A three year old female Rottweiler dog was presented with clinical signs of chronic diarrhoea, severe weight loss and sporadic vomiting. Histopathology revealed intestinal lymphangiectasia with lipogranulomatous lymphangitis. Intestinal lymphangiectasia represents a pathological dilatation of the intestinal lymph vessels and is the most common cause of protein-losing enteropathy in the dog. This paper reports a clinical case with a short review of literature

Branquinho, Joana

Faísca, Pedro

Mestrinho, Lisa

Morais de Almeida, Pedro

English

Universidade Lusófona: Revistas científico-culturais

Branquinho et al                                                                              Intestinal lymphangiectasia in a dog   6A CASE OF INTESTINAL LYMPHANGIECTASIA WITH LIPOGRANULOMATOUS LYMPHANGITIS IN A FEMALE ROTTWEILER DOG  UM CASO DE LINFANGIECTASIA COM LINFANGITE GRANULOMATOSA NUMA CADELA ROTTWEILER  Joana Branquinho, Lisa Mestrinho, Pedro Faísca, Pedro Morais de Almeida  1Centro de Investigação em Ciências Veterinárias (CICV), Faculdade de Medicina Veterinária, Universidade Lusófona de Humanidades e Tecnologias, Campo Grande, 376, 1749 - 024 Lisboa    Abstract: A three year old female Rottweiler dog was presented with clinical signs of chronic diarrhoea, severe weight loss and sporadic vomiting. Histopathology revealed intestinal lymphangiectasia with lipogranulomatous lymphangitis. Intestinal lymphangiectasia represents a pathological dilatation of the intestinal lymph vessels and is the most common cause of protein-losing enteropathy in the dog. This paper reports a clinical case with a short review of literature..     Resumo: Uma cadela, fêmea, de raça Rottweiller de três anos de idade apresentou-se com sinais clínicos de diarreira crónica, perda de peso grave e vómito esporádico. A histopatologia revelou uma linfangiectasia intestinal com linfangite lipogranulomatosa. A linfangiectasia intestinal consiste numa dilatação patológica dos vasos linfáticos intestinais, sendo a causa mais frequente de enteropatia com perda de proteína no cão. Este trabalho consiste na apresentação do caso clínico e numa breve revisão da literatura  INTRODUCTION  Intestinal lymphangiectasia (IL) is an uncommon disease but an important cause of protein-losing enteropathy in the dog. The major morphological abnormality that characterizes this disease is marked dilation of intestinal lymphatic vessels in the mucosa, submucosa and serosa (Finco et al., 1973; Melzer & Sellon, 2002; Batt & Hall, 1989). It has been recognized as a clinical entity in humans since 1961 and has been first described in dogs in 1968 (Waldmann, 1966; Campbell et al., 1968; Finco et al., 1973; Mattheeuws, 1974). The clinical signs of IL can be quite variable. Many dogs with IL exhibit nonspecific signs, such as anorexia or lethargy. Diarrhoea is one of the most consistent clinical signs associated to this disease, although not seen in all patients (Griffiths et al., 1982; Melzer & Sellon, 2002). Effusions or oedema, more often pure transudates effusions, may develop when serum albumin concentrations fall below 1.5 g/dl (Melzer & Sellon, 2002). Laboratory abnormalities can support the IL diagnosis; however they are neither specific nor pathognomonic of the disease (Kull et al., 2001).   CASE DESCRIPTION A three year old female Rottweiler, 45 kg b.w. was admitted for consultation at the teaching hospital of the Veterinary University (FMV-ULHT) with a two months history of chronic diarrhoea, severe weight loss and sporadic vomiting. The owner described large amounts of brown watery stools, with no mucus or fresh blood, 3 to 4 times a day and no tenesmus. The dog was eating well, was alert and responsive, although he had lost 13 kg in two months.   Previous exams performed by the referring vet revealed hypoproteinemia (3.2 g/dL, Revista Lusófona de Ciência e Medicina Veterinária                                                                      4: (2011) 6-11                                                      7reference range: 5.0 to 7.2 g/dL), lymphocytosis (5.7x109/L, reference range: 0.8 to 5.1x109/L) and thrombocytopaenia (84x109/L, reference range: 117 to 460x109/L). The diarrhoea did not respond to various antibiotic treatments or dietary management (hypoallergenic diet) and there was no complete improvement of symptoms.   On admission, clinical examination revealed mild abdominal discomfort, distended abdomen and emaciation. Blood, biochemical profile, abdominal ultrasound and radiography were performed.  Hematological findings showed mild lymphocytosis (5.7x109/L, reference range:0.8 to 5.1x109/L) and thrombocytopaenia (84x109/L, reference range:117 to 460x109/L). Biochemical profile showed moderate hypoproteinemia (4.2 g/dL, reference range: 5.0 to 7.2 g/dL) with hypoalbuminemia (1.7 g/dL, reference range: 2.3 to 4.0 g/dL).  Cholesterol level was border line, 112 mg/dL (reference range: 110 to 321 mg/dL). Liver was apparently normal with alanine aminotransferase of 50 u/l (reference range: 47 to 254 u/l). Urinalysis was within normal limits.  Radiographic exam was unremarkable except for a slight splenomegaly (figure 1).           Figure 1 – Lateral abdominal radiograph showing slight splenomegaly  Abdominal ultrasound examination revealed an increase of the small intestinal wall (8 mm), with normal layering, mild hipermotility and preserved function. Some intestinal segments had dilated lumen with anechoic content.  It was identifiedmild splenomegaly with normal echogenicity and architecture, without focal or diffuse abnormalities. The colon had some faecal content and the mesenteric lymphnodes were normal (figure 2).             Figure 2 – Transverse ultrasonogram of some sections of small intestine illustrating increase of the wall with normal layering.  At that time, the animal was medicated with metronidazol at a dosage of 15mg/kg, twice daily (Flagyl®, Sanofi-Aventis) and amoxicilin potenciated with clavulanic acid at a dosage of 12,5mg/kg, twice daily (Synulox®, Pfizer). Pancreatic enzymes were prescribed at a dosage of one capsule twice daily, with meals (Kreon®, Solvayfarma) as well as an ultra-low-fat diet supplemented with peanut oil. Cimetidine at a dosage of 5mg/kg, twice a day (Tagamet®, Smith Kline & French) and Vitamin B12 at a dosage of 1000 µg/dog once a week, for six weeks, (OHB12 5000 µg, Jaba Recordati).  Clinical and imaging findings were compatible with the following differential diagnosis of protein-losing enteropathy (ex: intestinal lymphangiectasia) and severe chronic enteritis (ex: severe small intestinal IBD- inflammatory bowel disease –, with SIBO- small intestinal bacterial overgrowth, acute ulcerative enteritis and small intestinal neoplasia (ex: alimentary lymphoma). Branquinho et al                                                                              Intestinal lymphangiectasia in a dog   8An exploratory celiotomy was recommended in order to collect intestinal and stomach full thickness biopsies.  To minimize the anaesthetic risk and post operative complications, a plasma transfusion was done to increase short-term the albumin level.  During the surgery, the presence of multiple small white nodules along ectasic lymphatic vessels on the serosal surface of the small intestine was evident. Furthermore, prominent mesenteric lymph vessels were distended with thick and chalky white paste (figure 3). Liver surface was irregular with visible alterations and a liver guillotine type biopsy was performed.            Figure 3 – Intraoperative image of distended and prominent mesenteric lymph vessels. Note the focal whitish points enlargements corresponding to lipogranulomas on the anti-mesenteric serosal surface.  Histopathological findings revealed a thicker intestinal mucosa due to lymphatic vessels ectasia and lymphoplasmacytic infiltrate in the lamina propria. The submucosa showed dilated lymphatic vessels, and in the subserosa, several lipogranulomes composed of foamy machrophages, were observed on the periphery of ruptured lymphatic vessels. The liver biopsy showed dilated lymphatic vessels in the periportal area, and mild hepatocyte vacuolar degeneration. The histopathological diagnosis was intestinal lymphangiectasia with lipogranulomatous lymphangitis and hepatic-lymphatic congestion with vacuolar degeneration.    DISCUSSION   IL is an uncommon disease in the general canine population, but is one of the most common causes of gastrointestinal protein loss. Its inheritance is still unknown but breeds with a higher incidence of IL due to inflammatory diseases include Basenjis, Soft-coated Wheaten Terriers, and Lundehunds (Melzer & Sellon, 2002; Littman et al., 2000; Landsverk & Gamlem, 1984). This disease can be primary or secondary and, in contrast to human IL, canine congenital IL is considered less common than acquired IL (Finco et al., 1973; Melzer & Sellon, 2002). Acquired IL is mainly idiopathic, but can also be recognized most frequently due to inflammatory processes that block lymphatic vessels and lymph flow. Other causes of increased pressure in lymph vessels include portal hypertension resulting from cirrhosis or heart disease (i.e., right-sided heart failure, pericardial effusion and pericarditis). Although, less frequently, we can also see cases with associated tumours of the intestinal wall, mesentery or even metastatic tumours (Melzer & Sellon, 2002; Louvet & Denis, 2004). Congenital IL, rarely reported, is caused by abnormally formed lymphatic vessels (Fogle & Bissett, 2007). The diagnosis of IL in dogs can be challenging. Clinical signs of IL can be highly variable, as many dogs with IL exhibit nonspecific signs such as lethargy or anorexia; however, diarrhoea remains the most common clinical feature, especially small bowel diarrhoea (Fogle & Bissett, 2007). Ascites, oedema, and hydrothorax are common in dogs with IL, mainly found due to decreased oncotic pressure secondary to hypoproteinemia, (especially hypoalbuminemia). In some dogs, clinical signs of thromboembolic disease, such as tachypnea and dyspnea due to pulmonary thromboembolism, may develop (Melzer & Sellon, 2002). Revista Lusófona de Ciência e Medicina Veterinária                                                                      4: (2011) 6-11                                                      9As previously described, laboratory findings in dogs with IL may suggest intestinal loss of lymph; however, they are not specific for a definitive diagnosis. Lymphopenia is the most frequent change supportive of IL, although in this case it was not observed. Anaemia and neutrophilic leukocytosis, (due to chronic inflammation) may be present in some dogs, however, not verified in this one. In this case, hypoalbuminemia was verified and this is the most consistent laboratory abnormality reported in canine IL. In some cases it can even be noticed pan-hypoproteinemia (Melzer & Sellon, 2002; Burns, 1982).  Hypocholesterolemia is another frequent biochemical alteration seen in canine IL although, was also absent in this case.  Other biochemical abnormalities reported include hypocalcemia secondary to overall loss of bound calcium resulting from hypoalbuminemia, and secondary to poor absorption as also vitamin D from the gut and by the lipogranuloma formation within the lymph vessels. Total serum calcium level is often decreased as an artefact of low serum albumin concentration (Melzer & Sellon, 2002; Burns, 1982; Fogle & Bissett, 2007; Mellanby et al., 2005). Thrombocytopenia, although unusual in IL cases, was seen in this dog. Some authors suggest this finding as a complication of the disease, such as thromboembolism or disseminated intravascular coagulation, however, no signs of these diseases were observed (Melzer & Sellon, 2002). The IL diagnosis is only confirmed by intestinal biopsy specimens (Kull et al., 2001). In this case surgical biopsy samples were performed by laparotomy due to the advantages of obtaining full-thickness lymphatic architecture and less disruption of the normal structure when compared to samples collected by endoscopy (Fogle & Bissett, 2007). The whitish spots observed in the small intestinal serosal surface and prominent dilated mesenteric lymph vessels corresponded to lipogranulomatous lymphangitis on histopathological examination. Not all cases of canine intestinal lymphangiectasia show this type of lesions and it is believed that this lipogranulomes result from an inflammatory foreign body type reaction. This inflammatory reaction is  rich with macrophages that appear not only due to the extravasation of lipid content, through dilated wall or ruptured lymph vessels, but also secondary to stagnated chylous and fat in perilymphatic tissues (Langley-Hobbs, 1993). Increased activities of liver enzyme and vacuolar changes in hepatocytes have been described in dogs with IL (Finco et al., 1973; Fogle & Bissett, 2007). In this case, although there were no changes in biochemical liver function, histological appearance of the liver was consistent with lymphatic congestion and vacuolar degeneration.   Urinalysis results are important as differential diagnosis for hypoalbuminemia secondary to renal protein lost (Melzer & Sellon, 2002). In this dog urinalysis results were unremarkable as in all IL cases. The gold of therapy in secondary IL cases includes treatment of underlying disease. In primary lymphangiectasia cases, treatment is basically supportive and symptomatic. Affected patients should have dietary modification with specific nutritional treatment, including low-fat food and supplements with adequate amounts of essential fatty acids, a reduction in long-chain triglycerides, because they stimulate the loss of lymph to the gastrointestinal lumen by chylomicron formation.  Long-chain triglycerides are not advisable in IL affected animals. Although there is some controversy about the mechanism of absorption for medium-chain triglycerides (MCTs), it is felt that MCTs can provide some of the favourable aspects helpful in recovering the patient’s body condition, without stimulating lymph loss (Peterson & Willard, 2003; Melzer & Sellon, 2002; Brooks, 2005). Branquinho et al                                                                              Intestinal lymphangiectasia in a dog   10 To ensure the success of nutritional treatment is also really important to choose high-quality and highly-digestible protein sources, so that we can minimize protein indigestion and reduce the production of toxins by bacterial flora. Immunosuppressive therapy with glucocorticoids may be useful in some specific cases, especially when the disease is secondary to an inflammatory cause. Prednisone at immunosuppressive doses (2 to 4 mg/kg/day) is commonly used in the initial management of many dogs with IL and mucosal inflammation.  In patients that respond poorly to glucocorticoids or in severe cases, azathioprine may be added (1 to 2 mg/kg or 50 mg/m2 PO q24–48h). In this case no glucocorticoids were prescribed. Antibiotherapy with metronidazole is also indicated not only because of its antimicrobial effectiveness, but also by their immuno-modulatory capabilities (Pibot et al., 2006; Hand & Novotny, 2002; Melzer & Sellon, 2002).  As demonstrated in this case, a favourable outcome could be achieved with specific dietary management and supportive therapy, without glucocorticoid therapy.  The main goal of treatment is the control of clinical signs, without cure. Previous studies reported a 2 years survival time after diagnosis (Hand & Novotny, 2002; Griffiths et al., 1982; Melzer & Sellon, 2002).    REFERENCES  Batt, R.M. & Hall, E.J. (1989). Chronic enteropathies in dog. J Small Anim Pract, 30(1),3-12.  Brooks, T. (2005). Case study in canine intestinal lymphangiectasia. Can Vet J, 46(12),1138-1142.  Burns, M.G. (1982). Intestinal lymphangiectasia in the dog: A case report and review. JAAHA, 18(1), 97–105.  Campbell, R. S. F., Brobst, D., & Bis-Gard, G. (1968). Intestinal lymphangiectasia in a dog.  J Am Vet. Med Ass, 153(8),1050-1054.  Finco, D. R., Duncan, J. R., Schall, W. D., Hooper, B. E., Chandler, F. W. & Keating, K. A. (1973). Chronic enteric disease and hypoproteinemia in nine dogs. J Am Vet Med Ass, 163(3),262-271.  Fogle, J.E. & Bissett, S.A. (2007). Mucosal immunity and chronic idiopathic enteropathies in dogs. Compend Contin Educ Pract Vet, 29(5),290-302.  Griffiths, G.L., Clark, W.T. & Mills, J.N. (1982).  Lymphangiectasia in a dog. Aust Vet J, 59(6),187–189.  Hand, M.S. & Novotny, B.J. (2002) Pocket Companion to Small Animal Clinical Nutrition, 4th ed. Topeka, Kansas: Mark Morris Institute, 640–646.  Kull, P.A., Hess, R.S., Craig, L.E., Saunders, H.M. & Washabau, R.J. (2001). Clinical, clinicopathological, radiographic, and ultrasonographic characteristics of intestinal lymphangiectasia in dogs: 17 cases (1996–1998). J Am Vet Med Assoc, 219(2),197-202. Landsverk, T. & Gamlem, H. (1984). Intestinal lymphangiectasia in the Lundehund. Scanning electron microscopy of intestinal mucosa. Acta Pathol Microbiol A, 92(5),353–362.  Langley-Hobbs, S.J. (1993). What is your diagnosis?  J Small Anim Pract, 34(4), 174.  Littman, M.P., Dambach, D.M., Vaden & S.L., Giger, U. (2000). Familial protein-losing enteropathy and/or protein-losing nephropathy in soft-coated wheaten terriers: 222 cases (1983–1997). J Vet Intern Med, 14(1), 68–80.  Louvet, A. & Denis, B. (2004). Ultrasonographic diagnosis-small bowel lymphangiectasia in a dog. Vet Radiol Ultrasound, 45(6),565–567. Revista Lusófona de Ciência e Medicina Veterinária                                                                      4: (2011) 6-11                                                      11 Mattheeuws, A., Derick, A., Thoonen, H. & Van Der Stock, J. (1974). Intestinal lymphangiectasia in a dog.  J Small Anim Pract, 15(12),757-761.  Mellanby, R.J., Mellor, P.J., Roulois, A., Baines, E.A., Mee, A.P., Berry, J.L., Herrtage & M.E. (2005). Hypocalcaemia associated with low serum vitamin D metabolite concentrations in two dogs with protein-losing enteropathies. J Small Anim Pract 46(7),345–351.  Melzer, K.J. & Sellon, R.K. (2002). Canine intestinal lymphangiectasia. Compend Contin Educ Pract Vet, 24(12),953–961.  Peterson, P.B. & Willard, M.D. (2003).  Protein-losing enteropathies. Vet Clin North Am Small Anim Pract, 33(5),1061–1082.  Pibot, P., Biourge, V. & Elliott, D. (2006). In: Encyclopedia of canine clinical nutrition. (1ª ed., pp. 106-122): Royal Canin.  Smith, S.J., Penninck, D.G., Keating, J.H. & Webster, C.R.L. (2007). Ultrasonographic intestinal hyperechoic mucosal striations in dogs are associated with lacteal dilation. Veterinary Radiology & Ultrasound, 48 (1), 51–57.  Van Kruiningen, H.J., Lees, G.E., Hayden, D.W., Meuten, D.J.,  Rogers, W.A. (1984). Lipogranulomatous lymphangitis in canine intestinal lymphangiectasia. Vet Pathol, 21 (4), 377-383.  Waldmann, T. A. (1966). Protein losing enteropathy. Gastroenterology, 50(3), 422-433.       

A CASE OF INTESTINAL LYMPHANGIECTASIA WITH LIPOGRANULOMATOUS LYMPHANGITIS IN A FEMALE ROTTWEILER DOG

Uma cadela, fêmea, de raça Rottweiller de três anos de idade apresentou-se com sinais clínicos de diarreira
crónica, perda de peso grave e vómito esporádico. A histopatologia revelou uma linfangiectasia intestinal com
linfangite lipogranulomatosa. A linfangiectasia intestinal consiste numa dilatação patológica dos vasos linfáticos
intestinais, sendo a causa mais frequente de enteropatia com perda de proteína no cão. Este trabalho consiste na
apresentação do caso clínico e numa breve revisão da literatura

Mestrinho, Lisa Alexandra

Almeida, Pedro Alexandre Morais de

ReCiL - Repositório Científico Lusófona

Branquinho et al                                                                              Intestinal lymphangiectasia in a dog  
 6
A CASE OF INTESTINAL LYMPHANGIECTASIA WITH LIPOGRANULOMATOUS 
LYMPHANGITIS IN A FEMALE ROTTWEILER DOG 
 
UM CASO DE LINFANGIECTASIA COM LINFANGITE GRANULOMATOSA NUMA CADELA ROTTWEILER 
 
Joana Branquinho, Lisa Mestrinho, Pedro Faísca, Pedro Morais de Almeida 
 
1Centro de Investigação em Ciências Veterinárias (CICV), Faculdade de Medicina Veterinária, 
Universidade Lusófona de Humanidades e Tecnologias, Campo Grande, 376, 1749 - 024 Lisboa  
 
 
Abstract: A three year old female Rottweiler dog was presented with clinical signs of chronic diarrhoea, severe weight 
loss and sporadic vomiting. Histopathology revealed intestinal lymphangiectasia with lipogranulomatous lymphangitis. 
Intestinal lymphangiectasia represents a pathological dilatation of the intestinal lymph vessels and is the most common 
cause of protein-losing enteropathy in the dog. This paper reports a clinical case with a short review of literature..    
 
Resumo: Uma cadela, fêmea, de raça Rottweiller de três anos de idade apresentou-se com sinais clínicos de diarreira 
crónica, perda de peso grave e vómito esporádico. A histopatologia revelou uma linfangiectasia intestinal com 
linfangite lipogranulomatosa. A linfangiectasia intestinal consiste numa dilatação patológica dos vasos linfáticos 
intestinais, sendo a causa mais frequente de enteropatia com perda de proteína no cão. Este trabalho consiste na 
apresentação do caso clínico e numa breve revisão da literatura 
 
INTRODUCTION 
 
Intestinal lymphangiectasia (IL) is an 
uncommon disease but an important cause 
of protein-losing enteropathy in the dog. The 
major morphological abnormality that 
characterizes this disease is marked dilation 
of intestinal lymphatic vessels in the 
mucosa, submucosa and serosa (Finco et al., 
1973; Melzer & Sellon, 2002; Batt & Hall, 
1989). 
It has been recognized as a clinical entity in 
humans since 1961 and has been first 
described in dogs in 1968 (Waldmann, 
1966; Campbell et al., 1968; Finco et al., 
1973; Mattheeuws, 1974). 
The clinical signs of IL can be quite 
variable. Many dogs with IL exhibit 
nonspecific signs, such as anorexia or 
lethargy. Diarrhoea is one of the most 
consistent clinical signs associated to this 
disease, although not seen in all patients 
(Griffiths et al., 1982; Melzer & Sellon, 
2002). Effusions or oedema, more often pure 
transudates effusions, may develop when 
serum albumin concentrations fall below 1.5 
g/dl (Melzer & Sellon, 2002). 
Laboratory abnormalities can support the IL 
diagnosis; however they are neither specific 
nor pathognomonic of the disease (Kull et 
al., 2001). 
 
 
CASE DESCRIPTION 
A three year old female Rottweiler, 45 kg 
b.w. was admitted for consultation at the 
teaching hospital of the Veterinary 
University (FMV-ULHT) with a two months 
history of chronic diarrhoea, severe weight 
loss and sporadic vomiting. The owner 
described large amounts of brown watery 
stools, with no mucus or fresh blood, 3 to 4 
times a day and no tenesmus. 
The dog was eating well, was alert and 
responsive, although he had lost 13 kg in 
two months.   
Previous exams performed by the referring 
vet revealed hypoproteinemia (3.2 g/dL, 
Revista Lusófona de Ciência e Medicina Veterinária                                                                      4: (2011) 6-11                                                    
 
 
7
reference range: 5.0 to 7.2 g/dL), 
lymphocytosis (5.7x109/L, reference range: 
0.8 to 5.1x109/L) and thrombocytopaenia 
(84x109/L, reference range: 117 to 
460x109/L). The diarrhoea did not respond 
to various antibiotic treatments or dietary 
management (hypoallergenic diet) and there 
was no complete improvement of symptoms.  
 
On admission, clinical examination revealed 
mild abdominal discomfort, distended 
abdomen and emaciation. 
Blood, biochemical profile, abdominal 
ultrasound and radiography were performed. 
 
Hematological findings showed mild 
lymphocytosis (5.7x109/L, reference 
range:0.8 to 5.1x109/L) and 
thrombocytopaenia (84x109/L, reference 
range:117 to 460x109/L). 
Biochemical profile showed moderate 
hypoproteinemia (4.2 g/dL, reference range: 
5.0 to 7.2 g/dL) with hypoalbuminemia (1.7 
g/dL, reference range: 2.3 to 4.0 g/dL).  
Cholesterol level was border line, 112 
mg/dL (reference range: 110 to 321 mg/dL). 
Liver was apparently normal with alanine 
aminotransferase of 50 u/l (reference range: 
47 to 254 u/l). 
Urinalysis was within normal limits.  
Radiographic exam was unremarkable 
except for a slight splenomegaly (figure 1). 
 
        
 
Figure 1 – Lateral abdominal radiograph showing 
slight splenomegaly 
 
Abdominal ultrasound examination revealed 
an increase of the small intestinal wall (8 
mm), with normal layering, mild 
hipermotility and preserved function. Some 
intestinal segments had dilated lumen with 
anechoic content.  It was identifiedmild 
splenomegaly with normal echogenicity and 
architecture, without focal or diffuse 
abnormalities. The colon had some faecal 
content and the mesenteric lymphnodes 
were normal (figure 2). 
 
 
 
 
 
 
 
 
 
 
 
 
Figure 2 – Transverse ultrasonogram of some 
sections of small intestine illustrating increase of the 
wall with normal layering. 
 
At that time, the animal was medicated with 
metronidazol at a dosage of 15mg/kg, twice 
daily (Flagyl®, Sanofi-Aventis) and 
amoxicilin potenciated with clavulanic acid 
at a dosage of 12,5mg/kg, twice daily 
(Synulox®, Pfizer). Pancreatic enzymes 
were prescribed at a dosage of one capsule 
twice daily, with meals (Kreon®, 
Solvayfarma) as well as an ultra-low-fat diet 
supplemented with peanut oil. Cimetidine at 
a dosage of 5mg/kg, twice a day (Tagamet®, 
Smith Kline & French) and Vitamin B12 at 
a dosage of 1000 µg/dog once a week, for 
six weeks, (OHB12 5000 µg, Jaba 
Recordati).  
Clinical and imaging findings were 
compatible with the following differential 
diagnosis of protein-losing enteropathy (ex: 
intestinal lymphangiectasia) and severe 
chronic enteritis (ex: severe small intestinal 
IBD- inflammatory bowel disease –, with 
SIBO- small intestinal bacterial overgrowth, 
acute ulcerative enteritis and small intestinal 
neoplasia (ex: alimentary lymphoma). 
Branquinho et al                                                                              Intestinal lymphangiectasia in a dog  
 8
An exploratory celiotomy was 
recommended in order to collect intestinal 
and stomach full thickness biopsies.  
To minimize the anaesthetic risk and post 
operative complications, a plasma 
transfusion was done to increase short-term 
the albumin level.  
During the surgery, the presence of multiple 
small white nodules along ectasic lymphatic 
vessels on the serosal surface of the small 
intestine was evident. Furthermore, 
prominent mesenteric lymph vessels were 
distended with thick and chalky white paste 
(figure 3). Liver surface was irregular with 
visible alterations and a liver guillotine type 
biopsy was performed. 
 
 
 
 
 
 
 
 
 
 
 
Figure 3 – Intraoperative image of distended and 
prominent mesenteric lymph vessels. Note the focal 
whitish points enlargements corresponding to 
lipogranulomas on the anti-mesenteric serosal surface. 
 
Histopathological findings revealed a thicker 
intestinal mucosa due to lymphatic vessels 
ectasia and lymphoplasmacytic infiltrate in 
the lamina propria. The submucosa showed 
dilated lymphatic vessels, and in the 
subserosa, several lipogranulomes composed 
of foamy machrophages, were observed on 
the periphery of ruptured lymphatic vessels. 
The liver biopsy showed dilated lymphatic 
vessels in the periportal area, and mild 
hepatocyte vacuolar degeneration. 
The histopathological diagnosis was 
intestinal lymphangiectasia with 
lipogranulomatous lymphangitis and 
hepatic-lymphatic congestion with vacuolar 
degeneration. 
  
 
DISCUSSION 
 
 IL is an uncommon disease in the general 
canine population, but is one of the most 
common causes of gastrointestinal protein 
loss. Its inheritance is still unknown but 
breeds with a higher incidence of IL due to 
inflammatory diseases include Basenjis, 
Soft-coated Wheaten Terriers, and 
Lundehunds (Melzer & Sellon, 2002; 
Littman et al., 2000; Landsverk & Gamlem, 
1984). 
This disease can be primary or secondary 
and, in contrast to human IL, canine 
congenital IL is considered less common 
than acquired IL (Finco et al., 1973; Melzer 
& Sellon, 2002). 
Acquired IL is mainly idiopathic, but can 
also be recognized most frequently due to 
inflammatory processes that block lymphatic 
vessels and lymph flow. Other causes of 
increased pressure in lymph vessels include 
portal hypertension resulting from cirrhosis 
or heart disease (i.e., right-sided heart 
failure, pericardial effusion and pericarditis). 
Although, less frequently, we can also see 
cases with associated tumours of the 
intestinal wall, mesentery or even metastatic 
tumours (Melzer & Sellon, 2002; Louvet & 
Denis, 2004). 
Congenital IL, rarely reported, is caused by 
abnormally formed lymphatic vessels (Fogle 
& Bissett, 2007). 
The diagnosis of IL in dogs can be 
challenging. Clinical signs of IL can be 
highly variable, as many dogs with IL 
exhibit nonspecific signs such as lethargy or 
anorexia; however, diarrhoea remains the 
most common clinical feature, especially 
small bowel diarrhoea (Fogle & Bissett, 
2007). 
Ascites, oedema, and hydrothorax are 
common in dogs with IL, mainly found due 
to decreased oncotic pressure secondary to 
hypoproteinemia, (especially 
hypoalbuminemia). In some dogs, clinical 
signs of thromboembolic disease, such as 
tachypnea and dyspnea due to pulmonary 
thromboembolism, may develop (Melzer & 
Sellon, 2002). 
Revista Lusófona de Ciência e Medicina Veterinária                                                                      4: (2011) 6-11                                                    
 
 
9
As previously described, laboratory findings 
in dogs with IL may suggest intestinal loss 
of lymph; however, they are not specific for 
a definitive diagnosis. Lymphopenia is the 
most frequent change supportive of IL, 
although in this case it was not observed. 
Anaemia and neutrophilic leukocytosis, (due 
to chronic inflammation) may be present in 
some dogs, however, not verified in this one. 
In this case, hypoalbuminemia was verified 
and this is the most consistent laboratory 
abnormality reported in canine IL. In some 
cases it can even be noticed pan-
hypoproteinemia (Melzer & Sellon, 2002; 
Burns, 1982).  
Hypocholesterolemia is another frequent 
biochemical alteration seen in canine IL 
although, was also absent in this case.  
Other biochemical abnormalities reported 
include hypocalcemia secondary to overall 
loss of bound calcium resulting from 
hypoalbuminemia, and secondary to poor 
absorption as also vitamin D from the gut 
and by the lipogranuloma formation within 
the lymph vessels. Total serum calcium 
level is often decreased as an artefact of low 
serum albumin concentration (Melzer & 
Sellon, 2002; Burns, 1982; Fogle & Bissett, 
2007; Mellanby et al., 2005). 
Thrombocytopenia, although unusual in IL 
cases, was seen in this dog. Some authors 
suggest this finding as a complication of the 
disease, such as thromboembolism or 
disseminated intravascular coagulation, 
however, no signs of these diseases were 
observed (Melzer & Sellon, 2002). 
The IL diagnosis is only confirmed by 
intestinal biopsy specimens (Kull et al., 
2001). 
In this case surgical biopsy samples were 
performed by laparotomy due to the 
advantages of obtaining full-thickness 
lymphatic architecture and less disruption of 
the normal structure when compared to 
samples collected by endoscopy (Fogle & 
Bissett, 2007). 
The whitish spots observed in the small 
intestinal serosal surface and prominent 
dilated mesenteric lymph vessels 
corresponded to lipogranulomatous 
lymphangitis on histopathological 
examination. Not all cases of canine 
intestinal lymphangiectasia show this type 
of lesions and it is believed that this 
lipogranulomes result from an inflammatory 
foreign body type reaction. This 
inflammatory reaction is  rich with 
macrophages that appear not only due to the 
extravasation of lipid content, through 
dilated wall or ruptured lymph vessels, but 
also secondary to stagnated chylous and fat 
in perilymphatic tissues (Langley-Hobbs, 
1993). 
Increased activities of liver enzyme and 
vacuolar changes in hepatocytes have been 
described in dogs with IL (Finco et al., 
1973; Fogle & Bissett, 2007). In this case, 
although there were no changes in 
biochemical liver function, histological 
appearance of the liver was consistent with 
lymphatic congestion and vacuolar 
degeneration.   
Urinalysis results are important as 
differential diagnosis for hypoalbuminemia 
secondary to renal protein lost (Melzer & 
Sellon, 2002). In this dog urinalysis results 
were unremarkable as in all IL cases. 
The gold of therapy in secondary IL cases 
includes treatment of underlying disease. In 
primary lymphangiectasia cases, treatment is 
basically supportive and symptomatic. 
Affected patients should have dietary 
modification with specific nutritional 
treatment, including low-fat food and 
supplements with adequate amounts of 
essential fatty acids, a reduction in long-
chain triglycerides, because they stimulate 
the loss of lymph to the gastrointestinal 
lumen by chylomicron formation.  
Long-chain triglycerides are not advisable in 
IL affected animals. Although there is some 
controversy about the mechanism of 
absorption for medium-chain triglycerides 
(MCTs), it is felt that MCTs can provide 
some of the favourable aspects helpful in 
recovering the patient’s body condition, 
without stimulating lymph loss (Peterson & 
Willard, 2003; Melzer & Sellon, 2002; 
Brooks, 2005). 
Branquinho et al                                                                              Intestinal lymphangiectasia in a dog  
 10
 To ensure the success of nutritional 
treatment is also really important to choose 
high-quality and highly-digestible protein 
sources, so that we can minimize protein 
indigestion and reduce the production of 
toxins by bacterial flora. 
Immunosuppressive therapy with 
glucocorticoids may be useful in some 
specific cases, especially when the disease is 
secondary to an inflammatory cause. 
Prednisone at immunosuppressive doses (2 
to 4 mg/kg/day) is commonly used in the 
initial management of many dogs with IL 
and mucosal inflammation.  In patients that 
respond poorly to glucocorticoids or in 
severe cases, azathioprine may be added (1 
to 2 mg/kg or 50 mg/m2 PO q24–48h). In 
this case no glucocorticoids were prescribed. 
Antibiotherapy with metronidazole is also 
indicated not only because of its 
antimicrobial effectiveness, but also by their 
immuno-modulatory capabilities (Pibot et 
al., 2006; Hand & Novotny, 2002; Melzer & 
Sellon, 2002).  
As demonstrated in this case, a favourable 
outcome could be achieved with specific 
dietary management and supportive therapy, 
without glucocorticoid therapy.  
The main goal of treatment is the control of 
clinical signs, without cure. Previous studies 
reported a 2 years survival time after 
diagnosis (Hand & Novotny, 2002; Griffiths 
et al., 1982; Melzer & Sellon, 2002).   
 
REFERENCES 
 
Batt, R.M. & Hall, E.J. (1989). Chronic 
enteropathies in dog. J Small Anim Pract, 
30(1),3-12. 
 
Brooks, T. (2005). Case study in canine 
intestinal lymphangiectasia. Can Vet J, 
46(12),1138-1142. 
 
Burns, M.G. (1982). Intestinal 
lymphangiectasia in the dog: A case report 
and review. JAAHA, 18(1), 97–105. 
 
Campbell, R. S. F., Brobst, D., & Bis-Gard, 
G. (1968). Intestinal lymphangiectasia in a 
dog.  J Am Vet. Med Ass, 153(8),1050-
1054. 
 
Finco, D. R., Duncan, J. R., Schall, W. D., 
Hooper, B. E., Chandler, F. W. & Keating, 
K. A. (1973). Chronic enteric disease and 
hypoproteinemia in nine dogs. J Am Vet 
Med Ass, 163(3),262-271. 
 
Fogle, J.E. & Bissett, S.A. (2007). Mucosal 
immunity and chronic idiopathic 
enteropathies in dogs. Compend Contin 
Educ Pract Vet, 29(5),290-302. 
 
Griffiths, G.L., Clark, W.T. & Mills, J.N. 
(1982).  Lymphangiectasia in a dog. Aust 
Vet J, 59(6),187–189. 
 
Hand, M.S. & Novotny, B.J. (2002) Pocket 
Companion to Small Animal Clinical 
Nutrition, 4th ed. Topeka, Kansas: Mark 
Morris Institute, 640–646. 
 
Kull, P.A., Hess, R.S., Craig, L.E., 
Saunders, H.M. & Washabau, R.J. (2001). 
Clinical, clinicopathological, radiographic, 
and ultrasonographic characteristics of 
intestinal lymphangiectasia in dogs: 17 cases 
(1996–1998). J Am Vet Med Assoc, 
219(2),197-202. 
Landsverk, T. & Gamlem, H. (1984). 
Intestinal lymphangiectasia in the 
Lundehund. Scanning electron microscopy 
of intestinal mucosa. Acta Pathol Microbiol 
A, 92(5),353–362. 
 
Langley-Hobbs, S.J. (1993). What is your 
diagnosis?  J Small Anim Pract, 34(4), 174. 
 
Littman, M.P., Dambach, D.M., Vaden & 
S.L., Giger, U. (2000). Familial protein-
losing enteropathy and/or protein-losing 
nephropathy in soft-coated wheaten terriers: 
222 cases (1983–1997). J Vet Intern Med, 
14(1), 68–80. 
 
Louvet, A. & Denis, B. (2004). 
Ultrasonographic diagnosis-small bowel 
lymphangiectasia in a dog. Vet Radiol 
Ultrasound, 45(6),565–567. 
Revista Lusófona de Ciência e Medicina Veterinária                                                                      4: (2011) 6-11                                                    
 
 
11
 
Mattheeuws, A., Derick, A., Thoonen, H. & 
Van Der Stock, J. (1974). Intestinal 
lymphangiectasia in a dog.  J Small Anim 
Pract, 15(12),757-761. 
 
Mellanby, R.J., Mellor, P.J., Roulois, A., 
Baines, E.A., Mee, A.P., Berry, J.L., 
Herrtage & M.E. (2005). Hypocalcaemia 
associated with low serum vitamin D 
metabolite concentrations in two dogs with 
protein-losing enteropathies. J Small Anim 
Pract 46(7),345–351. 
 
Melzer, K.J. & Sellon, R.K. (2002). Canine 
intestinal lymphangiectasia. Compend 
Contin Educ Pract Vet, 24(12),953–961. 
 
Peterson, P.B. & Willard, M.D. (2003).  
Protein-losing enteropathies. Vet Clin North 
Am Small Anim Pract, 33(5),1061–1082. 
 
Pibot, P., Biourge, V. & Elliott, D. (2006). 
In: Encyclopedia of canine clinical nutrition. 
(1ª ed., pp. 106-122): Royal Canin. 
 
Smith, S.J., Penninck, D.G., Keating, J.H. & 
Webster, C.R.L. (2007). Ultrasonographic 
intestinal hyperechoic mucosal striations in 
dogs are associated with lacteal dilation. 
Veterinary Radiology & Ultrasound, 48 (1), 
51–57. 
 
Van Kruiningen, H.J., Lees, G.E., Hayden, 
D.W., Meuten, D.J.,  Rogers, W.A. (1984). 
Lipogranulomatous lymphangitis in canine 
intestinal lymphangiectasia. Vet Pathol, 21 
(4), 377-383. 
 
Waldmann, T. A. (1966). Protein losing 
enteropathy. Gastroenterology, 50(3), 422-
433. 
 
 
 
 
 
 


A case of intestinal lymphangictasia with lipogranulomatous lymphangitis in a female rottweiler dog

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A CASE OF INTESTINAL LYMPHANGIECTASIA WITH LIPOGRANULOMATOUS LYMPHANGITIS IN A FEMALE ROTTWEILER DOG

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