Introduction

The clinical manifestations of systemic coagulopathies in cats have been sparsely documented. Reported findings include hematomas, otic and conjunctival hemorrhage, melena, petechiae, hematochezia, and pleural effusion.^1–3 Here, we report novel abdominal ultrasound findings in a cat with a systemic coagulopathy, which, if identified, should prompt the clinician to order urgent blood coagulation testing.

Contemporary standard of care was provided to the animal described in this report.

Case Report

A 3 yr old female spayed Sphynx cat was presented to her local veterinary emergency room for a 24 hr history of vomiting, lethargy, anorexia, and vocalizing when picked up. Physical examination revealed pain on palpation of the kidneys and a large, nonturgid bladder. A small volume of blood was present on the right side of her mouth, although the owner had noted that the cat had been chewing and rubbing on the carrier on the way to the clinic. The remainder of her physical examination was normal. A complete blood count, serum biochemistry profile, and urinalysis were unremarkable (Supplementary Spreadsheet 1). A single-view lateral radiograph of the thorax and cranial abdomen (including the retroperitoneum and kidneys) was normal. An abdominal ultrasound was performed by a diplomate of the American College of Veterinary Radiology. The renal corticomedullary definition was very mildly reduced, and there was no evidence of pyelectasia. The perinephric fat was diffusely hyperechoic, and there was a scant amount of anechoic retroperitoneal effusion. The attending radiologist thought these changes to be most consistent with interstitial or glomerulonephritis, with infectious, inflammatory, toxic, infiltrative, and systemic inflammatory disease processes considered as possibilities. The urinary bladder was moderately distended, and there was mild mesenteric lymphadenomegaly, measuring up to 5.4 mm in thickness, thought to most likely be representative of reactive lymphadenopathy. The remainder of the abdomen was normal, including her gastrointestinal tract, which exhibited normal thickness with appropriate wall layering definition, and her adrenal glands, which measured 2.7 mm (left) and 2.9 mm (right) in thickness.

The patient was referred to our facility ∼9 hr later. She was admitted to the hospital and placed on IV fluids^a (9 mL/hr). The following morning, a physical examination revealed a small volume of blood in the left side of the oral cavity and a small volume of hematochezia. Her fundus, examined with retroillumination, appeared normal. A complete blood count revealed anemia (packed cell volume 18%; laboratory reference interval [RI] 30–46%), reticulocytosis (101 K/µL; RI 0–50 K/µL), neutrophilia (22.7 K/µL; RI 2.0–12.0 K/µL), and thrombocytopenia (130 K/µL with occasional large platelets and no aggregates; RI 200–500 K/µL). Slight anisocytosis and polychromasia were observed on a blood film review, consistent with the mild reticulocytosis. A serum biochemistry profile showed hypoalbuminemia (1.9 g/dL; RI 2.8–3.9 g/dL), total hypocalcemia (8.6 mg/dL; RI 9–12 mg/dL), low creatinine (0.8 mg/dL; RI 0.9–2.0 mg/dL), and hyperglycemia (156 mg/dL; RI 70–140 mg/dL). Urinalysis, collected via cystocentesis, showed a specific gravity >1.035, hematuria (>75 red blood cells per high-powered field), pyuria (16–30 white blood cells per high-powered field), and proteinuria (urine protein to creatinine ratio 0.8). The urine was grossly brown/red and opaque. Aerobic urine culture showed no growth. Prothrombin (RI 8.7–12.9 s) and partial thromboplastin (RI 10.5–22.9 s) times were prolonged (both >100 s). Serum fasting bile acids and D-dimers were within the laboratory RI. A focal urinary tract ultrasound^b was performed ∼24 hr following the initial study by a radiology resident directly supervised by a diplomate of the American College of Veterinary Radiology. The entire retroperitoneal space was persistently diffusely hyperechoic with thickened, lobular fat now interspersed with hypoechoic material (Figures 1, 2). These findings were thought to represent diffuse retroperitonitis or retroperitoneal edema of unknown etiology with associated retroperitoneal effusion. Both kidneys were normal in structure (Figure 2), and the urinary bladder was moderately distended with fluid and contained a gravity-dependent collection of echogenic material. There was persistent mild, hyperechoic mesenteric lymphadenomegaly, measuring up to 6 mm in short axis. Fine-needle aspirates of the retroperitoneal space were obtained using 23-gauge and 25-gauge 1.5” needles. Cytology was of adequate cellularity, and many erythrocytes were observed. There were mildly increased numbers of segmented and nondegenerative neutrophils, and remaining leukocytes and platelets were found in proportion with the peripheral blood. No erythrophagia or evidence of erythrocyte breakdown products, such as hemosiderin or hematoidin, were observed in the samples from the retroperitoneal fat. These findings were thought to be consistent with either acute hemorrhage and mild neutrophilic inflammation or blood contamination. Aerobic and anaerobic cultures showed no growth. Fine-needle aspirates of the mesenteric lymph nodes were of fair cellularity with many lysed cells. The intact cells observed were primarily lymphocytes, which were predominantly (>90%) small and mature, with lower numbers of intermediate lymphocytes and plasma cells. Although the overall cellularity of the lymph node aspirate was low, the lymph node aspirate was consistent with aspiration of unremarkable lymphoid tissue or mild reactive lymphoid hyperplasia, given the mild mesenteric lymphadenopathy noted. Following her ultrasound, the cat became hypotensive and obtunded. A blood type and cross-match were performed, and she was treated with a fresh frozen plasma (8 mL/kg) bolus to rapidly replenish clotting factors, followed by a whole blood transfusion (13 mL/kg) administered over 4 hr given the clinical suspicion for progressive hemorrhage and the suboptimal size of the administered unit of plasma. She also received vitamin K (phytonadione 5 mg/kg subcutaneously once). No other medications were administered. She had no further hematochezia or oral bleeding and started eating, and her packed cell volume remained stable (23%) the following morning. She was discharged that day with 4 wk of oral vitamin K (phytonadione 1.5 mg/kg q 8 hr). Brodifacoum, bromadiolone, chlorophacinone, dicoumarol, difenacoum, difethialone, diphacinone, or warfarin were not detected in whole blood^c. Her prothrombin and partial thromboplastin times were normal 2 days, 1 mo, and 3 mo following cessation of vitamin K therapy, and she had no further signs of bleeding.

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Discussion

This case demonstrates that hyperechoic retroperitoneal fat can be an early manifestation of coagulopathy in cats. Although this cat eventually developed hematochezia and regenerative anemia, the initial finding of hyperechoic retroperitoneal fat in the absence of these signs led to a clinical suspicion of interstitial/glomerulonephritis as opposed to a systemic coagulopathy. Ultrasound findings in cats with coagulopathies have not been previously described, although abdominal radiographs in eight cats were reportedly normal.^1,4 In dogs, peritoneal effusion, retroperitoneal effusion, and gastric wall thickening have been reported,^5–7 and, although not reported in previous feline radiographic studies, this case shows that retroperitoneal effusion may also be a feature of coagulopathies in cats. The cause of the hyperechoic retroperitoneal fat in this case is unknown. Hyperechoic fat is typically associated with inflammation,^8,9 and, as cavitary blood is known to incite inflammation,^10,11 retroperitoneal bleeding may have induced steatitis. Alternatively, hemorrhage may have originated directly from the retroperitoneal fat. The cytology findings could support either possibility, and it is unknown whether the samples obtained from the retroperitoneal space were more representative of the fat or the interspersing hypoechoic fluid. The mildly increased numbers of neutrophils may represent either steatitis or peripheral blood contamination; similarly, the high numbers of erythrocytes may represent either hemorrhage or peripheral blood contamination. The presence of platelets and absence of erythrocyte breakdown products or erythrophagocytosis suggests either blood contamination or acute hemorrhage, given that erythrophagocytosis takes ∼1 day and hemosiderin and hematoidin at least 3 days to become apparent.^12,13 Given that the initially scant volume of retroperitoneal anechoic material increased in volume and became echogenic between the two ultrasound studies within 24 hr, which also coincided with the development of anemia, acute, active hemorrhage is considered most likely. Why bleeding in the retroperitoneum appeared before more common sites of hemorrhage (e.g., subcutaneous space, ocular, gastrointestinal, thoracic, and peritoneal cavities)^1,5 in this case is unknown. With hindsight, more significance should have been placed on the cat’s oral bleeding, rather than assuming this to be an effect of the cat chewing and rubbing its face on the carrier on the way to the clinic.

The cause of the mild mesenteric lymphadenomegaly is also unknown, given the poor cellularity and low number of intact cells obtained on fine-needle aspiration. Reactive lymphadenitis, secondary to gastrointestinal hemorrhage or retroperitoneal steatitis, is possible. Either of these causes may have been responsible for the cat’s initial presenting complaint of vomiting, lethargy, anorexia, and vocalizing when picked up. The gravity-dependent collection of echogenic material in the bladder likely represented blood clots¹⁴; however, hematuria could not be confirmed given the possibility of peripheral blood contamination from cystocentesis. Similarly, the white blood cells observed on urinalysis likely originated from the peripheral blood.

Given that no vitamin K epoxide reductase antagonists were detected in the cat’s blood, the cause of the coagulopathy remains unknown. Brodifacoum, bromadiolone, chlorophacinone, dicoumarol, difenacoum, difethialone, diphacinone, or warfarin were tested in whole blood, as this assay is commercially available^d. Ingestion of these agents is unlikely given the low limit of detection of the liquid chromatography–mass spectrometry assay used (brodifacoum <0.01 ppm, bromadiolone <0.02 ppm, chlorophacinone <0.2 ppm, dicoumarol <0.01 ppm, difenacoum <0.02 ppm, difethialone (0.07 ppm), diphacinone (<0.2 ppm), or warfarin (<0.02 ppm) but cannot be excluded given that the blood concentration of these agents required to induce coagulopathy in cats is, to our knowledge, unknown. Ingestion of another vitamin K epoxide reductase antagonist (e.g., diphenadione, coumachlor, coumafuryl, coumatetralyl, pindone, valone, or sulfaquinoxaline) is also possible.

Conclusion

Systemic coagulopathy should be considered as a differential for hyperechoic retroperitoneal fat in cats, especially in the absence of other clinical features suggestive of regional inflammation. The cause of the coagulopathy in this case remains unknown.