Case discussions of gastroenterology
Esophageal Disturbances
Chronic Regurgitation Is not an uncommon clinical presenting complaint to the veterinarian. First,
differentiation between vomiting and regurgitation is essential.
Diagnostic testing available to aid in evaluation of the esophagus includes thoracic radiographs, Live
time video for endoscopy and endoscopy. Occasionally static radiography is used with barium to
evaluate for pathology. It should be noted that thoracic radiographs are insensitive for many
esophageal conditions and are best used to document large masses, foreign bodies and/or overt
megaesophagus. Additionally, utilization of barium with standard radiography will pick up obvious
foreign bodies, neoplasia, esophageal strictures (in many cases) and vascular ring anomalies.
Occasionally, barium may provide information regarding motility. Knowledge regarding what normal
motility patterns are may help to interpret this when present. Endoscopic evaluation can be particularly
helpful in these cases when visual structural disease is present however, in many cases disease may be
understated on endoscopy (esophagitis) or completely underappreciated (esophageal dysmotility,
megaesophagus)
Clearly, video fluoroscopy is most well-suited to detecting disturbances in esophageal motility and/or
dynamic disease processes such as gastroesophageal reflux disease and/or hiatal hernias. This also
provides crude assessment of structural disorders. However, of course these studies are going to
underestimate mucosal disease.
Most common cause for regurgitation clinical practice is likely esophagitis this is an underappreciated
disturbance and standard imaging generally is ineffective at documenting presence. Therefore, if
thoracic radiographs are unremarkable, consideration to empirical therapy for esophagitis may be
appropriate in the right context prior to considering further diagnostic testing.
A rare cause of esophageal disease is eosinophilic esophagitis. This is an unusual common seen in the
veterinary patients. Has been reported in one dog and recently been documented in a cat (pending
publication). This condition is common in people and may be related to allergic hypersensitivity.
Occasionally, clinical response to dietary manipulation with respect to regurgitation has been
appreciated in the past without a diagnosis of eosinophilic esophagitis. Therefore, consideration to diet
trials for patients with regurgitation, particularly young patients should be employed. Patients that are
not responsive to treatment may require corticosteroids.
A common clinical scenario in practice is the presence of brachycephalic patients and regurgitation. Any
brachycephalic patient that is reported to be “vomiting” should be questioned highly about
regurgitation. These patients are thought to have a higher incidence of gastroesophageal reflux disease
and/or hiatal hernias. The negative pressure generated from increased inspiratory effort results in a
sucking force within the thoracic cavity and ultimately reflux mediated disease.
Correction of anatomical factors that contribute to inspiratory distress can aid in management all
regurgitation. Many patients can be treated effectively medically, with acid suppressive and promotility
medications. The author believes that individualized therapy is essential in managing these cases
successfully. Some patients exhibit responses to Pepcid and metoclopramide. However, the majority
patients require proton pump inhibitors and/or cisapride or erythromycin to facilitate a lower
esophageal tone.
These patients may also exhibit inflammatory disease elsewhere as was suggested in one veterinary
paper documenting inflammatory gastritis/enteritis in many patients that had endoscopy performed. As
with all other disorders, the interpretation of gastritis in the setting of a patient that is regurgitating
should be cautiously evaluated. In other words, does the biopsy fit the clinical picture.
The episode:
Occasionally, patients will present with episodes of one of the following symptoms: panting, pacing,
vocalization, drooling, anxiety, heart swallowing and/or more typical regurgitation. Is the author’s
opinion that these could potentially represent regurgitation events and subsequent esophagitis. Is not
uncommon to hear these clinical signs arising during recumbency and/or nighttime. This is a common
association and people is thought to be associated with exacerbation of esophagitis.
Current evidence supporting this clinical diagnosis is lacking. A recent study could not definitively
correlate clinical signs of” suspected reflux esophagitis” with changes in esophageal pH. Therefore,
further work needs to be performed to definitively document what is occurring with these events.
Some people may exhibit pain associated with non-acid reflux and could therefore explain some of
these patients.
However as with other clinicians, response to treatment with acid suppression and/or promotility
medications has been effective in some cases to minimize/resolve these events. Individualized titration
of different proton pump inhibitors and/or therapies may help to control the symptoms in some
patients.
Acute illness
Occasionally, acute onset gastrointestinal signs are manifestation of chronic disease. A not so
uncommon scenario is a patient that presents for acute onset perceived nausea (hypersalivation) and
lack of appetite. Each occasionally, gastric neoplasia can be causative. It is important to note that
gastric neoplasia and/or other gastric lesions may easily be missed by abdominal imaging including:
abdominal ultrasound and abdominal radiographs. Therefore, it is reasonable to consider endoscopic
evaluation in the setting of acute disease when the patient signalman and/or lack of response to
conventional therapy is seen. Additional presentations that occur with gastric neoplasia include
anorexia without any other clinical signs for hematemesis on multiple occasions. Isolated hematemesis
is not necessarily pathologic in the setting of acute gastritis. However, recurrent nature warrants
endoscopy.
Along similar lines, occasionally patients can present with acute onset of gastrointestinal signs, where
symptomatic therapy may be appropriate. As clinicians we must understand when symptomatic therapy
is appropriate and when symptomatic therapy is inappropriate. Occasionally, physical examination may
be unremarkable and patients could potentially still have surgical disorders. Therefore, clinical history
should be included in your algorithm as to whether or not you choose to perform additional diagnostics.
For instance, patients with clinical histories of foreign body ingestion or known grazing behavior
(patients on steroids, phenobarbital), additional diagnostic should be considered. In general, any
patient exhibiting abdominal discomfort, chronic signs of disease regardless of owner’s interpretation
(loss of muscle mass, weight loss, chronic vomiting) should have further abdominal imaging
performance. Additionally, diagnostic investigation with ultrasound may miss relatively obvious foreign
objects due to the subtleties and/or gas, whereas radiographs may obviously detect foreign material.
Chronic anorexia
Similar to gastric neoplasia, patients with primary brain tumors (less commonly other brain
disturbances) may have anorexia as their only presenting complaint. These animals may have no
gastrointestinal signs or other physical exam changes consistent with pathology. After extensive workup
both metabolic and imaging, consideration should be made to performing endoscopy and/or MRI.
While these conditions are relatively uncommon, persistent anorexia over several weeks may want this
relatively aggressive diagnostic workup. An additional cause of anorexia without any clinical signs is liver
disease. However, the majority of patients with liver disease will show elevations in liver values and/or
historically had elevation in the past fish however, that being said, serum bile acid testing should be
considered in any patient with persistent anorexia.
Histiocytic colitis
Histiocytic colitis is an uncommon form of ulcerative colitis in boxers and French Bulldogs. This
condition can occur in the other atypical breeds and is thought to likely be a alteration in immune
clearance of intracellular organisms (failed autophagy). These patients present for chronic large bowel
diarrhea associated with hematochezia and tenesmus. Clinical response is poor to traditional therapy
and endoscopic evaluation is necessary to document the disease. Biopsy changes reveal histiocytic
inflammation and sub categorization via FISH will document the presence of the organism
(enteroinvasive E. coli) within tissue. Occasionally, this can affect the small intestine in rare cases.
Recently, clinical response to historically effective antibiotic therapy has been documented. Cornell
laboratory has provided antibiotic sensitivity testing off of biopsies. This requires the foresight of
collecting biopsies and submitting them directly to the lab without formalin fixation. Therefore, in any
case where the disease is suspected, acquisition of non-formalin fixed biopsies is recommended.
Large bowel diarrhea
Chronic intermittent large bowel diarrhea characterized by tenesmus, hematochezia, mucoid stool
without weight loss and/or vomiting is frequently responsive to antibiotics unfortunately, some of these
patients may require chronic antibiotic therapy to maintain remission. Is important to note that some of
these patients can stabilize their gastrointestinal tract and recurrence can be prevented by adding fiber
supplementation. As previously stated, fiber can provide if I can prebiotic effects as well as providing
local chronic health through short-chain fatty acid production. Therefore, cases of antibiotic responsive
colitis and/or chronic colitis of no known etiology may benefit from fiber supplementation. It is
important also to note that fiber supplementation can be given in the form of a diet or supplemented to
pre-existing diets. It is the author’s opinion that some cases of antibiotic responsive diarrhea could be
synonymous with fiber responsive colitis as fiber alone sometimes prevents the need for antibiotics. In
general, when a patient has antibiotic responsiveness, the author likes to start all her courses of
antibiotics with transition to high-fiber diets and/or exogenous supplementation. Following a 4-6 week
course of antibiotics, they are discontinued/tapered.
Pyloric outflow tract obstructions:
The majority of patients that present for pyloric approach tract obstructions present with vomiting as
their main presenting complaint.
Occasionally, patients may present for evaluation of abdominal distention as a sole clinical complaint
additionally, clinical signs may be intermittent in these patients.. Often times, workup for primary
gastric disease resulting in hypomotility and/or systemic/metabolic disturbances that are associated
with decreased gastric emptying times should be evaluated for. In some cases, particularly m or local
obstruction (neoplasia, granulomatous disease, or foreign bodies). Middle-aged to older male dogs
(Chihuahua, Shitzu), a pyloric outflow tract obstruction associated with pyloric hypertrophy should be
considered. Additional causes of pyloric obstruction should also be ruled out.
Radiographic evaluation may reveal a “gravel sign” or “Sieve sign” suggesting a chronic partial pyloric
obstruction. A good ultrasonographer for should be able to identify thick of the wall within the pyloric
region to see whether or not this is likely. It should be noted that a small percentage of patients will be
missed with ultrasound. Endoscopic diagnosis is the hallmark of diagnosis. Endoscopic visualization
reveals hyperplasia of the pylorus and occasionally, histologic features are relatively unremarkable on
endoscopic biopsies due to partial thickness sample acquisition. Classically, these patients present for
abdominal distention and/or chronic vomiting or weight loss. Surgical intervention for chronic
hypertrophic pyloric gastropathy is recommended.
Chronic anemia
Occasionally, patients present for anemia that is intermittently present and regenerative. Additional,
whole clues on your CBC is the presence of a microcytic, hypochromic anemia. It should be noted that
many patients lack microcytosis or hypochromasia. Gastrointestinal blood loss is not an uncommon
cause for this presentation. Documentation of melena may not be appreciated in these patients as the
volume of blood loss is not substantial enough to result in melena. It is very uncommon for there to be
significant blood loss from any other site, results in a regenerative anemia without obvious detection
(respiratory, urinary, pleural cavity). Abdominal workup including ultrasound and/or abdominal
radiographs is often times unremarkable. Additionally, barium may or may not reveal an answer.
Small mucosal lesions are frequently missed on this form of study. Gastric ulcerations are almost always
missed on these studies unless associated with the mass. Therefore, endoscopic evaluation efficiently
recommended. It should be noted that only a small portion of the gastrointestinal tract is evaluated
with the endoscope. Therefore, the endoscope should be completely buried to not miss more distal
lesions. Additionally when possible, lower gastrointestinal endoscopy with ileoscopy is recommended.
Rare occasions, bleeding gastrointestinal masses can be missed on all diagnostic tests and surgical
exploration is needed. This too can miss lesions. Surgeons can only palpate the serosal aspect of the
gastrointestinal tract. Therefore, superficial mucosal lesions will always be missed. Coordination of
endoscopy with surgery (at the time of surgery) can potentially provide a diagnosis when neither test
alone was capable.
Malabsorptive disease:
In general, patients that are ingesting adequate calories with appropriate commercial/balanced diets
should maintain their body weight. If they are not, one must suspect one of the following: increased
caloric demands (hyperthyroidism), decreased energy utilization (diabetes mellitus), decreased
intestinal function (diffuse enteropathies) and/or alterations in pancreatic function.
Patient gastrointestinal malabsorption may present with limited to no gastrointestinal histories. Subtle
findings appreciated on physical examination including poor hair coat and/or loss of muscle mass may
be appreciated. The most common presenting clinical complaints are chronic weight loss, vomiting
and/or diarrhea. However, as stated above they may present for incidental discovery of
hypoalbuminemia or changes in stool volume. Generally speaking increases in stool volume without an
complementary change in diet volume and/or type, suggests changes in absorptive capacity.
In the workup of these patients, abdominal imaging and routine bloodwork should be performed.
Routine bloodwork should include: CBC, chemistry, T4, urinalysis and consideration should be made to
performing cortisol, ACTH stimulation test, gastrointestinal panel (TLI, cobalamin, folate).
In some patients, with hypoalbuminemia, owners are reluctant to perform biopsies in the setting of
minimal gastrointestinal signs and/or image changes, despite hypoalbuminemia. In these cases,
consideration to documenting protein loss from the gastrointestinal tract through an alpha protease
inhibitor assay may be of value.
Following appropriate evaluation, imaging could be considered prior to considering histopathology.
Imaging made side an opportunity to perform minimally invasive tests (aspirate, percutaneous biopsy,
etc.) without the need to perform endoscopy or surgery. However, it is important to note that
abdominal ultrasound is nonspecific for many patients with these disorders. In other words, mild
intestinal thickening or lymphadenopathy do not define a specific etiology and histopathology is still
required. Additionally, many patients may have a normal ultrasound, suggesting a “normal”
gastrointestinal tract. This could not be further from the truth, the clinical presentation strongly argues
that biopsies are needed.
Biliary obstruction
While biliary obstruction is an uncommon cause of clinical illness in veteran medicine, recent
interventional advances in therapy may be important when needed. Most common cause of biliary
obstruction in canine patients is chronic pancreatitis resulting in extra luminal compression of the
common bile duct. The majority of these patients will resolve over time if the pancreatitis is allowed to
recover. Some of these patients may develop progressive biliary obstruction that becomes related to a
primary stricture rather than pancreatitis itself. Differentiating the patient with pancreatitis from that
that gets a stricture is difficult at times. Patients with inactive pancreatitis (resolving pain, improved
appetite, normalization of PLI) and persistent/progressive changes consistent with extrahepatic biliary
obstruction are likely to have strictures. Whereas patients with active pancreatitis could potentially
have both. Therefore, serial evaluation and interpretation in light of the current clinical signs may help
to determine whether or not biliary intervention is needed. Occasionally, decompressive courses the
centesis can be performed safely in many patient to allow time for the pancreatitis to resolve.
Feline patients frequently develop extrahepatic biliary obstruction secondary bacterial
cholangitis/cholecystitis/choledochocitis. Thickening of the common bile duct and development of
exudate/concretions appear to be the most common causes in this scenario. Additional clinical causes
and cats include inflammatory bowel disease and/or neoplasia add the major duodenal papilla.
Serial ultrasounds evaluating for progressive distention of the common bile duct and/or development of
intrahepatic bile ducts within the liver should be performed. Ultrasound changes may not detect
marked distention of the gallbladder. In other words, gallbladder size does not definitively rule out
extrahepatic bile duct obstruction. Particularly in cats, chronic cholangitis (noninfectious or historically
treated infectious) can result in marked distention of the common bile duct with torqued wasabi and
measurements exceeding the “normal” common bile duct dimensions. In these patients, the distention
of the bile duct is likely associated with loss of elasticity over time, rather than pressure expansion from
obstruction. Surgical intervention is not recommended in these patients.
Historical intervention for these patients might have included surgical cholecystectomy, with occasional
rerouting procedures. Additionally, placement of stents at surgery across the major duodenal papilla
have been performed. Recently, interventional placement of stents using endoscopic assistance has
been made possible.
Refractory inflammatory bowel disease:
It is not uncommon for a patient to present with refractory inflammatory bowel disease. Is crucial in
this scenario that the clinical history be reevaluated to ensure that it is accurate (regurgitation vs.
vomiting, etc.). Additionally, the previous information that led to the diagnosis should be reevaluated
(review of biopsies in light of the clinical history and image changes).
Of course, patients with inflammatory bowel disease may develop complicating factors including
infection (Giardia, Cryptosporidium, etc.) or may have other diseases altogether. A common condition
that is overlooked at times is the presence of exocrine pancreatic insufficiency. Historically, it was
believed that this disease only existed in young German shepherds. Additionally, the clinical
presentation is classically associated with large-volume diarrhea, steatorrhea and ravenous appetite.
Clearly, older patients with less than typical presentations exist. Therefore performing a TLI is essential
in any refractory case and is ideally recommended for any patient associated with malabsorption prior
to the acquisition of biopsies. Another cause that is occasionally missed has a cause for progressive
weight loss is occult neoplasia. Patients may continue to maintain a good appetite with neoplasia and
progressive weight loss may be appreciated. Therefore, radiographic evaluation of the thoracic cavity
and abdominal imaging to screen for neoplastic disease is recommended. Along these lines, chronic
metabolic derangements including severe azotemia, severe chronic respiratory disease and/or hepatic
disease may be associated with some degree of weight loss. In other words, anytime patient is showing
progressive weight loss despite “appropriate” intervention, further diagnostic workup may be indicated.
Occasionally, patients with inflammatory bowel disease are truly refractory and modifications in diet
and/or medications are needed. The addition of cyclosporine is commonly used. However, alternative
immunomodulatory therapy may be essential. More importantly, it should be noted that synergism
between diet, immunosuppression and/or manipulation of bacterial flora (prebiotics, probiotics,
antibiotics) may be more effective than any one of these alone.
Interpreting a patient not biopsy
It is not uncommon for patients that present with acute onset disorders may end up having surgical
intervention and/or exploratory surgery for suspected surgical disease. These patients may have
biopsies obtained during these procedures. It is critical that the presence or absence of inflammation on
the biopsy does not alone warrant immunosuppressive therapy. In other words, a patient with an acute
history in which the clinical diseases resolved or fixed surgically, should not have lymphoplasmacytic
biopsies be interpreted as inflammatory bowel disease. As previously stated, the diagnosis of an
inflammatory enteropathy is based not only on histology but on the clinical diagnosis of chronic
gastrointestinal signs, absence of other concurrent disease processes and lack of response to dietary
and/or therapeutic trials.
One of the difficult things as a clinician is to ignore information that is provided on a biopsy. Patient
with inflammatory bowel disease do not histologically change over time on repeat biopsies despite
effective therapy. Therefore, it is reasonable to assume that small subset of patients may have had
historical gastrointestinal disease with persistent histopathological changes, despite the presence of a
functional gastrointestinal tract.
Hemorrhagic gastroenteritis:
This is a condition of unknown etiology may be thought to be related to Clostridial will organisms.
Patients with hemorrhagic gastroenteritis have a very acute to peracute presentation characterized by
hemoconcentration and normal to sub normal albumin/protein levels. Aggressive supportive care with
fluid therapy is indicated in these patients with many severe cases requiring colloid therapy to provide
intravascular support.
The subject of controversy recently is the need for antibiotic therapy. Recent studies have documented
no clinical benefit using metabolic therapy in these cases. However, the author believes that this is a
flawed study and that patients exhibiting fever, shock, hypoglycemia and/or severe ulceration
potentially benefit. Additionally, that paper also exhibited a quicker return to normal bowel movements
with antibiotic therapy.
Occasionally, patients will have clinical presentations that resemble hemorrhagic gastroenteritis. One
such condition is the presence of an intussusception particularly at the ileocolic junction. Patients that
are of unusual signalment with abdominal pain and North the presence of an abdominal mass should
have this entertained. These patients may present with severely hemorrhagic diarrhea and acutely
progressive shock. Rapid diagnosis using radiography and/or abdominal ultrasound is needed. It is
important to note that not all patient has a known risk factor for intussusception or has a palpable
abdominal mass or has a visible abdominal mass on radiographs.
Chronic Giardia
Giardia is a common cause of acute onset diarrhea and can be a cause of chronic ongoing diarrhea.
Diagnostic testing including zinc sulfate fecal centrifugation and/or highly sensitive fecal antigen tests
will help identify the potential presence of infection.
Following treatment for Giardia with appropriate intervention metronidazole, fenbendazole or febantal
may still yield positive fecal antigen testing. Additionally, some patients will continue to have positive
Giardia testing (cysts and antigen tests for several weeks following treatment. Repeat evaluation at 14
days with a zinc sulfate centrifugation usually shows clearance.
It is important to note that some patients with Giardia may have persistent antigen positive testing
without clinical signs for prolonged periods and it is uncertain whether or not these patients have
persistent infection or not. In this setting, documenting the presence or absence of Giardia cysts is
important to determine the significance of this finding. Patient without cyst documentation following
three consecutive samples of zinc sulfate centrifugation, probably should not be treated without other
concurrent clinical signs. In the setting of a multi-dog household, consideration of isolation of those
with positive antigen testing from those with negative antigen testing may be appropriate. However,
some animals will continue to be antigen positive indefinitely without ever showing clinical signs or
developing cyst shedding. Therefore the significance of this is uncertain. Additionally, hygiene including
cleaning the environment, washing environmental formites and/or bathing can be importance in
reducing reexposure to the organism.
If persistent infection is documented (manifested as clinical signs and cyst shedding), repeat treatment
with standard therapies may be considered or transitioning to novel strategies may be appropriate
(Albendazole, Ronidazole, Tonidazole, Quniacrine, Ipronidazole, Furazolidone).
Therefore, in short, if a patient is referred for chronically positive antigen testing without any evidence
of clinical signs and/or cyst shedding, then further diagnostic workup is not indicated in treatment is not
advised.
Protein losing enteropathy
Protein losing enteropathy is a group of disorders associated with protein loss from the gastrointestinal
tract. Some of these conditions may be associated with significant malabsorption or they may just be
associated with a declining albumin and no outward clinical signs.
Common clinical conditions associated with protein losing enteropathies include: inflammatory bowel
disease, intestinal neoplasia, infectious enteropathies (fungal disease, etc), food hypersensitivity, ulcers,
chronic intussusception, lymphangectasia. One more recently described, relatively common is atypical
hypoadrenocorticism. This is frequently misdiagnosed due to the lack of electrolyte changes and the
atypical age group (middle-aged or older). Laboratory diagnosis of this condition may be performed
with a baseline cortisol (documenting a cortisol level <1) and and ACTH stimulation test documenting
cortisol levels <1.5 (both pre-and post ). All patients undergoing potential endoscopy should have a
baseline cortisol prior to the procedure. Patients with structural disease on ultrasound unlikely to have
an abnormal ACTH level, therefore this is probably unnecessary in these patients. Clinical suspicion for
the disease should exist and patient with protein losing conditions, hypocholesterolemia, nonregenerative anemia, hypoglycemia and lack of stress leukogram (most common finding).
Patients with confirmed atypical Addison’s disease may potentially have primary pituitary disease or
more likely adrenal disease. Performing an aldosterone level and/or ACTH level may provide some clues
to the etiology. Patients with adrenal disease may have concurrent subnormal aldosterone levels and
generally will have high ACTH levels. Whereas patients with pituitary disease will have normal
aldosterone levels and will have a low ACTH level .
Feline infectious peritonitis
Feline infectious peritonitis frequently presents with more classic presentation of effusive disease with a
high-protein effusion. These patients may exhibit multisystemic signs characterized by courier retinitis,
hepatitis, fever, anorexia, hyperglobulinemia, hypoalbuminemia and/or granuloma formation within the
abdominal cavity, thoracic cavity and/or CNS. In general, the protein content of the fluid will usually be
>2.5 g/deciliter, have a modified transudate cell count characterized by a mixture of mononuclear cells
(neutrophils, lymphocytes, macrophages).
Occasionally, patients will present with abdominal effusion that is atypical for the disease process.
Characterized by significant percentage of neutrophils. In this setting, in the context of a neutrophilic,
high-protein, febrile, acutely ill patient, the impulse is to consider surgical exploration. Additionally, the
author has documented patients with evidence of “septic” lactate and glucose levels in the peritoneal
fluid when compared to peripheral blood. Abdominal exploration will usually reveal multifocal disease
within the abdominal cavity consistent with granulomas. It is important to note that many patients can
have quite widespread disease without alterations on ultrasound.
It is my opinion that any young cat that presents with abdominal effusion and chronic fever should be
suspected of having FIP. A definitive diagnosis often times requires histopathology to document the
presence of viral particles within macrophages/granulomas. Nonsurgical diagnostic testing including
PCR/IHC off of abdominal fluid may provide some value when enough macrophages are present within
the fluid to allow for a documentation of viral antigen. All tests in this scenario frequently have false
negative results. Therefore, it should be emphasized to the owner that diagnosis cannot be confirmed
reliably and some patients even with surgical intervention.
Occasionally patients will present with FIP confined to the intestinal tract. Focal abdominal masses have
been appreciated in some patients of varying ages. Surgical excision has resulted in long-term remission
in some patients. Currently, no particular effective treatment plan exists. The author believes that
there is some value in feline interferon and recent evidence suggests that there may be a benefit to
using poly prenyl immunostimulant. It is the author’s opinion that any young cat with an abdominal
mass should be suspected as having FIP or other benign disease processes in the majority of cases.
Polyps:
Patients commonly present animal hospital for hematochezia. It is important to differentiate the
common colitis patients from those with local structural disease and that do not have colitis. Patients
with colitis typically have the following acute onset clinical signs, mucus production, tenesmus and
concurrent diarrhea. Patients with constipation occasionally have blood along the surface of the stool
as a result of local abrasive properties of the firm stool. These patients, as expected, have significantly
firm stool. Patients with normal stool quality and blood laced on the surface of the stool should always
be suspected to have local disease. These patients generally have some structural disorder that leads
intermittently and coats the surface of the stool. In short , the more normal the stool with blood = local
mucosal disease.
Differential diagnosis for patients with this form of bleeding include colonic polyps, colonic neoplasia,
strictures, fibrosing colitis, foreign bodies, etc. Regardless of the patient’s age, colonoscopy should be
recommended.
A common differential diagnosis is colonic polyps. These are benign lesions associated generally in the
terminal/descending colon to anorectal junction. Given their small, delicate nature, rectal examination
may miss these easily even one present within palpable range. Careful, gentle palpation of the mucosa
circumferentially mail out better documentation on exam. These lesions are not thought to be
associated with neoplastic progression. However, recurrence following surgical and/or interventional
removal is possible/common. Recurrence may occur at the surgical site and/or other additional sites
throughout the colon. Colonoscopy will help to document the progression of lesions that are proximal
to the surgeon’s capabilities. Additionally, application of endoscopic mucosal resection techniques
(polypectomy, EMR) may be utilized at the time of the procedure.
Other polyps are occasionally seen within the gastrointestinal tract, most notably in the stomach of dogs
and cats. She is polyps generally arise from the pyloric antrum and are usually clinically asymptomatic.
The author is appreciated some of these causing mucosal bleeding or obstruction of the pylorus.
Documentation via endoscopy with biopsy is recommended in these cases. Occasionally, ultrasound
may miss these lesions due to gas within the stomach interfering with careful sonographic interrogation.
Endoscopic resection techniques can be employed to remove these lesions.
One final location classically described in cats for polyp formation is within the proximal duodenum.
These polyps have been associated with severe hemorrhage and need for transfusion in some animals.
These lesions can be easily missed on ultrasound due to the gas interface in that region. Additionally,
inexperienced endoscopists can miss the lesion easily despite intubation of the duodenum. Careful
protraction of the endoscope with insufflation will allow for appropriate visualization at the pyloricduodenal junction. These lesions, also can be removed endoscopic in many cases.
Antibiotic responsive diarrhea:
Occasionally patients present with chronic diarrhea that is responsive to antibiotics. These patients
were previously believed to of had small intestinal bacterial overgrowth. Evaluation of quantitative
bacterial cultures, revealed that significant changes in bacterial concentrations have not been present in
these animals. In light of the recent evidence suggesting the importance of bacterial flora and its effect
on gastrointestinal health, it is not hard to believe that dysbiosis could potentially influence disease.
Patients that have historically shown antibiotic responsive may need chronic antibiotic therapy to
maintain gastrointestinal health. Whereas others may be effectively treated with antibiotic courses for
4-6 weeks. Another population of antibiotic responsive patients exists. These patients represent those
with acute onset, fulminant diarrhea over one months time. Diagnostic imaging in these patients is
generally unremarkable and no evidence of metabolic/systemic disease exist. The rapid, fulminant
onset without any evidence to support chronicity may suggest that bacterial alterations may be present.
Documentation of altered fecal flora on fecal cytology (homogenous population) may be suggestive in
these cases. Some of these patients exhibit no response to “traditional” antibiotics (metronidazole,
Tylosin). Whereas, they may respond to atypical antibiotic therapy (fluoroquinolones).
Therefore, antibiotic therapy could be appropriate with atypical (generally conserved) antibiotics in
some patients with acute (bordering on chronic), fulminant diarrhea. It is not routinely recommended
to use these antibiotic trials unless the clinical picture fits and no other information suggests more
serious disease (weight loss, hypoalbuminemia, hypocobalaminemia, anorexia, image changes
consistent with disease, etc.).
Chronic pancreatitis:
Chronic pancreatitis was historically considered a highly underdiagnosed condition. Histologic evidence
of ongoing chronic pancreatitis is present in many older patients (both cats and dogs). This is defined by
the presence of fibrosis and pancreatic inflammation on histopathology. However, any of these patients
exhibit no clinical features consistent with pancreatitis. Since the relatively wide acceptance that this
histologically is more common than we anticipated, chronic pancreatitis is more widely diagnosed and is
probably overdiagnosed in clinical patients.
In other words, it is an uncommon cause of clinical disease despite a relatively common clinical diagnosis
in sick patients. Clinical signs of pancreatitis include: vomiting, anorexia, abdominal pain and/or
generalized lethargy. It is expected that most patients exhibiting chronic vomiting from pancreatitis
likely will not have a good appetite. Therefore, the presence of chronic intermittent vomiting with
maintenance of a normal diet is atypical for patients with pancreatitis dominating the clinical picture.
Additionally, diarrhea has a soul complaint is unusual. Therefore, whenever considering the diagnosis,
one must correlate it with the clinical picture.
Given the overlapping clinical signs, the diagnosis may be difficult. Additionally, the presence of a
positive “diagnosis” (ultrasound changes, biopsy changes, PLI changes) may not be reflective of the main
clinical symptoms reported. In other words, to conditions may exist within a patient. Ultrasound
changes with chronic pancreatitis can be nonspecific and generally are characterized by widening of the
pancreas, dilation of the pancreatic duct, changes in echogenicity of the pancreas and/or presence of
nodularity. Unfortunately, correlation of these findings with histopathologic changes has not been
definitively shown. Additionally, these changes are frequently persistent on ultrasound/static,
suggesting that a “diagnosis” can be made of chronic pancreatitis any time an ultrasound is performed
whether or not that patient is symptomatic or not, further complicating the diagnosis.
Patient with chronic pancreatitis as their main presenting clinical complaint will frequently have one or
more type of presentation. One common scenario is waxing and waning signs of illness. In these
patients, documenting fluctuations within the pancreatic lipase immunoreactivity testing may be of
value. Correlating clinical illness with high and clinical normalcy with low/normal PLI results can be
helpful in establishing a diagnosis. Other patients may exhibit signs of chronic illness. These patients
will typically continue to exhibit high PLI.
Treatment of this condition is difficult and generally involves supportive care (fluid therapy, anti-emetic
therapy and appetite stimulants). Patient with waxing and waning conditions are generally armed with
supportive medications at home to intervene at the earliest convenience, thereby minimizing trips to
the hospital. Patients with chronic recurrence and/or chronic persistent clinical signs may warrant from
immune modulation. The author suspects that immune modulation is ineffective at controlling
pancreatitis in our veterinary patients. However, that being said, some patients exhibit clinical response
to treatment. This is likely a reflection of additional steroid responsive disorders (i.e. inflammatory
bowel disease). Therefore, biopsy acquisition is always recommended in these patients prior to these
trials.
It is important to note that many dogs have histologic evidence supporting chronic pancreatitis as well.
It appears to be a less common scenario in dogs but one present, thought restriction is considered the
mainstay of therapy. Occasionally, patients will exhibit no clinical signs except the development of
exocrine pancreatic insufficiency and/or diabetes late in life. A breed that has been historically
overrepresented to develop fleet onset exocrine pancreatic insufficiency is the Cavalier King Charles
Spaniel.
Portosystemic shunts
Portosystemic shunts are classically associated with clinical signs compatible with hepatic
encephalopathy. It should be noted that some of these patients are clinically asymptomatic and will
never exhibit symptoms. Other clinical presentations documented include lower urinary tract disease,
polyuria/polydipsia, poor recovery from anesthesia and/or decreased growth. Alternatively, there is a
population of animals that exhibit no signs of encephalopathy but vague symptoms.
Typically, patients with portosystemic shunts have serum bile acid elevations >80. However, it should
be noted that some patients have relatively mild serum bile acid elevations. Additionally, some patients
have the inverse elevation (elevated pre-prandial bile acids). Therefore, pre-and postprandial bile acid
testing should be performed in any patient suspected of this disorder. Additionally, no “cutoffs” are
reliable in differentiating patients with portal venous hypoplasia (MPD) from that of true portosystemic
shunts. Ammonia levels can be used to aid in diagnosis as they are specific to patients with
portosystemic shunting (congenital or acquired). Unfortunately, this assay may be complicated by time
sensitive, sample handling issues.
Ultrasound diagnosis requires a highly skilled radiologist and patients. Certainly, in the hands of an
experienced radiologist, >90% of patients will have evidence supporting a portosystemic shunt. This is a
patient size and mobility and gastrointestinal contents at the time of the procedure. Regardless,
circumstantial information can be gleaned from ultrasound supporting a potential diagnosis of
portosystemic shunt. This may include, cystic or renal calculi, renomegaly, microhepatica, altered portal
vein to aortic or portal vein to caudal vena cava ratios. More specific circumstantial evidence including
alterations in portal flow and/or turbulence within the portal vein may be suggestive.
Finally, the most definitive diagnostic test is a CT portogram. This represents a highly accurate
evaluation of the vasculature, quantifying the number and location of portosystemic shunts. It provides
the clinician with some information regarding portal blood flow and surgical planning. Is thought to be
more sensitive than surgical exploration.
In some cases of portosystemic shunt, chronic gastrointestinal signs may be appreciated. These signs
may include decreased appetite, intermittent vomiting, intermittence diarrhea, weight loss and/or
overall poor body condition. Therefore, they should be considered in any patient with chronic
gastrointestinal signs at any age. Although, young patients certainly should be higher consideration.
Portosystemic shunts are quite diverse in their clinical presentations and imaging/gross appearance of
the liver may be quite varied from normal to nodular.
Recently, a protein C level was suggested to provide differentiation between patients with portal venous
hypoplasia and those with portosystemic shunts. While this does provide reasonable discrimination
between the two populations and can be used to further support diagnostic testing and/or not doing
diagnostic testing, some overlap does exist between the two populations. Because this represents a
synthetic property of the liver, a reduced protein C level, whether or not it is related to a portosystemic
shunt or to portal venous hypoplasia (MVD) may present with clinical signs compatible with
encephalopathy. Whereas those with a normal protein C level, whether or not a portosystemic shunt or
MVD is present, generally will not exhibit clinical signs. This test is used in patients with low clinical
suspicion for portosystemic shunting to justify monitoring without further diagnostics (CT, liver biopsy).
Similar to patients with portosystemic shunts, patients with chronic liver disease may not show any
clinical signs except vague changes in appetite and/or weight loss. Therefore, in a patient with
significant a biliary changes on imaging and/or bloodwork with vague symptoms, this should be
considered on the differential diagnosis list.