the next day and swore that the next time he traveled to a foreign city he would bring all the sustenance and comforts he needed with him.

  3. Maurice, Herbert's college colleague, was feeling rather lucky that he did not acquire the diarrhea that his friend suffered with. Two weeks after their trip to Mexico, Maurice, while sitting in his modern literature class (Mad Magazine in Our Culture-101) began to experience mild abdominal discomfort. He did not pay much attention to this as he thought it might be due to hot peppers and peanut butter sandwich he had had for lunch. That night he had more abdominal cramps and one loose stool with mucus. Three days later the pain was still present in his abdomen, plus he was experiencing mild nausea and a feeling of abdominal distention.

    At this point he decided not to go to class, Basket Weaving211, as he felt ill. It was just as well that he didn't go because soon after arising he experienced severe tenesmus and passed a grossly bloody loose stool with much mucus. Now Maurice was worried and went to the student health service feeling somewhat confused that he had diarrhea two weeks after his Mexican trip, whereas his buddy Herbert got diarrhea on the way home.

    Physical examination at the student health service revealed that Maurice had 103 temperature orally, had a BP of 130/ 78, pulse 116 and regular, and diffused abdominal tenderness. The areas of more pronounced tenderness were located in the caecum and ascending colon. Maurice's liver was slightly enlarged and slightly tender. The rest of the physical examination was within normal limits.

    The physician assistant who examined the patient was quite concerned about Maurice and after collecting data and blood and stool, called the physician on call, Dr. Ben Gay. The physician examined the patient including performing a rectal examination and confirmed the PA's findings. It was decided to admit Maurice to the infirmary for further work-up. Last night Maurice had another bloody stool and Dr. Gay decided to perform a sigmoidoscopy on the patient to rule out ulcerative colitis, regional enteritis, polyps or whatever. Sigmoidoscopy revealed areas of ulcerations of the colon with normal mucosa interspersed. Material from the mucosal lesions were aspirated and sent to the lab for analysis.

    By this time, his CBC had returned and showed a hemoglobin of 14.5 grams and a WBC of 16,000 with 75% polymorphonuclear cells. Flat plate of the abdomen showed some generalized distention of the bowel with no suggestion of bowel obstruction or mass lesion.

    The material aspirated from the colon during sigmoidoscopy showed many RBCs, a few WBCs, and nothing else abnormal. Dr. Gay ordered daily stool cultures for bacteria, ova, and parasites. Maurice was placed on intravenous fluids and bed rest and seemed to improve slightly. On the third day after admission, his fourth stool examination after admission revealed the typical trophozoites of Entamoeba histolytica. Dr. Gay prescribed a regimen of metronidazole for Maurice and the patient showed rapid clinical improvement.

  4. The day of his daughter's wedding had finally arrived, and Mr. Larry Frugal was happy and excited but worried about how much the wedding would cost. The couple wanted to have the ceremony in a forest which made Larry happy because it saved him the price of renting a hall. About 75 people were invited and the food for this event was being prepared by Larry's other daughter's high school cooking class. The menu was just as Larry's daughter, Daisy, had ordered - turkey Rockefeller. Because the wedding was on Saturday afternoon, the food was cooked Friday morning (school closed on Saturday, of course). The food was allowed to cool slowly at room temperature, to be rewarmed shortly before the wedding.

    The wedding itself was magnificent, the day was perfect temperature in the low 80s and the minister, a defrocked Shinto priest, conducted a beautiful service, all in Sanskrit. The food was devoured - every drop was consumed. Everyone agreed it was the best wedding they had ever been to.

    At 3 a.m. the bridegroom was preparing to consummate his now legal union and he suddenly noticed that his wife was gone. He did hear moans and groans from the bathroom, however, but figured that it was normal for a bride to be anxious. Daisy's husband became more concerned, however, as he heard the toilet flushing over and over again. He begged entrance and found his wife lying on the floor moaning because of severe abdominal cramps and crying that for the past hour she had had six watery bowel movements. What a way to start married life! Quite upset by now, the young husband phoned his new mother-in-law for advice. She was unable to come to the phone, the father-in-law said, as she was in the bathroom suffering from abdominal cramps and diarrhea. What a family, the bridegroom exclaimed!

    Getting more and more worried, the young spouse put his new wife in the back of his Honda and drove to the nearest hospital emergency room which happened to be St. Mary Detrimental Hospital. When he arrived, it looked like an instant replay of the wedding; 20 people from the wedding were there standing in line, with numbers in their hands, waiting their turn to see the health care practitioner. All of the people had the same general complaints, abdominal cramps and profuse diarrhea.

    The PA and doctor on duty were in a tizzy. The laboratory technician who was called in was swamped with blood counts and specimen cups full of watery stools. The first five stool examinations from the first five patients were examined for fecal leukocytes and none was found; ruling out the possibility at this time of an epidemic of bacterial gastroenteritis.

    It was decided that this mass diarrhea episode was most probably an enterotoxemia secondary to clostridium perfringens. No food was available for analysis as it was all consumed. All patients recovered spontaneously in two or three days except Grandpa Frugal who has a heart condition and a pacemaker. He went into shock but recovered nicely with the administration of intravenous fluids.

  5. Marvin Grepz, age six months, was a delightful child - always smiling, playful and very much what his mother, Greta, had always wished for. He never had "three-month colic" like his cousin did. Marvin was being breast fed and gaining and growing just like the book said he should.

    Greta decided it was time to wean Marvin as they were moving, and she needed more time to arrange the new house. She weaned him to whole milk just as all of her girlfriends had done. By this time they had moved to their new home. After being on whole milk for one week and off of breast milk entirely, Marvin became a monster - screaming day and night, vomiting three or four times a day and filling his diapers with loose mucoid stools seven or eight times a day. Greta was quite upset by this time but attributed Marvin's changed habits to the move and the fact that she was not able to spend as much time with him as before because she was getting the new house in order.

    Finally, Greta could take no more of this and took him to their family health care practitioner. The examination revealed that Marvin was quite irritable and showed a poor recent weight gain, but was otherwise normal. The urinalysis was normal and so was the CBC. Stools were examined with methylene blue for leukocytes and also with Wright's stain. The only WBCs that were found were an increase in eosinophils in the stool mucus. Stool cultures were sent to the lab.

    Marvin's doctor took a very careful history from Greta including a detailed dietary history. He found that Greta began to feed him whole milk, strawberry cobbler, tomato soup and orange juice all in the same week - all these foods were new to Marvin but Greta felt like he needed new foods to stimulate his appetite. The doctor decided to put the baby on a food elimination diet - all the new foods he had been given were stopped for two weeks and offered again one at a time. All went well. During the time that Marvin was off of these foods he became his old self again and thrived beautifully - until whole milk was reintroduced and then the abdominal pains, vomiting and diarrhea began again. The whole milk was again stopped and Marvin ws placed on a soybean formula whereby all of his symptoms disappeared. The doctor said that Marvin most likely was allergic to milk, and though this diagnosis is difficult to prove, his response to the elimination diet revealed this to be the most likely possibility.

  6. (6) Ms. Maisha Pupick is a 22-year-old graduate student from Israel studying in the United States. During the first few months of her stay in this country, she felt wonderful but during the last two or three months she has been feeling poorly. Her symptoms are not dramatic or acute or specific for anything - just increased tiredness, some loss of appetite and mild weight loss, occasional nausea and vomiting episodes and mucoid stools. Maisha figured that all of these symptoms could be explained on the basis of homesickness, of having to adjust to a new culture and school or possibly due to the fact that her lovelife was zip.

    Maisha enrolled in a meditation class and felt somewhat better for a while, but soon her old symptoms returned with the addition of bloody stools and tenesmus. At times her bowel movements consisted of tenesmus followed by small "squirts" of bloody mucus. On two occasions she soiled her bed and night clothes during sleep. Now this young student was getting quite concerned. She also noticed that she was running a low grade temperature. Maisha decided that the time had come for medical intervention and she went to see a physician.

    The doctor was also concerned as the patient looked even sicker than the complaints she voiced implied. It was decided that Maisha should be admitted to the hospital for diagnostic evaluation. In the office the patient showed evidence of recent weight loss, a temperature of 101 degrees orally, some pallor of the oral mucosa and nailbeds and tenderness in her lower abdomen. Rectal examination revealed narrowing of the rectal lumen.

    The results of her laboratory tests in the hospital were as follows: Hemoglobin 11.5 grams, WBC 17,000 with 80% polymorphonuclear leukocytes, sedimentation rate 45. Stool cultures were negative for pathogenic bacteria or parasites.

    Sigmoidoscopy was performed the day after admission and visualization of the rectum and sigmoid area revealed loss of the normal mucosal vascular pattern; friability of the mucosa when it was swabbed; edema; ulceration; and purulent mucosal exudate noted in the anal canal.

    A barium enema was performed the next day and this showed shortening and straightening of the rectosigmoid and sigmoid area, a very symmetrical mural involvement with small ulcerations and loss of normal haustral markings as well as a "lead-pipe" appearance of the descending colon.

    The diagnosis of chronic ulcerative colitis was made and Maisha was given salicylazo-sulfapyridine by mouth (Azulfidine) plus several hydrocortisone retention enemas. Her rectal bleeding stopped and she felt better. She was placed on a soft diet and given stool softeners. Maisha improved steadily and decided to change her lifestyle. She fell in love with the medical resident, married him, and lived relatively happily thereafter (with occasional mild recurrences of her ulcerative colitis).

OBJECTIVE 5 - Questions

1. Elmer F. has diarrhea today - three watery bowel movements without blood or mucus. Preceding the onset of the diarrhea he vomited twice. He feels somewhat weak and has muscle pains and occasional abdominal cramps. Two days ago his wife and oldest son had the same complaints, but they are improved. What would be your advice to Elmer?

2. What would you expect Elmer's watery stool to be composed of? If you stained a sample of his stool with methylene blue, what would you expect to see under the microscope in terms of WBC? What would you expect his stool cultures and peripheral CBC to reveal?

3. Little Kitty G. loves to play with her pet turtle Myrtle (a dirty little beast; Myrtle not Kitty). Kitty experienced a bout of diarrhea this week - several days of loose, green slimy stools with some gross blood in the stools. Her temperature was 101.6 degrees and she complained of colicky abdominal pain. What might her diagnosis be? How would you prove it? How would you treat her?

4. Victor is a world traveler and usually experiences no problems with his occupation except an occasional "hangover" and an occasional bout of jet lag. During the past month, however, he has been experiencing abdominal discomfort plus diarrhea alternating occasionally with constipation. When his stools are loose, they are profuse and contain what looks like pus and mucus. The last three stools contained gross blood and were associated with tenesmus. What investigations would you undertake to diagnose his problem? What treatment would you offer if parasites were found?

5. Harriet Schmeck, a graduate student at Sam Houston Institute of Technology, has recently been on an archeological dig in South America in an attempt to get her master's degree. The food has been terrible and the weather quite warm and humid. During the past four weeks, she has been feeling poorly. She has had diarrhea intermittently as have her colleagues, but now she has been feeling some malaise and running a temperature of 101 degrees orally. She has lost six pounds in the last three weeks. Harriet became more concerned recently when she noted bloody diarrhea with occasional squirts of bloody mucus. Her abdominal cramps, which previously were mild, now became more intense and her appetite dwindled. Harriet became worse one weekend and was sent to a hospital in the United States. What diagnosis would you consider as causing her GI complaints? How would you proceed to diagnose her problem? How would you treat her?

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OBJECTIVE 1 Answers to Questions in Section 2.1.1

1. The most common cause of acute gastroenteritis in this country is an acute nonbacterial gastroenteritis, usually viral. Its frequency is second only to the common cold as a cause of illness in the U. S.

2. The great danger in this otherwise benign self-limiting disease is dehydration.

3. The normal formed stool is usually 60-70% water by weight. Liquid stools generally contain 80X or more water by weight.

4. The increase in water content of diarrheal stools can be due to impaired water absorption by the intestinal mucosa or increased secretion of water by the intestinal mucosa.

5. Acute nonbacterial gastroenteritis is characterized by sudden onset of nausea and vomiting followed by explosive diarrhea with or without abdominal cramps. There can also be myalgia, anorexia and low grade fever.

6. The typical stool in acute viral gastroenteritis consists of water and stool remnants. Blood, pus and mucus are usually absent.

7. The two most common bacterial gastroenteritides in the U. S. are those caused by salmonella or shigella.

8. Salmonella gastrointestinal infections are usually transmitted from animals to man and occasionally from man to man.

9. The greatest single source of human salmonella infections in the U. S. is the vast reservoir of salmonella in lower animals.

10. A typical attack of acute salmonella gastroenteritis is mild, brief, self-limiting and consists of sudden onset of colicky abdominal pain and loose watery stools that can be slimy, green and smell like rotten eggs. Low grade temperature elevation can occur as well as abdominal tenderness. The symptoms generally subside spontaneously in 2-5 days.

11. Salmonella gastrointestinal infections primarily involve the small intestine, producing edema and Inflammation of the mucosa. Shigella infections, on the other hand, produce mucosal changes mainly in the rectum and sigmoid area consisting of diffuse mucosal swelling and petechial hemorrhages in mild cases; severe cases have a fibrinous exudate with necrosis of the mucosa and the development of shallow ulcers. Shigella actually involves the entire colon but the maJor changes are in the rectum and sigwoid.

12. The stools of patients with shigellosis are watery, relatively odorless, contain mucus, are yellow-green and commonly contain blood, whereas the stools of patients with salmonellosis are loose, slimy, smell like rotten eggs and green in color, but do not commonly contain blood.

OBJECTIVE 1 - Answers to Questions in Section 2.1.1

13. Giardia lamblia and Entamoeba histolytica are the two most important parasites in terms of gastroenteritis in the U. S.

14. Giardiasis is a disease of the small intestine and is acquired through ingestion of cysts of the parasites which are passed in human feces and spread through the ingestion of contaminated water.

15. Amebiasis is a disease of the large intestine. The cyst of the ameba is the infective form. Man passes cysts in his stools and transmission occurs by ingestion of food or water contaminated by human fecal matter.

16. The common name for bacterial enterotoxemia is food poisoning. The two most common causes in this country are the enterotoxins produced bv staphylococci and those produced by Clostridium perfringens.

17. The clinical features of staphylococcal food poisoning are sudden intense nausea followed by explosive vomiting and intense abdominal cramps. Diarrhea can occur but is a less important feature. Clostridium perfringens food poisoning is marked by abdominal cramps and profuse diarrhea; vomiting is not a prominent feature.

18. In bacterial gastroenteritis, the clinical features of the disease are probably due to invasion of the mucosa of the intestine by the bacteria whereas in bacterial entrotoxemias the clinical features are probably due to a toxin produced by the bacteria.

19. Milk is the most common food allergen. Gastrointestinal symptoms caused by food allergens include diarrhea, abdominal distention, abdominal pain, vomiting and flatulence.

20. The "typical" patient with ulcerative colitis is apt to be a young adult female living in a northern urban area, well educated and well above the national average economically. There is also a possibily of a positive family history for the disease (5-10% of ulcerative colitis patients have such a history).

21. The major clinical manifestations of ulcerative colitis include diarrhea, rectal bleeding, abdominal pain, fever and weight loss. Tenesmus with "squirts" of bloody mucus are distinctive for this disease.

22. Regional enteritis is referred to in the literature by such names as regional ileitis, Crohn's disease, transmural colitis or granulomatous colitis.

23. The most common clinical presentations of regional enteritis are diarrhea, colicky abdomen pain and weight loss.

24. Functional gastrointestinal diseases comprise a variety of complaints referable to the G.I. tract in which no gross organic lesions can be found and the clinical manifestations are probably the result of altered physiological mechanisms. Functional gastrointestinal abnormalities may be regarded as aberrations of the secretory activities or motor activities or both, of a gastrointestinal segment.

25. Rectal involvement occurs in almost all patients with ulcerative colitis and in only 20% of patients with granulomatous colitis.
Ulcerative colitis more commonly affects the rectum and left side of the colon most severely, affecting the entire bowel circumference and producing continuous lesions. Granulomatous colitis more commonly affects the right side of the colon, sometimes affecting one wall of the intestine, sparing the opposite wall, and producing patchy lesions on the intestinal wall.
Perianal fistulae and internal fistulae are common in granulomatous colitis and uncommon in ulcerative colitis.
Cancer of the colon is relatively common in ulcerative colitis and uncommon in granulomatous colitis.
Ulcerative colitis usually involves only the mucosa and submucosa of the intestine; granulomatous colitis involves all layers of the intestinal wall.

OBJECTIVE 2 Answers to Questions in Section 2.1.2

1. Stool cultures of patients with acute nonbacterial gastroenteritis are generally nonproductive. The usual cause is presumably viral. Growing viruses is a time consuming and relatively expensive procedure and in individual cases the isolation of a specific virus on stool culture would not necessarily mean that the agent has caused the illness as a considerable percentage of asymptomatic individuals will grow the same virus from their stools. By the time the report returned from the lab in terms of virus culture, the patient would have recovered from this self-limiting disease. CBCs in these patients are usually normal.

2. Outside of the collection of data, i.e. a thorough history and complete physical, the major diagnostic tool in the diagnosis of such diseases as shigellosis and salmonellosis is a stool culture for the purpose of identifying the causative bacterial pathogen.

3. Examination of the stool of leukocytes is a rapid method of distinguishing the presence or absence of a bacterial etiology in patients with gastroenteritis. The presence of leukocytes on a smear of the patient's stool or of mucus obtained from a rectal swab gives an indication of the bacterial etiology of the gastroenteritis.

4. Giardiasis can be diagnosed by the demonstration of cysts or trophozoites of Giardia lamblia in stool specimens or in the duodenal fluid. The most reliable method involves examination of a smear of biopsied duodenal mucosa stained by giemsa solution. A substantial number of symptomatic patients will have negative stool cultures for this parasite.

5. The diagnosis of gastroenteritis due to Entamoeba histolytica is best established by identification of the trophozoites or cysts of ameba in the patient's stool.

6. The exact etiology of a bacterial enterotoxemia can only be established if samples of the ingested contaminated food can be shown to contain large numbers of enterotoxin producing bacteria.

7. Skin testing for food hypersensitivity is generally of little or no value as these tests are not very accurate.

EXERCISE 2-b Answers to Questions in Section 2.1.2

8. The most important tools in the diagnosis of ulcerative colitis are sigmoidoscopy and barium enema.

The typical sigmoidoscope findings are: loss of mucosal vascular pattern, edema and ulceration of the mucosa, friability of the mucosa upon swabbing, purulent mucosal exudate.

Typical barium enema findings include straightening and shortening of the rectosigmoid area with symmetrical involvement of the bowel wall with small ulcerations, a loss of normal haustral markings and a "lead pipe" appearance of the descending colon.

9. Barium enema studies in patients with granulomatous colitis reveal "skip" areas of involvement of the bowel (rather than continuous involvement), fistulae, strictures of the bowel wall, coarse mucosal ulcerations and, usually, noninvolvement of the rectum.

10. There are no laboratory and/or x-ray determinations that are diagnostic of functional bowel diseases. Most of the time the diagnosis can be made from the history and physical examination. The laboratory and/or x-ray studies in such patients are usuallv within normal limits. *****


EXERCISE 3 DISCUSSION
OBJECTIVE 3 - Answers to Questions in section 2.1.3

1. Both diphenoxylate and atropine act to decrease the gastrointestinal motility. This action permits more water to be reabsorbed from the fecal material and thus increases the consistency of the fecal material. Magnesium salts are demulcents which means that they relieve the irritation which is causing the increase in gastrointestinal motility. Psyllium seeds are hydrophilic and absorb excess water in the bowel and form a gelatinous mass. Because the bowel water has been incorporated into the gelatinous substance, there is less water available which results in the elimination of a firmer stool. 2. The oral administration of antibiotics can cause an alteration in the normal gastrointestinal bacterial flora. These changes can result in a variety of symptoms which include diarrhea, gas build- up and a decrease in nutrient absorption. In addition, many antibiotic agents can cause a direct irritation of the gastrointestinal mucosa which is usually manifested as nausea and vomiting.

EXERCISE 4 DISCUSSION OBJECTIVE 4 - Answers to Questions in Section 2.1.4

  1. The essence of the treatment for patients with acute gastroenteritis is: a) allowing time for the mucosa of the bowel to regenerate by putting the bowel to relative "rest"; and b) replacement of lost water and electrolytes to prevent dehydration.
  2. Antibiotics are not indicated in the treatment of acute viral gastroenteritis as the antibacterial agents will not destroy the viral agents and may actually interfere adversely by altering the fecal flora or in some instances irritating the intestinal mucosa.

    Most patients with salmonella gastroenteritis have a relatively benign self-limiting course and do not require antibiotic therapy. Patients with mild to moderate disease do not have a shorter duration of illness when they receive antibiotic therapy and the use of antibacterial agents may actually prolong the carrier state. For patients with severe salmonella intestinal infections, chloramphenicol or ampicillin can be used.

    Any antimicrobial therapy offered to patients with acute shigellosis actually results in a bacterial cure rather than a clinical cure as the typical patient with acute shigellosis has a self-limited course. Antibiotic therapy in such patients can reduce the excretion of bacteria in the stool and reverse the pathologic process in the bowel. Ampicillin can be used if the bacteria are sensitive.

    Patients with enterotoxemia due to Staphylococcus aureus or Clostridium perfringens generally do not require antibiotics as the disease is usually self-limited and the antibacterial agents are not effective against the toxins causing the disease.

  3. Antidiarrheal medications, such as opiates, inhibit propulsive movements of the intestine, decrease peristalsis and allow more time for intestinal water absorption; however, these drugs can cause fluid retention within the bowel great enough to mask depletion of extracellular fluid. These drugs, therefore, do not necessarily decrease the loss of fluid from the gut but can sequester this fluid in distended loops of bowel.

    Opiates should not be administered to patients with bacterial gastroenteritis, such as salmonellosis or shigellosis, as by giving such drugs one may be interfering with nature adversely. That is to say, diarrhea, especially in patients with bacterial gastroenteritis, can be a mechanism whereby the body rids itself of pathogenic organisms. The body normally attempts to decrease the time of contact between invasive bacteria and intestinal mucosal cells by producing diarrhea. Because opiates interfere with this process, i.e. by decreasing peristalsis and prolonging contact of invasive bacterial and intestinal mucosa, the patient could actually become worse.

  4. Metronidazole is an effective medication against Giardia lamblia and is currently also the most useful drug for patients with amebic dysentery.
  5. Most patients with bacterial enterotoxemia have a self-limited course. Restoration of fluid and electrolyte balance is the primary focus of therapeutic endeavor. Nausea, vomiting and diarrhea can be treated symptomatically. There is no specific therapy for this disease.
  6. In treating a patient with a food allergen, one attempts to determine the food or foods that are likely to be the cause of the symptomatology by way of a dietary history. The food or foods that are suspected should be eliminated from the diet for two or three weeks and then reintroduced one by one at 3-5 day intervals to see if symptoms recur. Once the suspected food is identified in this manner, it should be eliminated from the diet if possible.
  7. One could treat the insidious form of ulcerative colitis with Azulfidine and topical steroids in the form of hydrocortisone suppositories or hydrocortisone retention enemas to help control the rectal bleeding.
  8. The major indications for surgery in patients with ulcerative colitis are massive intestinal bleeding, perforation of the bowel, intractable disease and a long history of symptomatic disease. When surgery is indicated the current procedure of choice is a total colectomy and ileostomy.
  9. Reassurance and an empathetic explanation to the patient of the benign nature of the disease is the treatment of choice for functional GI disease.

    OBJECTIVE 5 - Answers to Questions in Section 2.1.5

    1. 1. Most probably Elmer is suffering from acute viral gastroenteritis as was his family. Because their course was apparently benign and self-limited, it is probable that his course will be the same. All he requires at this time is the ingestion of clear liquids such as 7-Up, tea, ginger ale, and Jello in an effort to allow his intestinal mucosa to regenerate and to prevent dehydration. If Elmer does not improve or in fact gets worse, he should be evaluated.
    2. If Elmer was suffering from acute viral gastroenteritis, which is by far the most common cause of diarrhea in this country, his stools would be composed of water and stool remnants. The stools would not contain pus, blood or mucus. The fecal leukocyte count using methylene blue stain would be normal. Stool cultures would not grow pathogenic organisms and his peripheral CBC should be within normal limits.
    3. It is a fairly safe bet that Little Kitty has Salmonella gastroenteritis which she contracted from Myrtle who excreted Salmonella in her stool and thus in the water in which she swam. Probably, after playing with Myrtle, Kitty inadvertently put her hands in her mouth and ingested the pathogenic bacteria.

      The diagnosis could be proved by culture of Kitty's stool and also by culturing Myrtle's swimming pool. A sample of Kitty's stool, stained with methylene blue, would probably reveal many polymorphonuclear leukocytes. We would expect that Kitty would have a normal peripheral CBC and abdominal x-rays.

      Kitty should respond to symptomatic treatment with careful attention given to her fluid and electrolyte balance. As Kitty has a mild to moderate degree of illness, antibiotics are not needed and she will probably experience a self-limited course.

    4. Stool cultures should be obtained to rule out bacterial gastroenteritis. Stool examinations were obtained for ova and parasites and amoebae were found. Victor received mentroidazole and recovered.
    5. Harriet, after admission to the hospital, continued to have loose bloody stools. Her stool cultures for Salmonella and Shigella were negative. Because of the locality of the archeological dig, her stools were examined for parasites and none was found, including an analysis of her duodenal fluid for Giardia lamblia. A diagnosis of ulcerative colitis was entertained and she was sigmoidoscoped.

      Sigmoidoscopy revealed loss of the normal vascular pattern of the intestinal mucosa, edema and ulceration of the mucosa, purulent mucosal exudate and a friable intestinal mucosa.

      Harriet was given a barium enema which showed straightening and shortening of the rectosigmoid and sigmoid area with symmetrical involvement of the bowel wall. Barium enema also revealed a loss of haustral markings and a "lead pipe" appearance of the descending colon.

      The diagnosis of ulcerative colitis was confirmed and she was given Azulfidine by mouth and hydrocortisone retention enemas. Harriet was given stool softeners, low residue diet and a chance to recover. She improved and decided to try for a somewhat less intense life - she became a medical educator.

    *****