Diarrhea is a symptom which is defined in several ways, most often by the number of daily bowel movements, but also by their consistency, their volume or weight. The patient focuses mainly on the consistency of his stools and their numbers, the quantitative aspect is more difficult to assess. The volume or weight of stool is the best definition of diarrhea (generally weighing more than 250 g / day for a subject having a Western diet). Stool weight value is nevertheless difficult to obtain outside of a hospital so that the number and consistency of stools are usually used in the first analysis to determine the existence of a diarrhea.
We talk about chronic diarrhea if symptoms persist for more than three to four weeks, at which time infectious hypotheses are less feasible in immunocompetent individuals.
This definition taking into account only the number and consistency of stools nevertheless has the disadvantage of including in the context of chronic diarrhea irritable bowel syndrome, which remains the most common cause of disorder transit in our region.
The etiologies of chronic diarrhea are very numerous (see Box 1). They make it difficult to establish a simplified strategy, but if the data of clinical and biological examinations a first line does not quickly turn to an accurate diagnosis, the current logic is to achieve first-line morphological explorations centered on endoscopic assessment with gastroscopy and colonoscopy with biopsies. This attitude is of great diagnostic value and helps to explain many chronic diarrhea.
DIAGNOSIS:
Examination:
The well reconstructed history of chronic diarrhea often distinguishes a functional table from one situation to the organic evidence.
The arguments in favor of an organic nature are: diarrhea lasting for at least two to three months;
– Continual diarrhea, especially at night;
– Significant weight loss.
Diarrhea characters are important to define:
– Time: Morning, postprandial any time both day and night;
– Imperious nature of stool;
– Like stools: afécales, fat, discolored, possible presence of undigested food eaten that day, presence of mucus, pus or blood.
The search for a trigger at the beginning of the symptoms is essential as, living in tropical countries, taking a new medicine, including an antibiotic, a nonsteroidal anti-inflammatory drug or other recently introduced.
The pathological context is to define: existence of diabetes, the system disease, chronic alcoholism, drug abuse, history of transfusion. Note ethnicity, a possible homosexuality, family history of cancer, inflammatory bowel disease or celiac disease.
The surgical history are important to clarify especially if they are gastrointestinal: intestinal resection, vagotomy, cholecystectomy, etc.
Chronic diarrhea usually not summarizes all of the clinical and other digestive symptoms or extradigestifs are important to recognize:
– Abdominal pain or fever are sometimes present, continuous or intermittent;
– The existence of vomiting, anorexia or polyphagia;
– Koenig syndrome which shows stenosis of the small intestine should be sought during the interrogation;
– Rectal bleeding or tenesmus may move towards a low intestinal origin;
– The existence of a fever, arthralgia, rash (erythema nodosum) can evoke an inflammatory colitis, a secretory flush syndrome (carcinoid), edema of the lower extremities finding, secondary to hypoproteinemia losing enteropathy;
– Signs in favor of a thyroid especially endocrinopathy be sought but their absence does not eliminate the diagnosis.
Clinical examination:
The clinical examination is of course an essential step:
– Abdominal palpation research mass, hepatosplenomegaly, peritoneal effusion;
– DRE eliminates anorectal tumor pathology;
– The proctology examination genupectorale position when possible is important to search for a fistula, fissure, perianal dermatitis or abnormal anoperineal static;
– The rest of the clinical examination aims to seek extradigestifs signs up towards a specific etiology (see below).
Laboratory tests:
An initial laboratory tests often helps clarify the situation: it must include complete blood count, erythrocyte sedimentation rate and C-reactive protein, a blood electrolytes, urea, creatinine, liver function tests complete. Stool culture and parasitology of stools must be prescribed if they were not made initially at the beginning of the diarrheal syndrome. An iron status, TSH, protein electrophoresis are also expected.
The search for immunosuppression is important and, in case of clinical suspicion, HIV serology is to prescribe the patient’s agreement.
After this survey, it is possible in most cases to suspect the etiology and mechanism of diarrhea.
Endoscopic examinations:
The next stage of exploration is represented by the endoscopic upper gastrointestinal endoscopy including a balance sheet and a ileocolonoscopy, usually performed at the same time during the same anesthesia. This assessment can detect a parietal lesion in the proximal small intestine and terminal and in the colon.
Colonoscopy:
It allows the discovery of the parietal colonic pathologies framework and the terminal ileum.
The first diagnosis always feared by patients is that of cancer. Colon cancer may indeed be responsible for chronic diarrhea. If one knows the prevalence of colonic adenomas during routine colonoscopies performed from the age of 50 (about 14 to 37%) the prevalence of polyps or cancers in patients undergoing colonoscopy for chronic diarrhea n is not known. This could be in the order of 33% for associated rectal bleeding.
Colonoscopy also allows the diagnosis of inflammatory bowel disease (Crohn’s disease and ulcerative colitis) and microscopic colitis (collagenous or lymphocytic colitis).
Systematic retrograde ileoscopy increases the diagnostic yield of colonoscopy.
In patients with chronic diarrhea with normal colonoscopy, a terminal ileitis is found in a third of cases.
Overall, ileocolonoscopy allows an etiologic diagnosis in 15 to 20% of the holders of chronic diarrhea patients, this figure may rise to 40% in cases of inflammatory bowel disease is suspected.
Upper gastrointestinal endoscopy:
The upper gastrointestinal endoscopy allows the search for ulcer disease, but especially the realization of distal duodenal biopsies that are essential for the diagnosis of malabsorption with finding villous atrophy or abnormal cell infiltration of the lamina propria.
Chief among these diseases, we must mention celiac disease, but Whipple’s disease much rarer, tropical sprue, gastroenteritis eosinophilic well documented by these biopsies.
Radiological examinations:
Scanner abdominopelvic:
The abdominopelvic CT scan with contrast of the small intestine or colon according to the diagnostic orientation is expected before the small bowel which ends the morphological assessment. The scanner enables particularly assess the state of the pancreas (tumor, calcifications), discover liver metastases, intra-abdominal mass, parietal abnormalities in the small bowel, peritoneal effusion subclinical.
Imaging of the small intestine:
The gold standard remains the small bowel.
However in his standard technique, sensitivity remains low. It can be replaced more recently by a enteroclysis performed after ingestion of water or the contrast medium in the small intestine with a probe placed beyond the ligament of Treitz.
The small bowel enteroscopy is little current use as long achievement difficult and does not allow a full exploration of the hail. A new technique (evaluation) of double balloon enteroscopy to facilitate progress could however change this. Videocapsule may have a place in certain diseases of the small intestine responsible for chronic diarrhea, particularly in the balance sheet expansion with Crohn’s disease.
Other tests:
In the absence of diagnostic examinations at the end of raised, the next examination is to provide a fécalogramme, preferably over three days which allows:
– Confirm diarrhea: weighing more than 300 g;
– Dosing steatorrhea (less than 6 g);
– To make a clearance of alpha-1 antitrypsin in case of hypoproteinemia electrophoresis to document a possible enteropathy.
False diarrhea:
If a false diarrhea, it must be on data from fécalogramme:
– Reassess the hypothesis of functional diarrhea;
– Seek a factitious diarrhea the dosage of laxatives in the stool or urine.
If signs of malabsorption:
If signs of malabsorption suggested by a massive weight loss, severe asthenia and fécalogramme, look for vitamin deficiency that clinical examination may suggest: anemic syndrome, skin lesions, mucous membranes, bone (osteomalacia) or neurological (to deficiency neuropathy ). Should be measured folate, vitamin B12, calcium and phosphate a practice, a dosage of vitamin D.
Steatorrhea exceeds 30 g is observed in case of extended parietal lesion of hail or severe exocrine pancreatic insufficiency.
The test that explores D xylose absorption of sugars in the proximal small level is no longer widely used, the information given by duodenal biopsies obtained easily using endoscopy advantageously replacing this assay. The Schilling test that studies the absorption of vitamin B12 with or without intrinsic factor is rarely useful because of the progress of other functional and morphological explorations.
Intestinal bacterial overgrowth:
On suspicion of intestinal bacterial overgrowth (vitamin B12 deficiency, steatorrhea), the review is to achieve a glucose breath test, the sensitivity is excellent with good specificity in the absence of prior antibiotic therapy within 15 days prior examination. This examination is, however, available only in specialized services.
Investigations of the pancreas:
For a chronic exocrine pancreatic insufficiency or clinically speaking, it takes at least 90% destruction of the pancreatic acini.
This phenomenon is so late in the natural history of chronic pancreatitis.
The study of pancreatic secretion after stimulation (secretin or cholecystokinin) is little used in clinical practice because of its highly invasive nature.
Pancreatic imaging comprises firstly an ultrasound, then above a scanner that lets you know the morphological state of the gland (hypertrophy, calcification) and deduce its functional state. This morphological approach can be complemented by endoscopic ultrasound, which can detect early signs of chronic pancreatitis and especially highlight a small tumor, endocrine.
Wirsungraphy retrograde selective catheterization of pancreatic can detect early chronic pancreatitis by objectifying a dilated pancreatic duct, the presence of intraductal stones and dilatation of both pancreatic and secondary channels. However there is a risk of pancreatitis spurt related to the review.
The images obtained by MRI wirsungo are also interesting and without iatrogenic risk, making it currently the preferred first line.
There is an excellent correlation between the data and data Wirsungraphy study of pancreatic secretion by tubing.
The study of serum enzymes (amylase and lipase) is not a reflection of the secretory capacity of the exocrine pancreas.
In contrast, the determination in the stool of some pancreatic enzymes, including elastase, seems interesting.Indeed, a single stool sample is needed to enable this technical Elisa assay. The sensitivity of this test is good, but it does recognize the existence of pancreatic insufficiency at a stage already evolved.
PABA test is an indirect technique to highlight the challenge cit exocrine enzyme but requires urine collection 6 hours after a test meal, the patient is fasting for the day. Its sensitivity remains good, but it is rarely used in clinical practice because of its technical requirements.
CHRONIC DIARRHEA ETIOLOGY:
The main causes of chronic diarrhea are presented in Box 1.
Box 1. Major causes of chronic diarrhea
Colonic
Colon cancer
Ulcerative colitis
Crohn’s disease
Microscopic colitis
Small bowel origin
Celiac disease
Crohn’s disease
Whipple disease
Tropical Sprue
Amyloidosis
Eosinophilic gastroenteritis
Primary intestinal Lymphangiectasia
Chronic intestinal pseudo-obstruction
Malabsorption of biliary salts
Lactase deficiency
Intestinal bacterial overgrowth
Hail Radiation
Lymphoma
Giardiasis
Pancreatic origin
Chronic pancreatitis
Pancreatic Cancer
Cystic fibrosis
Endocrine
Hyperthyroidism
Diabetes
Hypoparathyroidism
Addison’s Disease
Tumor secreting hormones (vipoma, gastrinoma, carcinoid)
Other etiologies
Factitious diarrhea
Surgical causes: bowel resection, Internal intestinal fistula
Drug Causes
Alcoholism
Autonomic neuropathy
Diarrhea mechanisms can be:
– Driving;
– Osmotic;
– Secretory;
– Volumogénique;
– Exudative.
Driving Diarrhea:
The clinical diagnosis of motor diarrhea is not always easy. The test carmine red (colored stool in less than eight hours after ingestion of carmine red, disappearing within 24 hours) may help. Stool volume is often not increased, but on the other hand they are numerous with the presence of food eaten that day. The stools are often compelling, without abdominal pain associated with no deterioration of general condition, without weight loss. Steatorrhea may be moderately increased, rule less than 15 g. The etiologies of these motor diarrhea are listed in Box 2. Note that the diagnostic far the most frequent motive is the diarrhea irritable bowel often occurring in people under 45 years.
Box 2. Leading causes of motor diarrhea
Endocrine Origin
Hyperthyroidism
Medullary Thyroid Cancer
Carcinoid syndrome
Neurological origins
Truncal vagotomy
Diabetic neuropathy
Shy-Draper syndrome (orthostatic hypotension)
Digestive origins
Small bowel resection
Reaching the small extent (postradique, Crohn)
Irritable bowel ++
Osmotic diarrhea:
Osmotic diarrhea is often difficult to distinguish from a motor diarrhea and are due to ingestion of solutes little to no absorbable.
The example of this type of diarrhea is caused by the ingestion of polyethylene glycol (PEG) to get a colonic wash before colonoscopy.
In pathology, little or no absorbed substances cause osmotic water use and electrolytes which increase the intraluminal fluid flow.
If the substance that causes diarrhea is fermentable, the saddle is acidic, frothy, hot, often determining a very embarrassing perianal dermatitis. Diarrhea stops when test of fasting.
The etiologies of these osmotic diarrhea are listed in Box 3.
Box 3. Main causes osmotic diarrhea
Deficiency disaccharidases
Lactase and sucrase-isomaltase
Osmotic laxatives
Magnesium sulphate and soda
Macrogol (PEG)
Lactulose
Lactitol
Antacid
Magnesia oxide
Hydroxide magnesia
Secretory diarrhea:
Secretory diarrheas are usually very heavy diarrhea than 500 g or 1 kg / 24 h sometimes associated with hypokalemia, metabolic acidosis or prerenal failure. It persists when fasting.
The causes are noted in Box 4.
Box 4. Main causes of secretory diarrhea
Irritant laxatives
Anthraquinone
Phenolphthalein and bisacodyl
Other drugs
Colchicine
Digitalis
Biguanide
Organ damage colic
Collagenous colitis and lymphocytic
Chronic inflammatory bowel disease
Villous adenoma (hypokalemia)
Familial adenomatous polyposis
Infectious causes
Giardiasis (common variable hypogammaglobulinemia)
Amoebiasis
Campylobacter
Salmonella
Cryptosporidiosis and microsporidiosis (if immunosuppression)
Cytomegalovirus and herpes virus
Endocrine tumors
Cholera endocrine (VIPoma, pheochromocytoma)
Diarrhea volumogénique:
The volumogéniques diarrhea are due to a flooding of the gut by an increase in digestive gastric secretory rates in particular in the framework and Zollinger Ellison syndrome.
The control of acid secretion by inhibitors of proton pump stops diarrhea.
Exudative diarrhea:
Exudative diarrhea have clinical signs in case of major protein loss: edema sloping white, soft and painless, sometimes hydrops or peritoneal effusion chylous (if lymphatic obstruction). The biological sign is hypoalbuminemia, sometimes profound, evocative if it is associated with hypogammaglobulinemia.
The main causes of exudative chronic diarrhea are noted in Box 5.
Box 5. Main causes of exudative diarrhea
Obstacle lymphatic drainage
Lymphoma
Pancreatic Cancer
Whipple disease
Primitive intestinal lymphangiectasia (Waldmann’s disease)
Out of the epithelial barrier
Bacterial or viral colitis (HIV)
Inflammatory colitis (chronic infl ammatory bowel disease)
Radiation enteritis
Digestive tumor ulcerated
Bacterial overgrowth
Polyposis Cronkhite-Canada
Disease Ménétrier
Lupus
Malabsorption:
The main causes of malabsorption are presented in Box 6.
Box 6. Main causes of malabsorption
Villous atrophy
Celiac disease
Tropical Sprue
Graft disease against the host GVHD (Graft vs. Host Disease)
Atrophy primitive ileal
Giardiasis
Other parietal lesions of the small intestine
Whipple disease
Mycobacterium avium (AIDS)
Lymphoma of the small bowel
Crohn’s disease extent
Hail Radiation
Eosinophilic Gastroenteritis
Parasitic
Giardia lamblia
Cryptosporidiosis (AIDS)
Microsporidiosis (AIDS)
Postsurgical
Hail short (less than 1 meter)
Ileal resection greater than 1 meter
Gastrectomy
Chronic bacterial colonization of the small intestine
Anses blind
Postsurgical strictures hail or not
Small bowel diverticulosis
Movement Disorders of the small intestine
Scleroderma
Chronic intestinal pseudo-obstruction
Amyloidosis
Exocrine pancreatic insufficiency
Chronic pancreatitis
Cancer of the pancreas head
Cystic fibrosis
Failure to bile salts
Cholestasis intra- or extrahepatic
Biliary fistula
Ileal resection
FREQUENTLY ETIOLOGIES:
Among the etiologies of chronic diarrhea, some need to be discussed as a priority.
Lactose intolerance in adults:
Deficits lactase adult must be classified into two distinct types:
– Primitive genetic deficiencies especially;
– Deficiencies secondary to many digestive disorders, infectious or relating to villous atrophy.
In case of primary deficiency, cit challenge concerns the lactase the brush border of the enterocyte, but there is no detectable histological alteration. This deficiency is final and its prevalence varies greatly among ethnic groups: rare among Caucasians (5-15%), it is much more common in Mediterranean and especially in blacks and Asians.Deficiency who moved from childhood worsens in adulthood. In adults under Western nutrition, the challenge usually accompanied cit no nutritional impact, lactose accounting for a small share of total calorie intake.
Ingested lactose present in the intestinal lumen determines postprandial osmotic diarrhea, often acid, irritating and a colonic fermentation responsible for flatulence.
Sometimes the symptoms can mimic an ordinary irritable bowel and this is food oriented questioning that can suggest the diagnosis.
Anyway there is in practice a frequent dissociation between lactase deficiency and symptoms of intolerance, administration of moderate amounts of milk is often tolerated and asymptomatic.
Definitive diagnosis, if necessary, may use either oral load test with lactose glycemic curve or the hydrogen breath test following lactose administration. The treatment is, of course, in the eviction of dairy products from the diet.
Celiac disease in adults:
Considered rare in adults, recent epidemiological surveys based on serological studies now available give a prevalence oscillating between 1 per cent to one per 500 subjects in different countries. This frequency contrasts with the relative rarity of the diagnosis and suggests both the existence of little or not symptomatic form as well as insufficiently recognized celiac disease.
Clinical picture:
The classic form (50%) corresponds to a range of hail damage with chronic diarrhea, weight loss, abdominal distension.
Extra-digestive presentation forms are common in adults and correspond to more limited living with hail macroou microcytic anemia, osteomalacia, iron deficiency, recurrent aphthous stomatitis, unexplained transaminase elevations, etc. The silent forms, unknown, corresponding to total or partial villous atrophy without any digestive symptom. This form is preferentially seek in diabetics, hypothyroid, if PBC, serum antibody deficiency antigliadin (IgA), in trisomy and parents first degree celiac patients.
Reviews:
If the disease is mentioned, look for anti-gliadin antibodies, particularly IgA, more specific, currently supplanted by endomysial antibodies and highly specific antitransglutaminases. The essential diagnostic criterion remains the detection of villous atrophy associated with intraepithelial lymphocytosis on the duodenal mucosa biopsies obtained during gastroscopy (Fig. 1, see also included in the color specifications). Definitive diagnosis must require villous regrowth after a gluten-free diet followed for 6 months. The treatment is based solely on the complete and final eviction of gluten found in cereals (wheat, rye, barley). There is frequently associated with autoimmune diseases. The risk of lymphoma (especially intestinal) is increased, as well as that of some epithelial cancers (hail, pharynx, esophagus). The endomysial antibody levels decreases if followed without gluten diet and can be a monitoring mode to enjoy the good adhesion to the plan.
Inflammatory bowel disease:
Ulcerative colitis and Crohn’s disease are inflammatory bowel diseases whose etiology is unknown. The incidence of Crohn’s disease has increased since half a century (× 6) while the prevalence of ulcerative colitis has remained stable. The peak incidence of these diseases is around the third decade.
Diagnosis:
Clinical picture:
The evolution unpredictable, is characterized by outbreaks of varying severity interspersed with remission.
The symptoms in the two diseases is often close, but rectal bleeding are often revealing in ulcerative colitis, anal fistula rather suggestive of Crohn’s disease. Chronic diarrhea is very common, often inaugural. Extradigestive manifestations, rheumatologic (arthralgia, back pain) skin (erythema nodosum) or mucosal (oral aphthous ulceration) may precede or be associated with gastrointestinal symptoms.
The abdominal pain of varying intensity, often located at the right iliac fossa in cases of Crohn’s disease: a terminal ileitis may mimic appendicitis.
We must seek the questioning the existence of Koenig syndrome, stenosis witnessed hail. Chronic diarrhea associated with anal fistula evokes a Crohn’s disease.
Reviews:
The sigmoidoscope allows the diagnosis of ulcerative colitis, rectal involvement is constant in this disease. Thrust there is always an inflammatory syndrome to look at chronic diarrhea.
Stool cultures and stool parasitology are necessary to eliminate an infectious colitis, main differential diagnosis.
Colonoscopy with ileoscopy allows in all cases the diagnosis and distinguished mostly ulcerative colitis inflammatory disease which is continuous from the rectum, Crohn’s disease whose disease is often discontinuous. Reaching the small exists only in Crohn’s disease (Fig. 2 and 3, see also Figure 3 in the color specifications). The perendoscopic biopsies can reveal granulomas (30 to 50% of Crohn’s disease) that can differentiate the two diseases. The evolving risk eventually after 10-15 years of evolution was the malignant, risk common to both diseases.
Treatment:
The medical treatment of moderate uses the 5 aminosalycilés. In case of more serious push corticosteroids whose action is fast systemically are needed. In steroid-forms, immunosuppressants (azathioprine, Imurel®) should be used. In case of very active or fistulizing Crohn’s disease, anti-TNF alpha antibody (eg, infl iximab, Remicade) give often spectacular, but unfortunately transient results, requiring maintenance therapy. Surgical treatment is considered only in case of failure of medical treatment. It may be indicated if emergency occurs fulminant colitis (megacolon) sometimes indicative of the disease.
Microscopic colitis:
Diagnosis:
They are responsible for chronic secretory diarrhea, sometimes severe water (15 to 20 bowel movements a day) fluctuating. This picture contrasts with a noisy condition often tainted with a macroscopically normal colonoscopy. Only biopsies allow us to recognize the diagnosis. Made of collagen colitis is distinguished by the presence of a thickened collagen strip under the surface epithelium and lymphocytic colitis which results in an increased number of intraepithelial lymphocytes in the surface epithelium.
Both diseases give a similar clinical picture and may only be distinguished by colonic biopsies. Biologically, there is no inflammatory syndrome and stool cultures are negative. The spontaneous evolution is sometimes limiting, but can also be interspersed with chronic remissions breakouts. There is a strong female in collagenous colitis.Autoimmune diseases (++ thyroid, connective tissue) are often associated. Lymphocytic colitis are sometimes caused by drugs (veinotonic, ranitidine, proton pump inhibitors, etc.) and in this case-limiting stopped the offending product.
Treatment:
The best current treatment seems to be the budesonide orally (Entocort®) or corticosteroids at low doses. The 5-aminosalycilés are less consistently effective.
Irritable colon and functional diarrhea:
The IBS includes a set of functional bowel symptoms including abdominal pain or discomfort associated with altered bowel habits (constipation or diarrhea), all lasting for at least 12 weeks based on criteria established during a consensus meeting Rome (cf. Constipation).
Among the signs suggesting this diagnosis, we must mention the urgency of bowel movements, their often postprandial, sensation of incomplete evacuation, bloating, emission of mucus associated with bowel movements (classical mucomembraneuse colitis).
We talk about irritable bowel to diarrheal trend there are more than 3 bowel movements per day, and irritable bowel syndrome with constipation predominant if there are less than 3 bowel movements per week. Disorders are often inconsistent with periods of spontaneous remission. Irritable Bowel Syndrome with diarrhea form is the most common cause of chronic diarrhea and should be briefly mentioned above in young subjects to avoid an excess of complementary examinations.
Treatment:
The antimotility like loperamide are effective, but relapse is the rule upon discontinuation of treatment.
Mucilage, by their hydrophilic property, can increase the viscosity of the stool and thus their urgency.
Dietary measures are often essential: the use of a more or less expanded residue diet is recommended, often followed spontaneously by patients.
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