The patient was a five-year-old, intact male biewer terrier weighing 6.6 kg. Since 2020, the dog had presented intermittent episodes of diarrhea, progressive weight loss, abdominal distension, and apathy. As the condition progressed, cavitary effusions developed (ascites and, subsequently, pleural effusion), along with low albumin concentration, decreased serum cholesterol, reduced circulating lymphocytes, and hematological alterations consistent with protein-losing enteropathy.

Throughout 2022, neurological signs suggestive of hepatic encephalopathy were also observed, including episodes of disorientation, seizures, and behavioral changes. The clinical history was further complicated by episodes of hematemesis, meteorism, abdominal pain, and inappetence. Imaging and laboratory examinations performed between late 2022 and early 2023 indicated hepatic alterations consistent with portal hypertension and reinforced the presence of PSS.

In March 2023, the patient developed caudal vena cava thrombosis, and anticoagulant therapy with enoxaparin sodium was initiated. During the same period, the dog developed non-regenerative normocytic normochromic anemia, requiring blood transfusion (packed red blood cells) and the use of erythropoietin under the guidance of the Hematology team. The case was also evaluated by a multidisciplinary team, including Specialists in Nephrology, Neurology, Cardiology, and Gastroenterology.

In January 2024, the patient presented urolithiasis in the urinary bladder, with associated dysuria. Surgical cystotomy was performed, and the calculi were submitted for analysis, which did not reveal significant abnormalities. In late 2024, following extensive clinical, laboratory, and imaging investigation, an endoscopic intestinal biopsy was performed, confirming the diagnosis of intestinal lymphangiectasia.

Therapeutic management was then directed toward dietary intervention with a low-fat diet enriched with medium-chain triglycerides, vitamin supplementation with Pet Protein®, microbiota-modulating antibiotics, and continuous cyclosporine administration aimed at immunosuppressive modulation to control the intestinal immune-mediated response. The patient currently remains under continuous clinical management and follow-up by an integrated team, with variable symptomatic control.

Over the five-year clinical course, there was progression of signs consistent with a chronic, multifactorial disease of complex evolution. The patient was periodically evaluated at different stages of the disease, exhibiting an intermittent clinical pattern frequently associated with gastrointestinal, systemic, and neurological disturbances.

Among the most common physical findings were episodes of marked abdominal distension, with visible enlargement of the lateral abdominal region, as well as the presence of free fluid in the peritoneal cavity, confirmed by imaging examinations and abdominocentesis. The clinical presentation also included pleural effusion, particularly in the right hemithorax, accompanied by a restrictive respiratory pattern and bilateral reduction of breath sounds on thoracic auscultation, consistent with ventilatory restriction secondary to fluid accumulation.

During periods of worsening gastrointestinal signs, abdominal palpation revealed increased sensitivity, heightened peristaltic activity, and clear signs of discomfort upon touch, suggestive of abdominal pain, particularly in the epigastric region. The body condition score fluctuated between 3 and 4/9, with notable muscle mass loss in the paravertebral region and pelvic limbs, especially during periods of prolonged anorexia.

Neurological signs were recorded throughout follow-up, notably episodes of seizures, increased muscle tone in all four limbs, opisthotonos, and prolonged motor recovery during the post-ictal period, particularly in the pelvic limbs. During a neurological consultation in August 2024, the patient presented a general neurological examination within normal limits, although the clinical history was consistent with reactive or genetically mediated epileptic seizures. Specialized follow-up was therefore recommended, with the indication of phenobarbital at a concentration of 40 mg/mL, to be administered only in the event of new seizure episodes. The neurological condition was attributed to possible hepatic encephalopathy, with clinical improvement observed following the instituted hepatic management.

Mucosal evaluation revealed variations ranging from mild pallor to a pearly appearance and mild icterus. Serial laboratory tests demonstrated persistent non-regenerative normocytic normochromic anemia, frequently associated with reduced lymphocyte counts. Due to progressive hematological decompensation, specific therapies were implemented, including the administration of erythropoietin and, in critical periods, transfusional support. In more advanced stages, cardiopulmonary auscultation identified a grade II/VI systolic functional heart murmur, likely secondary to severe hypoproteinemia, which showed partial regression after correction of serum protein levels.

Laboratory and imaging examinations performed throughout follow-up revealed findings consistent with protein-losing enteropathy and hematological disorders associated with chronic hepatic dysfunction. Serum albumin remained persistently below the reference range, reaching 1.6 g/dL in October 2024 (reference range: 2.6-4.0 g/dL), accompanied by significantly reduced lymphocyte counts at different time points, such as October and November (424/µL and 396/µL; reference range: >1,000/µL), suggesting systemic lymphatic impairment (Appendix A).

Serum bile acid testing performed in August 2024 (Appendix B) showed values within the normal range in the preprandial phase (4.3 µmol/L; reference range: 0-5 µmol/L), but with a slight increase in the postprandial phase (40.8 µmol/L; reference range: 0-15 µmol/L), a finding suggestive of reduced hepatic clearance and consistent with hepatobiliary dysfunction or the presence of PSS when correlated with the patient’s clinical history.

In November 2024, the patient exhibited a progressive decline in hematocrit, with values of 18% on the 15th and 17% on the 18th, along with an unremarkable reticulocyte count, characterizing non-regenerative normocytic normochromic anemia. Given the severity of the condition, treatment with recombinant erythropoietin and packed red blood cell transfusion was initiated. In December, a satisfactory hematological response was observed, with hematocrit increasing to 62% (Appendix C).

Abdominal ultrasonography performed in November 2024 (Figure 1) revealed a hyperechoic image (arrow) consistent with caudal vena cava thrombosis, associated with distension of the portal vein and diffuse reduction in intestinal motility. These findings, together with the clinical presentation, supported the suspicion of a severe abdominal vascular disorder, and anticoagulant therapy with enoxaparin was promptly initiated, followed later by clopidogrel.

Figure 1

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