Types of Small Intestinal Inflammatory Bowel Disease
Forms of small intestinal IBD include lymphocytic-plasmacytic enteritis (LPE), eosinophilic enteritis (EE), granulomatous enteritis, regional enteritis, and neutrophilic enteritis (see ). Furthermore, certain breed-specific patterns of disease are recognized, including Basenji enteropathy and the PLE/protein-losing nephropathy (PLN) syndrome of soft-coated Wheaten Terriers. Although the histopathologic findings of these disorders may differ, the etiopathogenesis is thought to be broadly similar.
LPE is the most common histopathological form of SI IBD, and is characterized by mucosal infiltration of lymphocytes and plasma cells ( ). LPE can be associated with lymphocytic-plasmacytic inflammation in other regions of the GI tract (e.g., lymphocytic-plasmacytic gastritis [see Chapter 56 ] and lymphocytic-plasmacytic colitis [see Chapter 58]). LPE in cats can be associated with inflammatory disease in the pancreas (see Chapter 10) and/or liver (see Chapter 61) as part of the “triaditis” syndrome.
Clinical signs of LPE are similar to other forms of IBD and are not pathognomonic. Severe LPE is reportedly prevalent in German Shepherd dogs, Shar-Peis, and pure-bred cats. The approach to diagnosing LPE is the same as for any other form of IBD. However, in both cats and dogs, it can be difficult to differentiate severe LPE from alimentary lymphoma. Exploratory celiotomy may be a preferable means of collecting biopsy material in cats, given both concerns over differentiation of LPE from GI lymphoma on endoscopic biopsy, and the concurrence of pathologic change in other organs. Given these diagnostic dilemmas, clonality studies assessing T-cell receptor rearrangements may assist in identifying low-grade lymphoma.3
EE is reportedly the second most common form of IBD and can be associated with disease elsewhere in the GI tract. On histopathologic examination, mucosal architectural disturbances (e.g., villus atrophy) are present in conjunction with a mixed infiltrate of inflammatory cells with eosinophils predominating ( ). The diagnosis has been problematic in the past because diagnostic criteria (e.g., degree of eosinophil infiltration) varied amongst pathologists. However, the WSAVA standards suggest clear diagnostic criteria (e.g., mild 5 to 10 eosinophils per ×40 field; moderate 10 to 20 per ×40 field; marked eosinophils dominate the tissue population).2 A diagnosis of EE should only be made once other causes of eosinophilic infiltration (e.g., endoparasitism and hypersensitivity disorders) have been eliminated. EE also may be associated with systemic eosinophilic disorders (e.g., hypereosinophilic syndrome) in both cats and dogs.
The condition can be seen in dogs and cats of any breed and age, although it is more common in younger adult animals. Boxers, German Shepherds, and Dobermans may be predisposed. The clinical signs reported are similar to other forms of IBD, although mucosal erosion and/or ulceration may occur more frequently and lead to hematemesis and melena. Concurrent PLE is also recognized, and severe eosinophilic gastroenteritis is also associated with spontaneous perforation of the GI tract.4
Basenji enteropathy is a severe, hereditary form of LPE that has been well characterized in Basenjis, although the mode of inheritance remains unclear. Vomiting and small intestinal diarrhea are the main clinical signs. A progressive PLE is often noted, and some severe cases develop spontaneous intestinal perforation. Intestinal lesions in Basenjis are characterized by increases in CD4+ and CD8+ T cells.5, 6 In addition to lymphocytic-plasmacytic gastritis, mucosal hyperplasia occur, and this is thought to be secondary to hypergastrinemia. Treatment is usually unrewarding, with progressive clinical signs and dogs dying within months of diagnosis. However, early aggressive combination treatment with glucocorticoids, antibacterials, and dietary modification may achieve remission in some cases.
A unique clinical syndrome has been reported in soft-coated Wheaten Terriers.7 Affected dogs may present with signs of PLE, PLN, or both. A genetic basis is likely and, although the mode of inheritance is not yet clear, a common male ancestor has been identified. An immune-mediated pathogenesis is likely and dietary hypersensitivity might be involved, as suggested by alterations in antigen-specific fecal immunoglobulin (Ig) E concentrations.8, 9 Signs of PLE tend to develop at a younger age than PLN, and clinical signs include vomiting, diarrhea, weight loss, and pleural and peritoneal effusions. Affected dogs are at risk of thromboembolic disease.10 Treatment is similar to that described for general IBD.
This rare form of IBD is characterized by the development of granulomas and mucosal infiltration with macrophages. This condition is likely to be the same as regional enteritis where ileal granulomas are reported.11, 12 Potential causes of granulomatous inflammation include Yersinia and mycobacterial infections, foreign-body reactions, and fungal diseases. In cats a pyogranulomatous transmural inflammation has been associated with feline infectious peritonitis (FIP) virus infection. Although there are similarities between this condition and human Crohn disease, intestinal obstruction and fistula formation are not observed. Conventional therapy for IBD is usually not effective and the prognosis is guarded, although a combination of surgical resection and antiinflammatory treatment was reported to be successful in one case.
Some inflammatory diseases may be characterized by infiltrates of neutrophils or by granulomatous inflammation, although these patterns are rare. If neutrophils are evident, an underlying bacterial infection should be considered. Alternatively, the neutrophilic infiltrate may have arisen from bacterial invasion secondary to mucosal barrier disruption from erosive or ulcerative lesions. Glucocorticoids are generally not recommended for such cases, unless they fail to respond to all other therapeutic modalities.
Proliferative enteritis is characterized by segmental mucosal hypertrophy of the intestine. It is most common in pigs, but a similar although very rare condition has been reported in dogs.13 There may be an underlying infectious etiology and Lawsonia intracellularis infection has been implicated but not yet been proven. Other potential infectious causes include Campylobacter spp. and Chlamydia.
Reportedly, IBD has an immune-mediated etiology and thus the GI associated lymphoid tissue likely plays a critical part in pathogenesis.14 Full details of the mucosal immune system are found in Chapter 3, while intestinal inflammation is reviewed in Chapter 4. Briefly, the intestinal mucosa has a barrier function (“immune exclusion”), and controls exposure of antigens to the gut-associated lymphoid tissue, which must generate protective immune responses against pathogens while remaining “tolerant” of harmless environmental antigens such as commensal bacteria and food. IBD develops when the normal decision-making process breaks down, leading to inappropriate immune responses and uncontrolled inflammation. Critical to the development of inflammation is a breakdown in tolerance to normal luminal antigens (particularly endogenous bacterial species). This loss of tolerance may result from disruption of the mucosal barrier leading to excessive antigen exposure to the underlying immune system, from dysregulation of normal mucosal immune system function, or from a combination of these processes. The end effect is uncontrolled inflammation, which is the result of activation of the many effector pathways. The inflammation can then lead to architectural disruption, resulting in adverse effects on function, which depend upon the part of the bowel affected.
Unfortunately, data that directly assess the pathogenesis of canine small intestinal IBD are limited, and many gaps in our understanding remain. Many studies have used histochemical and immunohistochemical techniques to quantify immune cell populations within the intestinal mucosa with variable results.14 For canine IBD, recent studies have suggested an increase in cells expressing Toll-like receptors-2, -4, and -9.15 Other studies have shown a decrease in certain lymphocyte populations (total T cells and IgG+ plasma cells), while others have shown increases (αβ T cells, CD4+ T cells, IgG+ plasma cells) as well as increased macrophage and granulocyte numbers.14 The confusion is compounded by the fact that in feline IBD, a disease with similar histopathologic changes to the canine form, the only reported difference from control samples was an increase in cells expressing major histocompatibility complex class II.16
Inconsistent results have also been seen with the studies conducted to date on soluble immunologic factors. Increased concentrations of acute phase proteins (e.g., C-reactive protein) have been documented in canine IBD in some,17 but not all studies.18, 19 Recent studies suggest decreased acute-phase proteins in feline IBD.20 Initial semiquantitative reverse transcriptase PCR (RT-PCR) studies suggested increased cytokine gene expression in canine chronic enteropathies,21 and this has been confirmed in one,22 but not all,23 more recent studies that have used real-time PCR methodology. Again, these results differ from feline studies, where histopathologic evidence on mucosal inflammation correlated with increases in a range of cytokines.24 Unfortunately, in all of these studies, gene expression alone was assessed, and not the functional protein. However, in a recent study, tumor necrosis factor (TNF)-γ protein was not detected in the serum of 15 dogs with IBD.16
The reasons for such discrepancies are not known but may relate to the fact that the chosen gold standard throughout was histopathology, which itself is variable and lacks consensus among pathologists.2 An alternative possibility is that the many studies have assessed patients in various stages of disease, and it may be that immunologic responses differ, and this lead some researchers to suggest the alternate name of “chronic enteropathy.”18
Many clinicians consider small intestinal IBD to be the most common cause of chronic vomiting and diarrhea in dogs and cats; however, given that large scale epidemiologic studies have hitherto not been conducted, the true prevalence of the condition is unknown. In reality, the condition may be overdiagnosed as a result of the ease with which endoscopic biopsy samples of the intestine can be collected, the current difficulties in interpretation of histopathologic specimens, and because alternative reasons for the clinical signs are inadequately eliminated during the diagnostic workup.
The studies that have been published to date suggest that canine SI IBD is most common in middle-aged animals and is uncommon in dogs younger than 12 months of age. Young and growing animals are most likely to suffer from either infectious causes of chronic diarrhea or adverse reactions to food components. No apparent gender predisposition has been reported. IBD can potentially occur in any breed of dog, although predispositions are reported for certain breeds (discussed previously). IBD can affect cats of any age or gender, although middle-aged animals are most commonly affected. Some pure breeds (e.g., Siamese) are said to be predisposed to IBD; the pattern of disease also differs in that concurrent histopathologic changes can be seen the intestine, pancreas, and liver (often termed triaditis) ( ). For instance, there may be concurrent LPE, lymphocytic cholangitis, and chronic lymphocytic pancreatitis.2 Interestingly, concurrence of IBD and pancreatitis has been reported in dogs,25 suggesting that the distinction between species may be less clear than previously thought.
A range of possible clinical signs is associated with both canine and feline SI IBD, but none are pathognomonic for the condition. Not surprisingly, a “small intestinal pattern” diarrhea is most commonly seen (e.g., increased volume, watery, altered color). However, mixed-pattern diarrhea can be seen if the IBD also involves the large intestine and, in occasional cases, a large intestinal pattern diarrhea occurs, most likely the result of prolonged SI diarrhea or the presence of agents that stimulate colonic secretion (e.g., bacteria, bacterial toxins, deconjugated bile acids, or hydroxylated fatty acids).
In cats, vomiting is often the predominant clinical sign of small intestinal IBD, and diarrhea may be only occasional or absent. This may, in part, be related to the fact that some cats do not use a litter tray and thus owners may be unaware of toileting habits. Vomiting is also seen in canine SI IBD although, in the authors experience, almost invariably accompanies, and is less severe than, diarrhea. Hematemesis or melena is usually associated with more severe disease, which has caused mucosal ulceration or erosion; although it can occur in any form of IBD, it appears to occur more often with EE.
Appetite changes can be variable in SI with some cases demonstrating polyphagia, others show differing severities of anorexia, or there may be no appetite change observed. If marked inflammation is present within the SI, significant malabsorption may result, and this can lead to weight loss. Such cases may also develop panhypoproteinemia, and two studies demonstrated that hypoalbuminemia is a poor prognostic indicator in IBD.18, 26 If marked hypoalbuminemia is present (e.g., serum albumin concentrations below approximately 1.5 g/dL), associated signs such as ascites and subcutaneous edema may develop. Thromboembolism and remote organ failure is seen in some patients with PLE. Other systemic consequences of IBD include thrombocytopenia and arthropathies and typical signs may be noted. However, such reports are rare,27 and in my opinion these are uncommon findings in both canine and feline IBD. Progression of disease is variable and, in some cases, signs may wax and wane.
General physical examination findings may include dehydration, alterations in demeanor, poor body condition, and signs of anemia if associated blood loss is severe. Abdominal palpation is an important component of the examination, and associated findings include (mild) abdominal discomfort, thickened intestines, turgid or thickened intestinal loops, and ascites (fluid thrill). Although rectal examination does not directly investigate the SI, it may reveal evidence of changes in fecal characteristics (e.g., melena).
In humans, activity indices are used to quantify disease severity in IBD, aiding the assessment of the response to treatment and allowing comparisons between published studies in the literature. Recently, an activity index was suggested for canine IBD (canine IBD activity index [CIBDAI]; ),17 and its use in the clinical setting provides a more objective measure of therapeutic response.18, 28 In one study, CIBDAI correlated with serum acute phase protein concentrations,17 although this was not confirmed by recent work.19 Clinicians must understand that increases in CIBDAI simply suggest an increase in severity of GI signs, and that high values do not confirm the diagnosis of IBD. For example, increased CIBDAI has been seen in dogs with food-responsive conditions, and values decreased on successful treatment.29 More recently, a variation of CIBDAI, the canine chronic enteropathy activity index (CCEAI; see ) was proposed.18 All of the same signs are scored as for the CIBDAI, but additional characteristics are also assessed (e.g., presence of ascites and/or peripheral edema, pruritus, and serum protein concentrations). A recent study shows that this correlates better with prognosis than the CIBDAI18; however, the advantage of improved performance may be offset by the requirement for blood sampling and serum albumin measurement. Time will tell which system is preferred by clinicians and researchers. Finally, an activity index for feline IBD (FIBDAI) was proposed, which makes use of histology, GI signs, serum total protein and phosphorous concentrations, serum alkaline phosphatase concentration, and endoscopic lesions.30
| Characteristic | CIBDAI | CCEAI |
|---|---|---|
| Attitude/activity | 0. Normal | 0. Normal |
| 1. Slight decrease | 1. Slight decrease | |
| 2. Moderate decrease | 2. Moderate decrease | |
| 3. Severe decrease | 3. Severe decrease | |
| Appetite | 0. Normal | 0. Normal |
| 1. Slight decrease | 1. Slight decrease | |
| 2. Moderate decrease | 2. Moderate decrease | |
| 3. Severe decrease | 3. Severe decrease | |
| Vomiting | 0. None | 0. None |
| 1. Mild (once/wk) | 1. Mild (once/wk) | |
| 2. Moderate (2 to 3/wk) | 2. Moderate (2 to 3/wk) | |
| 3. Severe (>3/wk) | 3. Severe (>3/wk) | |
| Stool consistency | 0. Normal | 0. Normal |
| 1. Slightly soft feces, fecal blood mucus, or both | 1. Slightly soft feces, fecal blood mucus, or both | |
| 2. Very soft feces | 2. Very soft feces | |
| 3. Watery diarrhea | 3. Watery diarrhea | |
| Stool frequency | 0. Normal | 0. Normal |
| 1. Mild increase (2 to 3/day) | 1. Mild increase (2 to 3/day) | |
| 2. Moderate increase (4 to 5/day) | 2. Moderate increase (4 to 5/day) | |
| 3. Severe increase (>5/day) | 3. Severe increase (>5/day) | |
| Weight loss | 0. None | 0. None |
| 1. Mild (<5%) | 1. Mild (<5%) | |
| 2. Moderate (5% to 10%) | 2. Moderate (5% to 10%) | |
| 3. Severe (>10%) | 3. Severe (>10%) | |
| Serum albumin | 0. Albumin >2.0 g/dL | |
| 1. Albumin 1.5 to 1.99 g/dL | ||
| 2. Albumin 1.2 to 1.49 g/dL | ||
| 3. Albumin <1.2 g/dL | ||
| Ascites and peripheral edema | 0. None | |
| 1. Mild ascites or peripheral edema | ||
| 2. Moderate ascites/peripheral edema | ||
| 3. Severe ascites/pleural effusion and peripheral edema | ||
| Pruritus | 0. No pruritus | |
| 1. Occasional episodes of itching | ||
| 2. Regular episodes, but stops when asleep | ||
| 3. Dog regularly wakes up due to itching | ||
| Final score | 0 to 3. Clinically insignificant disease | 0 to 3. Clinically insignificant disease |
| 4 to 5. Mild IBD | 4 to 5. Mild IBD | |
| 6 to 8. Moderate IBD | 6 to 8. Moderate IBD | |
| ≥9. Severe IBD | ≥9. Severe IBD |
Given that none of the clinical signs and physical examination findings that are seen with IBD are pathognomonic, further investigations are essential in order to make a diagnosis. Because the term idiopathic IBD should be restricted to use in cases in which intestinal inflammation is found without an obvious underlying cause, all other etiologies must first be excluded. Therefore detailed preliminary diagnostic investigations must be performed, prior to acquisition of GI biopsy samples, to ensure that other etiologies are excluded. Investigations include fecal analyses, routine hematologic analysis, clinical chemistry, urinalysis, assay of serum TLI, pancreatic lipase immunoreactivity, and diagnostic imaging. Although none of these tests is diagnostic for IBD, they help to eliminate the possibility of extraintestinal disease (e.g., pancreatitis, hypoadrenocorticism, renal failure, and hepatic failure), anatomic intestinal disease (e.g., tumor or intussusception), and other known causes of intestinal inflammation. Diagnostic imaging in particular allows the clinician to determine whether focal or diffuse intestinal disease is present, allowing selection of the most appropriate method of intestinal biopsy. In many cases, standardized therapeutic trials can help to confirm the diagnosis, by eliminating other possible causes of intestinal inflammation.
In companion animals with SI IBD, hematologic examination is frequently unremarkable. Changes in white blood cells that are occasionally observed include mature neutrophilia, neutrophilia and left shift, and eosinophilia, but none are pathognomonic. Reactive “atypical” lymphocytes may be seen in patients with LPE, and lymphopenia can occur if lymphangiectasia is present. If anemia is present, it may be a reflection of either chronic inflammation or chronic blood loss. Iron-deficiency anemia, with a microcytic hypochromic pattern, also has been reported in IBD,31 and thrombocytosis also may be seen.31
In many patients with SI IBD, clinical biochemistry is unremarkable. If PLE is present, serum concentrations of both albumin and globulin can be decreased. Confirmation of PLE requires the absence of significant liver changes (e.g., marked enzyme elevations, low urea, low glucose) on clinical chemistry, or the absence of anemia on complete blood cell count, and of proteinuria on urinalysis. However, fecal α1-PI measurement may help. Hypocholesterolemia may suggest malabsorption, but this finding is not pathognomonic. Ionized hypocalcemia and hypomagnesemia are also reported.32, 33 Intestinal inflammation in dogs may cause a reactive hepatopathy with mild to moderate (two- to fourfold increases) in liver enzyme (i.e., alanine transaminase [ALT] and alkaline phosphatase) activities. In contrast, as a consequence of their shorter half-lives, liver enzyme increases are less common in feline IBD, and marked elevations in ALT more commonly occur secondary to alimentary lymphoma than feline IBD.34
Fecal flotation is very important in eliminating parasitic causes of mucosal inflammation. In most cases of SI IBD, these tests yield negative results. When occasional positives do occur, determining the significance can be problematic, as these organisms can be found in the stool of healthy animals. Although trial therapy may be considered, clinicians should exercise caution given concerns over the development of therapeutic resistance.
Measurement of serum folate and cobalamin is available for both dogs and cats, and deficiency of these substances is associated with IBD. Recent work has highlighted the importance of hypocobalaminemia in cats,35 and hypocobalaminemia is also a negative prognostic indicator in chronic enteropathy in dogs18 as well as other alimentary tract diseases such as EPI.36 Although such alterations are not pathognomonic, deficiencies in IBD suggest the need for more aggressive therapy against the primary disease, and also the need for parenteral supplementation. This is particularly important, because cobalamin deficiency may itself have systemic metabolic consequences and cause intestinal dysfunction,37 and anecdotal evidence suggests that the response to immunosuppressive therapy for IBD may be suboptimal until cobalamin deficiency is resolved.
Radiographic and ultrasonographic studies are most commonly used to eliminate other possible diseases rather than to make a diagnosis of SI IBD. However, when used in conjunction with specific clinical signs and laboratory testing, the information from imaging studies enables an appropriate choice of a biopsy method (e.g., upper or lower GI endoscopy, or exploratory celiotomy). Ultrasonography in IBD patients can help to document mesenteric lymphadenopathy.38, 39 Although intestinal wall thickness can be measured, one study suggests that this measure is of limited value in the diagnosis of SI IBD.40 In fact, the only occasions when the bowel wall was notably thickened was when edema was present secondary to marked hypoproteinemia. A recent study suggests that different ultrasonographic patterns can help to differentiate chronic enteropathies with different etiologies.41 Loss of normal intestinal layering is more commonly seen with neoplasia than IBD.
Intestinal biopsy is essential to prove the presence of intestinal inflammation and confirm a diagnosis of SI IBD; either endoscopy or exploratory celiotomy can be used. During endoscopy, the gross appearance of the intestinal mucosa can also be observed. Intestinal inflammation may be indicated by findings such as increased granularity, irregularity, and friability with the presence of erosions, ulceration, and spontaneous hemorrhage. However, these findings are not pathognomonic, and correlation between gross inspection and histopathology is poor.18, 28 Limitations of endoscopy include small sample size, superficial and often fragmented samples, and the fact that tissue can only be collected from proximal regions and (occasionally) the distal ileum. Exploratory celiotomy and full-thickness biopsy may be necessary, although this is more invasive and wound healing can be problematic if severe hypoproteinemia is present.42 Nonetheless, the approach may be more suitable for cats, given the tendency for concurrent hepatic and pancreatic involvement,43 the difficulties in differentiating IBD from small-cell lymphoma in endoscopic duodenal biopsies,34 and the reliability of the small size of endoscopic biopsies that are often collected in this species.
The pattern of histopathologic changes in biopsy specimens depends upon the type of IBD. Histopathologic assessment of intestinal biopsies remains the gold standard for diagnosis of many intestinal diseases, but has marked limitations, most notably variable quality of tissue specimens obtained endoscopically44 and poor agreement between histopathologists.45 The latter may be a result of the subjective nature of interpretation of the degree of inflammation, the patchiness of inflammation, or the presence of edema (caused by hypoproteinemia) leading to difficulties in assessing cell density.
It can be difficult to distinguish severe LPE from lymphoma, particularly when endoscopic biopsy samples are examined. This may be a result of the fact that infiltration of malignant lymphocytes is patchy, that inflammatory change may accompany alimentary lymphoma (and predominate in some areas), or that lymphocytic infiltration is deep to the area sampled. Cases of feline alimentary lymphoma can be missed if duodenal endoscopic biopsy samples are used in histopathologic assessment, rather than full-thickness specimens.34 Hence, it may be preferable to collect surgical specimens in this species, and this approach gives the added advantage that other organs can be sampled (e.g., liver and pancreas) when checking for “triaditis.”
The standards published by the WSAVA GI Standardization Group2 hopefully will improve the reliability of IBD diagnosis.18, 28 Ultimately, the primary clinician should interpret histopathology results cautiously and try to relate them to the clinical presentation. Results should be questioned if the histopathologic diagnosis does not fit the clinical picture or the response to apparently appropriate therapy is poor. In some cases repeat biopsy (e.g., by exploratory celiotomy) may be required.
Many research techniques have been developed to assess alterations of the immune system that occur in IBD. Examples include immunohistochemical characterization of immune cell populations,46, 47, 48, 49 measurement of gene expression for cytokines by RT-PCR,21, 22, 23 assessment of T-cell clonality,3 measurement of mucosal perinuclear antineutrophilic antibody (pANCA),50 and measurement of mucosal P-selectin expression.51 Although these techniques have not been widely adopted for clinical diagnosis, there may be potential for future application. In particular, assessment of T-cell clonality may prove to be a useful tool to differentiate LPE from low-grade lymphoma.3 In addition, there may be benefit in development of mucosal pANCA and P-glycoprotein expression for helping to predict response to therapy.50, 51
In many cases, clinicians can use an organized therapeutic plan to help confirm the diagnosis, and determine the optimal therapy for a particular case. Unless the animal is debilitated, single therapeutic modalities are instigated sequentially, and the owner is asked to record precisely in an event diary the frequency and nature of clinical signs. The clinician can then review the diary and calculate disease severity using one of the recognized scoring schemes (see ). Although response to treatment can inevitably be judged more objectively, clinicians should still be cautious that therapy might have only invoked a placebo effect. My favored order of treatment trials is anthelmintic/antiparasitic medication, dietary modification, antibacterial trials, and, finally, trial immunosuppressive therapy.
Regardless of the histologic type of IBD, treatment usually involves a combination of dietary modification, antibacterials, and immunosuppressive therapy. Most recommendations are based upon individual experience because objective information of efficacy is generally lacking, and no randomized controlled clinical trials have been conducted. A staged approach to therapy is recommended whenever possible, but may not be appropriate in seriously ill patients (e.g., those with severe hypoproteinemia) where immediate intervention with combination therapy may be essential. Where sequential therapeutic trials ar
Anatomy of the Canine Stomach, Small and Large Intestine
The small intestine (SI) is, in essence, an interface between the external environment and the body, and is both an absorptive surface and a barrier; it must digest and absorb nutrients while excluding antigens and microbes and eliminating fecal waste. It faces a frequently changing dietary and bacterial intake, and yet has to maintain a dynamic but balanced microflora within its lumen while being intermittently exposed to pathogens. All of its functions—mixing and propulsion, secretion, digestion, absorption, regulation of blood flow, immunologic reaction and tolerance, and elimination—are fully integrated through both local and remote neuroendocrine and immunologic mechanisms (see Chapter 1). It thus has a complex task and requires specialized anatomic arrangements to perform them.
The SI is basically a tube, beginning at the pylorus of the stomach and ending at the ileocolic valve. However, this tube is ultimately in continuity with the external environment, proximally from the mouth via the esophagus and stomach, and distally to the anus via the large intestine ( ).1, 2, 3 It is relatively short, reflecting the typical dietary intake of cats and dogs. It is approximately 1 to 1.5 meters long in adult cats and ranges from 1 to 5 meters in adult dogs, in proportion to the size of the individual. It is divided arbitrarily into three anatomic segments: the duodenum proximally, then the jejunum, and finally the ileum distally (see ).
The first part of the SI, the duodenum, comprises approximately 10% of its total length. It passes from the pylorus dorsally and to the right, at the level of the ninth intercostal space, and is immobilized by the hepatoduodenal ligament. It then turns caudally into the descending duodenum in contact with the right flank, turning again at the caudal flexure near the pelvic brim. It is in close association with the common bile duct and the head and right limb of the pancreas, which lie in its mesentery.
The common bile duct and one pancreatic duct enter the duodenum via the major papilla. In dogs an accessory pancreatic duct often enters at a minor papilla more distally and slightly more ventrally ( ), but there is a range of variations in the actual number of ducts and their drainage pattern from the pancreas (see Chapter 60). The papillae are notable endoscopic landmarks in dogs, but may not be obvious in cats.
The distal duodenal flexure, where the duodenum courses to the left side of the abdomen (see ) is often at the limit of the reach of a standard 1-meter gastroscope, except in cats and small dogs. In dogs the antimesenteric side of the duodenum is marked by a line of whitish, mucosal depressions signifying the presence of specialized lymphoid areas, the Peyer patches (see ). Secretory Brunner glands and annular mucosal folds are features of the human proximal duodenum, but are not present in dogs and cats. After the distal duodenal flexure, the ascending limb of the duodenum crosses the midline and ends at the level of L6 close to the root of the mesentery near the left kidney, with a mesenteric attachment to the colon, the duodenocolic ligament.
The middle part of the SI, the jejunum, arises as an indistinct structural and functional transition from the duodenum and forms the majority of the SI. The jejunum is loosely suspended in the middle of the peritoneal cavity in a dorsal mesentery, forming mobile loops, and is potentially palpable throughout its length in cooperative and nonobese patients. The mesentery is normally a continuous sheet that is folded to allow the SI to loop within the peritoneal cavity, unlike in humans where segments of the duodenum (and colon) are retroperitoneal. The mesentery carries the vascular, lymphatic, and nervous connections between the SI and the rest of the body.
Defects in the mesentery, most often traumatic in origin, can allow internal hernia formation and small intestinal incarceration. An outpouching of the dorsal mesentery of the stomach forms the greater omentum. This structure functions as a protective, immunologic organ, having the ability to migrate to sites of intraperitoneal inflammation and potentially prevent leakage from an intestinal perforation and seal off pockets of infection.
Approximately the last 30 cm of the SI comprises the ileum. The transition from jejunum to ileum in humans is based on changes in diameter, color, and the presence of Peyer patches; in dogs and cats the distinction has been arbitrarily based on the extent of attachment of the ileocolic ligament. In fact the basic structure of the ileum is no different from the rest of the SI and it is not clearly demarcated microscopically from the jejunum. However, it does have some unique functional characteristics, such as the absorption of bile salts and cobalamin. It is also a site of dense lymphoid follicle expression. Meckel diverticulum, a remnant of the embryonic omphalomesenteric duct, found in the ileum of approximately 2% of people and a potential source of bleeding, obstruction, intussusception, and volvulus, is not reported in dogs and cats. The ileum ends at the ileocolic valve in close association with the cecocolic junction.