STUDENT PAPER COMMUNICATION ÉTUDIANTE

Case study in canine intestinal lymphangiectasia

Thomas A. Brooks

Abstract — A 9.52 kg, 9-year-old, spayed female beagle was presented with the chief complaint of
abdominal distention of 1 week’s duration. A presumptive diagnosis of canine intestinal lymphan-
gectasia was arrived at by exclusion of other causes for the patient’s ascites. The patient was success-
fully treated with dietary modification and immunosuppressive therapy.

Résumé — Une femelle Beagle stérilisée de 9,52 kg, âgée de 9 ans, a été présentée pour une disten-
sion abdominale qui durait depuis une semaine. Un diagnostic présomptif de lymphangiectasie a été
retenu par exclusion des autres causes reliées à l’ascite. Le patient a été traité efficacement par une
modification de son alimentation et par une thérapie immunosuppressive.
(Traduit par Docteur André Blouin)
Can Vet J 2005;46:1138–1142

A 9.52 kg, 9-year-old, spayed female beagle was pre-

sented to the Fox Valley Veterinary Clinic (North
Aurora, Illinois, USA) with the chief complaint of
abdominal distention of 1 wk duration (Figure 1). The
physical examination was relatively unremarkable, except
for ascites with a pronounced abdominal fluid wave and
a body condition score (BCS) of 2.5/5, based on a scale
where a score of 1/5 is severely emaciated and a score of
5/5 is morbidly obese. From the history obtained from
the client at the time of presentation, the patient’s attitude
and appetite were normal, but for about 3 wk prior to
presentation, her stools were semisoft in the early morn-
ing, became progressively looser through the day, and
eventually became unformed. There was no change in
the frequency of defecation, though defecation seemed
to be taking more time. Sporadic episodes of vomiting
Figure 1. Patient at initial presentation
had been noted, and the dog had had a dry, intermittent
cough since being adopted 2 y previously. She was cur-
rently being treated with a hyposensitization program for Hyperadrenocorticism was considered as a possible
inhalant allergies to Tyrophagus putrescentiae, a type of cause for the dog’s “potbelly” appearance, because older,
grain mite, and had been for a period of approximately spayed, female beagles have been reported to be at an
9 mo at the time of presentation. The patient was not on increased risk for developing this disease (1), but this
any other medications. was thought to be less likely in light of the history and
physical examination. So 2 broad categories of conditions
causing ascites were focused on 1) Forms of right-sided
heart failure that could cause congestion in the systemic
Winner of the CVMA Pet Food Certification vasculature, such as tricuspid valve regurgitation, pul-
Nutrition Award monic stenosis, pericardial effusion, pericarditis, and
Atlantic Veterinary College, University of Prince Edward heartworm disease; and 2) forms of hypoalbuminemia
Island, 550 University Avenue, Charlottetown, Prince Edward caused either by decreased albumin production or
Island C1A 4P3. increased albumin loss, resulting in low intravascular
oncotic pressure. The decreased albumin production
Address all correspondence and reprint requests to
would be due to a hepatic insufficiency (HI), while the
Mr. Brooks.
increased albumin loss could be due to a protein-losing
Thomas Brooks’ current address is 405 Oak Street, North nephropathy (PLN), protein-losing enteropathy (PLE),
Aurora, Illinois 60542, USA. acute or chronic blood loss, or starvation. With the
Mr. Brooks will receive 50 free reprints of his article, courtesy client’s approval, the patient was admitted for preliminary
of The Canadian Veterinary Journal. diagnostic tests.

1138 Can Vet J Volume 46, December 2005

Table 1. Selected biochemical and complete blood cell count results
Day Day Day Day Day Day Day Day
Normal range 0 15 22 48 62 78 97 181
Total protein 51–78 g/L 25 27 31 30 36 34 44 44
Albumin 25–36 g/L 11 13 13 14 20 18 24 22
Globulin 28–45 g/L 14 14 18 16 16 16 20 22
Cholesterol 2.89–8.48 mmol/L 3.03 2.59 4.34 3.08 2.28 2.89 4.16 3.89
Calcium 2.05–3.09 mmol/L 2.07 2.07 2.24 2.02 2.20 2.27 2.57 2.05
AST (SGOT) 5–55 /L 60 52 49 60 28 34 26 43
CK 10–200 /L 335 271 168 427 151 132 128 166
Absolute lymphpocyte count 1000–4800/L 476 — 344 585 246 565 534 860
AST — aspartate aminotransferase; CK — creatinephosphokinase

Blood was submitted for a complete blood (cell) count
(CBC), biochemical analysis, values for postprandial bile
acid, and an antigen heartworm test. Thoracic radiographs
were taken to evaluate the heart and look for evidence of
pleural effusion. A lead II electrocardiograph (ECG) was
also taken.
Results from the antigen heartworm test (Heska Solo
Step HC; Heska Corporation, Fort Collins, Colorado,
USA) were negative, and no evidence of heart disease
was apparent on either the ECG or the thoracic radio-
graphs. Evaluation of the rest of thorax and visible
extrathoracic structures showed no evidence of pleural
effusion, but the liver did appear small. In light of these
findings and the normal cardiac auscultation during the
physical examination, right-sided heart disease was ruled
out and the ascites was attributed to hypoalbuminemia,
most likely due to HI, PLN, or PLE.
An abdomenocentesis was performed and ultrasono-
graphs of the abdomen were taken. The abdomenocen-
tesis yielded a clear transudate, with no cellularity on
cytologic examination. The fluid had a specific gravity
of 1.006 and total solids  2.0 g/100 mL. The ultraso-
nographs showed no abnormalities, except for the marked
ascites and what appeared to be a small liver. No nodular-
ity was seen within the liver, which appeared homoge-
nous and hyperechoic. A tentative diagnosis of liver
fibrosis resulting in HI was made, and the client was
given a guarded prognosis.
With client consent, an ultrasound-guided liver biopsy
was obtained. An activated clotting time (ACT) was
performed to quickly screen for abnormalities of the
intrinsic clotting factors that may have been affected by
the HI. The results of the ACT were within normal limits,
so the patient was premedicated with atropine sulfate
(generic; Phoenix Scientific, St. Joseph, Missouri, USA),
0.04 mg/kg bodyweight (BW), SC, and sedated with
meditomidine (Domitor; Pfizer, Exton, Pennsylvania,
USA), 8.8 g/kg BW, IM, and butorphanol tartrate
(Torbugesic; Fort Dodge Animal Health, Fort Dodge,
Iowa, USA), 0.22 mg/kg BW, IM. In addition to provid-
ing sedation, these agents also provided analgesia for the
procedure. Four liver samples were collected percutane-
ously. The patient was released later that night with no
treatment prescribed, pending the results of the biopsy
and other tests.
Results of the biochemical, postprandial bile acids
values, and the CBC were received the following day
(Table 1, day 0). Mildly elevated aspartate aminotrans-
ferase (AST; SGOT) and creatinephosphokinase (CK)
levels were noted and attributed to the muscle loss noted
in the physical examination (low BCS). All other liver
function tests were within the normal ranges, including
the postprandial bile acids. The patient was moderately
panhypoproteinemic. Most of the remaining biochemi-
cal results were within the normal limits and those that
were not were easily attributed to individual variation.
Results from the CBC were within normal limits, except
for moderately low absolute lymphocyte and eosinophil
counts. The interpretation of these results excluded
hyperadrenocorticism, HI, and acute or uncompensated
chronic blood loss. Two days later, the exclusion of
HI was further supported by liver biopsy results that
showed only mild hydropic degeneration with attendant
cholestasis.
Having ruled out HI and acute blood loss as a cause
for the hypoalbuminemia, PLN, PLE, and semicompen-
sated for chronic blood loss became the next 3 most
likely causes. Chronic blood loss and PLN were the
easiest to rule out diagnostically. The client confirmed
that there had been no melana or frank blood in the
stools, and 3 fecal flotations and a direct fecal smear
ruled out gastrointestinal parasites as a possible cause
for chronic blood loss. So these results, in conjunction
with results from the CBC and the history, ruled out
chronic blood loss. A urine sample, collected via cysto-
centesis, showed only trace protein. The urinalysis results,
in conjunction with normal renal values obtained from
the earlier biochemical analysis, were used to rule out a
PLN. A urine protein:creatinine ratio could have been
used to further evaluate for renal protein loss (2), but this
was not considered necessary in this case.
By exclusion, PLE was left as the final cause for the
hypoalbuminemia (3). The differential diagnoses for PLE
include generalized disorders, as well as primary gastro-
intestinal diseases (2,3). The generalized disorders
include congestive heart failure, nephrotic syndrome,
and metastatic neoplasia. No evidence was found in the
diagnostic tests that had been done that would indicate
any of these general disorders as a cause for the hypo-
proteinemia, leaving primary gastrointestinal causes for
investigation.
The primary gastrointestinal causes for PLE can be
divided into 2 broad categories: 1) disorders that increase
mucosal permeability and 2) lymphatic disorders (3).
Increased mucosal permeability can be further divided
into disorders of parasitism; mechanical obstruction,
such as intussusception and chronic foreign body; and
inflammation, such as food allergies and inflammatory

Can Vet J Volume 46, December 2005 1139

bowel disease (IBD). Lymphatic disorders can be caused
by intestinal lymphangiectasia (IL) and lymphosarcoma.
Results from the previous diagnostic tests ruled out
parasitic and mechanical causes for increased mucosal
permeability. Food allergies and IBD caused by food-
related allergies were not considered likely differential
diagnoses, because the patient’s diet consisted of only a
specially formulated low allergen food (Hill’s prescrip-
tion diet canine z/d low allergen; Hill’s Pet Nutrition,
Topeka, Kansas, USA). Results from the physical exam-
ination and imaging studies discounted generalized or
localized lymphosarcoma, so the top differential diagno-
ses became IL and IBD due to non-food-related allergies,
with IL being the more likely, because it is the most
common disorder associated with PLE (2,4). The only
way to definitively diagnose either of these conditions is
histologically through collection of intestinal biopsies
via endoscopy or laparotomy (2,3,5,6). Endoscopy has
the advantages of being less invasive and allowing visu-
alization of lesions to biopsy, provided that the condition
is not focal and outside the effective reach of the endo-
scope. Laparotomy has the advantage of allowing visual
evaluation of all of the abdominal organs, including the
entire gastrointestinal tract and the gastrointestinal lym-
phatics. However, it is associated with a high occurrence
of postsurgical complications, including death or dehis-
cence due to delayed wound healing associated with
hypoalbuminemia (2–7). A concern in collecting a biopsy
sample by either method is that mild forms of the disease
may not yield appreciable lesions and a diagnostic
sample may not be obtained (6). In this patient, an endo-
scopic biopsy would have been the preferred choice, but
the client was not interested in having a biopsy taken via
either method, due to the cost of endoscopy and possible
complications of laparotomy. In the client’s opinion, the
patient’s quality of life was still favorable, based on the
patient’s good attitude and appetite, so it was decided to
repeat the biochemical analyses to reevaluate the panhy-
poproteinemia and perform a fecal alpha-1 proteinase
inhibitor (fecal 1-PI) test to screen for PLE. Fecal
1-PI is of a similar molecular weight to albumin, but,
unlike albumin, it is resistant to proteolytic degradation
within the gastrointestinal tract. Therefore fecal 1-PI
can be used as a marker for the intestinal loss of albumin
(8). Although the fecal 1-PI test has a high sensitivity
for hypoalbuminemia in cases of PLE, its specificity is
low. However, the specificity can be increased by ruling
out other causes of hypoproteinemia (8), such as was
done in this case. The client was also willing to institute
a conservative treatment for IL, which consisted of a
dietary change to reduce long-chain triglycerides (LCT)
in the diet. Long-chain triglycerides in the diet stimulate
the loss of lymph to the gastrointestinal lumen through
chylomicron formation (9). There is some evidence that
LCT may be proinflammatory, which could also stimulate
the loss of lymph from inflamed lacteals (6). It has been
reported that reducing the presence of LCT in the diet
can decrease lymph flow 10-fold in the mesentary (6). It
was hoped that a fat restrictive diet (Hill’s prescription
diet r/d; Hill’s Pet Nutrition) would decrease lymph loss
to the gastrointestinal lumen, enough to reduce the
patient’s hypoalbuminemia and ascites. In addition, the
hyposensitization treatments for inhalant allergies were
1140
stopped to reduce inflammatory stimuli in general,
though there was no evidence to suggest that those anti-
gens were causing a direct problem.
The patient was admitted to hospital to ensure proper
sample handling during the collection of the stool sam-
ples for the fecal  1 -PI test and thus minimize the
chances of receiving a false negative. Although fecal
1-PI is resistant to degradation in the gastrointestinal
tract, it degrades if left at room temperature. Freezing
will slow this process, but repeated freezing and thawing
must be avoided, because it accelerates the degradation.
Three stool samples from 3 separate defecations were
collected for the fecal 1-PI test and the patient was
released. The samples for fecal 1-PI testing were sub-
mitted to the Gastrointestinal Laboratory, Texas A&M
University, College Station, Texas, USA. Expected turn-
around time for the test was about 3 to 4 wk. A recheck
examination was scheduled to coincide with the return
of the fecal 1-PI test results. Blood was also collected
at this time for biochemical analyses. The results of these
analyses (Table 1, day 15) were similar to those of the
original analyses. The patient was still moderately pan-
hypoproteinnemic. Although hypoalbuminemia is the
most consistent clinicopathologic finding in IL, globulin
levels are often affected as well, and panhypoprote-
innemia is supportive of a diagnosis of IL (6,7). Special
attention was also paid to cholesterol and calcium levels,
because these values, when low, are also supportive of a
diagnosis of IL. Hypocholesterolemia is attributed to
gastrointestinal loss and lipid malabsorption. Hypocalce-
mia is mainly an artifact of low serum albumin concen-
tration, but it may be exacerbated by decreased intestinal
calcium absorption (6). Cholesterol levels in the patient
were mildly decreased and calcium levels were at the low
end of the normal range. In hindsight, the CBC should
have been repeated to monitor the absolute lymphocyte
count, because lymphopenia is a relatively consistent
finding in patients with IL and, when present, lends
additional support to a diagnosis of IL (6,7).
About 1 wk after initiating the new diet, the patient
was presented for vomiting. Two days prior to presenta-
tion, the patient had vomited about half a meal of food,
shortly after feeding. On the day of presentation, the
patient vomited 3 times in a 10-minute period, shortly
after feeding. The vomitus contained food all 3 times,
but frank blood was also noted with the 3rd vomition.
A physical examination yielded the same findings as at
the time of the original presentation for ascites. The
patient was given aminopentamide hydrogen sulfate
(Centrine; Fort Dodge Animal Health), 0.2 mg, IM, as a
fast onset antiemetic. The following medications were
prescribed for use at home: metoclopramide HCl
(generic; PLIVA, East Hanover, New Jersey, USA),
5 mg, PO, q8h for 5 d and sucralfate (generic; Merckle
GmbH, Blaubeuren, Germany), 0.5 g, PO, q8h for 5 d,
as an antiemetic and gastroprotectant, respectively. It was
thought that the vomiting might be due to the increased
volume of the fat restrictive diet that was being fed com-
pared with the volume of the previous diet. The increased
volume was necessary to maintain an equivalent caloric
intake. The client was advised to feed smaller meals more
frequently, to prevent over-filling the stomach. Another
biochemical analysis and CBC were performed to make
Can Vet J Volume 46, December 2005
Table 2. Any individual sample  15.0 g/g is
consistent with protein-losing enteropathy
Sample A Sample B Sample C
Fecal -1 PI (g/g) 29 51.7 53.2
sure that the vomiting did not indicate a more compli-
cated problem. The results of the biochemical analyses
and CBC (Table 1, day 22) showed some improvement
in the levels of total protein, globulin, cholesterol, and
calcium. Albumin and absolute lymphocyte values
remained relatively unchanged.
The results of all 3 fecal 1-PI test samples were
consistent with PLE (Table 2). On physical examination,
the ascites was less pronounced than on original presen-
tation, but it was still prominent. No other significant
changes were noted on physical examination. The client
reported that the consistency of the stools had improved
slightly, but that they were still soft with a gradual pro-
gression to being loose as the day progressed. There had
been no further vomiting since the last physical examina-
tion. The client also felt that the patient’s attitude had
been a little quieter lately, but her appetite was normal.
Based on the clinical signs, fecal 1-PI test results, and
biochemical and CBC profiles collected thus far, it was
felt that IL was the underlying condition for this PLE.
Obtaining a biopsy was discussed again as a means to
get a definitive diagnosis, but the client did not consider
that this was necessary when weighed against the costs
involved and possible complications. The use of cortico-
steroids as an immunosuppressive agent to reduce inflam-
mation of the assumptively inflamed lacteals of the
intestine, and thus decrease loss of lymph to the gastro-
intestinal lumen (2,4,5), was considered, but the client
was reluctant to start a medication that would be needed
indefinitely. It was decided to continue the dietary
therapy for another month and then, if there was no
improvement, to add corticosteroids to the treatment
regimen. Blood was submitted for a biochemical analy-
sis and CBC, with an additional follow-up biochemical
analysis and CBC scheduled in 2 wk, and another, at the
time of the recheck physical examination, in 4 wk.
The results of the biochemical analysis and CBC
(Table 1, day 48) did not show any improvement over the
previous results; however, the results from the 2-week
follow-up (Table 1, day 62) did show an improvement of
the total protein and albumin values, although both were
still below the reference range. The cholesterol and
absolute lymphocyte values were at their lowest since
original presentation. No change in treatment was made
at this time.
At the 4-week recheck and physical examination, the
patient seemed a bit depressed. There was no appreciable
change in the ascites since the last examination. Although
the patient’s weight had remained at 9.5 kg, the BCS was
reevaluated as only a 2/5 and the hair coat was dull in
appearance. No other abnormalities were found. The
client reported that although the appetite remained good,
the patient was lethargic and uninterested in the daily
routine, except for mealtimes. Although the most recent
biochemical analyses had shown some small improve-
ment in the hypoalbuminemia, the general well-being of
Can Vet J Volume 46, December 2005
Figure 2. Patient after 4 d of corticosteroid treatment.
the patient appeared to have declined. Prednisolone
(generic; Vetamix, Shenandoah, Iowa, USA) was dis-
pensed at an immunosuppressive dosage of 2 mg/kg BW,
PO, q12 h for 5 d, then to be decreased to 1 mg/kg BW,
PO, q12h for at least 6 wk or until a change in clinical
signs was seen (4). If remission of the disease was
obtained, the dose would be lowered to the lowest effec-
tive dose to maintain remission of clinical signs (4). On
day 78, there were no significant improvements (Table 1,
day 78), but the cholesterol and absolute lymphocyte
values had returned to approximately their levels at
day 48. A recheck examination in 2 wk was scheduled.
Four days after beginning the prednisolone, the client
reported that the ascites was gone and that the patient’s
attitude was brighter and she was more active (Figure 2).
In addition, the client felt that the consistency of the
stools had improved, although they remained soft. The
patient was reweighed and the 1 mg/kg dose of pred-
nisolone adjusted to reflect the current weight of 7.25 kg.
It was felt that medium-chain triglycerides (MCTs) could
be helpful in regaining the patient’s body condition.
Although there is debate about the mechanism of absorp-
tion for MCTs, it is felt that MCTs can provide some
of the favorable aspects, mainly increased calories, of
dietary lipids, without stimulating lymph loss (5).
Medium-chain triglycerides’ oil was not readily available
from the practice’s regular suppliers or local pharmacies,
but an alternative source was found at a local health food
store. Pure coconut oil, which is an MCT, was added to
the diet at 1 tablespoon, q12h. It has been reported that
MCT oil is unpalatable to most patients, but the client
reported that the patient found the pure coconut oil very
palatable. The plan for recheck was modified and a
follow-up examination, biochemical analyses, and CBC
were scheduled for in 3 wk.
At the follow-up examination, the patient was bright,
alert, and active. The client reported that the patient was
active and playful at home and that the consistency of
the stools had continued to improve but were occasion-
ally soft. The patient’s weight had increased to 7.62 kg.
No evidence of ascites was appreciated (Figure 3). The
only abnormalities noted were a BCS of 2.5 and a dull
hair coat. The biochemcal analyses and CBC were
repeated (Table 1, day 97). The albumin and globulin
levels had increased to a point where the patient was now
1141

Figure 3. Patient after approximately 1 mo of corticosteroid
treatment.
only mildly panhypoproteinemic. The cholesterol and
calcium values were within the reference ranges, though
the absolute lymphocyte count remained relatively
unchanged. It was decided to continue the prednisolone,
as planned, and to continue the pure coconut oil in the
diet until a BCS of 3/5 was attained.
Although regular monitoring of protein levels would
have been appropriate (3,4), the client felt the patient was
doing well and it was unnecessary. Fecal consistency was
used as an indicator of corticosteroid effectiveness in
determining the lowest effective every-other-day (eod)
dose. The patient had been maintained free of clinical
signs at a level of 2.5 mg of prednisolone eod. A BCS of
3/5 was attained at a body weight of 9.07 kg, at which
time the pure coconut oil was removed from the diet. The
3/5 BCS has been maintained on the fat restricted diet.
Biochemical analyses and a CBC were obtained 181 d
after the original presentation (Table 1, day 181). The
albumin, globulin, cholesterol, and calcium values were
relatively unchanged from the last biochemical analysis
at 97 d. The CBC showed an increase in the absolute
lymphocyte count, although it was still below the refer-
ence range.
1142
The 3 cornerstones for treatment of IL include address-
ing the underlying cause, the use of anti-inflammatory
medications, and dietary modification. But as is demon-
strated by this case, a favorable outcome can be achieved,
even if the underlying cause cannot be determined.
Unfortunately, resolution is rare and in most cases remis-
sion of clinical signs is the best that can be achieved for
patients with IL. Even in patients where remission can
be attained, the longest reported survival time after diag-
nosis of IL is 2 y (6). As of this writing, 507 d since
the initial presentation for ascites, the patient remains
free of clinical signs on a maintenance dose of 2.5 mg
(0.28 mg/kg) of predinisolone eod. and continues to
maintain a BCS of 3/5 on the restricted fat diet.
Acknowledgments
The author thanks the veterinarians and staff of Fox Valley
Veterinary Clinic for their advice and encouragement.
CVJ
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Can Vet J Volume 46, December 2005