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Compendium May 2012 (Vol 34, No 5)

Clinical Snapshot: Periumbilical Ecchymotic Hemorrhage in a Rat Terrier

by Michael O. Childress, DVM, MS, DACVIM

    Case Presentation

    A 7-year-old, castrated rat terrier presented for emergent evaluation of lethargy and inappetence of 4 days’ duration. Shortly before presentation, the dog’s owners had found it hiding in a secluded area of the house. While attempting to rouse the dog, the owners noted that it was ataxic in all four limbs and exhibited inappropriate mentation.

    On physical examination, the patient was noted to be mentally dull but responsive to stimulation. The dog was tachycardic (pulse rate: 170 bpm, reference range: 70 to 160 bpm) and tachypneic (respiratory rate: 60 breaths/min, reference range: 20 to 40 breaths/min). Systolic blood pressure, measured by Doppler sphygmomanometry, was 80 mm Hg (reference range: 124 to 178 mm Hg). Mucosal pallor and mild abdominal distention were noted. On visual inspection of the ventral abdomen, a well-demarcated region of periumbilical ecchymotic hemorrhage (FIGURE A) was apparent. No other areas of cutaneous or mucosal hemorrhage were identified. A minimum database consisting of a complete blood count, a serum biochemistry panel, and urinalysis revealed moderate normocytic, normochromic anemia (hematocrit: 20.4%, reference range: 37% to 55%) and marked hyperproteinemia (total serum protein concentration: 10.6 g/dL, reference range: 4.8 to 6.9 g/dL) characterized by hyperglobulinemia (7.4 g/dL, reference range: 1.7 to 3.8 g/dL) and a normal serum albumin concentration (3.1 g/dL, reference range: 2.3 to 3.9 g/dL).

    1. What is the name for the lesion depicted in Figure A? What is the pathogenesis of this lesion?
    2. Based on the pathogenesis of the lesion in Figure A and review of the clinical and clinicopathologic data presented, what are some possible causes of the dog’s condition?
    3. What further diagnostic tests would you recommend at this point?

    Answers and Explanations

    1. Periumbilical ecchymotic hemorrhage is known as Cullen sign after Thomas Cullen, the British obstetrician who first described this lesion in association with ruptured ectopic pregnancy in humans. Its presence indicates hemorrhage into the peritoneal or retroperitoneal space.1–4 Cullen sign develops when free peritoneal or retroperitoneal blood dissects along fascial planes into the subcutaneous space and accumulates at the umbilicus. Intraabdominal hemorrhage may also traverse small congenital defects in the peritoneum near the umbilicus to accumulate in the periumbilical subcutaneous tissues.1 In humans, Cullen sign has been described in association with necrotizing hemorrhagic pancreatitis, intraabdominal malignancy, perforating duodenal ulcer, and coagulopathy and as a complication of percutaneous liver biopsy; peritoneal or retroperitoneal hemorrhage is a common feature of all of these conditions.3,4 Cullen sign has been reported in a dog with suspected adrenal gland neoplasia1 and in two dogs following blunt abdominal trauma.2

    2. The presence of Cullen sign, abdominal distention, anemia, and signs of hypovolemic shock (mucosal pallor, tachycardia, tachypnea, hypotension) suggest acute hemoabdomen in this dog. In the absence of a history of trauma, abdominal neoplasia is the most likely cause of hemoabdomen in dogs; ruptured tumors of the spleen and liver are most frequently implicated.5 Other nontraumatic etiologies for hemoabdomen include gastric dilatation-volvulus, splenic or liver lobe torsion, anticoagulant rodenticide toxicosis, or other coagulopathies.5

    The marked hyperglobulinemia in this patient is highly suggestive of lymphoid neoplasia, such as multiple myeloma, lymphoma, lymphoid leukemia, or extramedullary plasmacytoma. However, hyperglobulinemia also may be associated with numerous acute or chronic infectious or inflammatory conditions, active liver disease, or nephrotic syndrome.6 Given the dog’s clinical presentation and laboratory results, lymphoid neoplasia of the liver and/or spleen with associated organ rupture and hemoabdomen was considered the most likely diagnosis.

    3. Abdominal imaging tests and abdominocentesis are indicated in this case to confirm the presence of hemoabdomen and identify the source of hemorrhage, if possible. Coagulation tests should be performed to rule out coagulopathy as a contributing factor to the development of hemoabdomen. Serum protein electrophoresis should also be performed to determine which serum proteins are responsible for the hyperglobulinemia.


    In this case, abdominal radiography revealed a soft tissue opacity in the midabdomen in the region of the spleen (FIGURE B), with patchy areas of mildly decreased serosal detail. Subsequent abdominal ultrasonography identified a 5-cm splenic mass of mixed echogenicity (FIGURE C) and numerous small, hypoechoic nodules scattered throughout the splenic parenchyma. Analysis of a fine-needle aspirate of the spleen revealed a marked lymphoplasmacytic proliferation suggestive of lymphoid hyperplasia or lymphocytic or plasmacytic neoplasia. Free abdominal fluid was also identified ultrasonographically. Abdominocentesis was performed, and a sample of hemorrhagic fluid with a packed cell volume of 25% was obtained, confirming the presence of hemoabdomen. Prothrombin time was normal at 7.6 seconds (reference range: 5.4 to 9.4 seconds), although partial thromboplastin time was prolonged at 15.8 seconds (reference range: 9.4 to 13.4 seconds). Serum protein electrophoresis revealed a monoclonal gammopathy. Monoclonal gammopathy is most commonly associated with lymphoid neoplasia in dogs, although it is occasionally associated with nonneoplastic disease, particularly ehrlichiosis and leishmaniasis.7 Given the presence of the splenic mass, infectious disease was considered an unlikely cause for this dog’s clinical presentation, and diagnostic testing for infectious diseases was not performed.

    The dog underwent emergency splenectomy, and the splenic mass was histopathologically identified as a hematoma. No histopathologic evidence of neoplasia was apparent in the spleen, even after evaluation of additional recut tissue sections. However, 3 days after splenectomy, the dog’s peripheral lymphocyte count had increased from 1.33 × 103 cells/µL to 10.36 × 103 cells/µL (reference range: 1.0 × 103 to 5.0 × 103 cells/µL). Flow cytometric evaluation of peripheral blood diagnosed chronic lymphocytic leukemia of B-cell origin. It was suspected that this neoplasm had secondarily infiltrated the spleen and precipitated splenic rupture and hematoma, although this could not be confirmed.

    Given the absence of identifiable neoplasia in splenic histopathology samples, ehrlichiosis could also be a plausible explanation for the monoclonal gammopathy and lymphocytosis identified in this dog. However, the lymphocytosis associated with canine ehrlichiosis typically consists of CD8+ T cells,8 as opposed to the B-cell lymphocytosis noted in this dog. Therefore, ehrlichiosis was considered less likely to be a causative or contributing factor to this dog’s clinical presentation. The owners elected no follow-up treatment for the dog, and it was discharged from the hospital 5 days after splenectomy, after which it was lost to follow-up.


    1. Schermerhorn T, McNamara PS, Dykes NL, et al. Cullen’s sign and haemoglobinuria as presenting signs of retroperitoneal haemorrhage in a dog. J Small Anim Pract 1998;39:490-494.

    2. Crowe DT, Todoroff RJ. Umbilical masses and discolorations as signs of intraabdominal disease. J Am Anim Hosp Assoc 1982;18:295-298.

    3. Harris S, Naina HV. Cullen’s sign revisited. Am J Med 2008;121:682-683.

    4. Meyers MA, Feldberg MA, Oliphant M. Grey Turner’s sign and Cullen’s sign in acute pancreatitis. Gastrointest Radiol 1989;14:31-37.

    5. Pintar J, Breitschwerdt EB, Hardie EM, et al. Acute nontraumatic hemoabdomen in the dog: a retrospective analysis of 39 cases. J Am Anim Hosp Assoc 2003;39:518-522.

    6. Lassen ED. Laboratory evaluation of plasma and serum proteins. In: Thrall MA, Baker DC, Campbell TW, et al, eds. Veterinary Hematology and Clinical Chemistry. Baltimore, MD: Lippincott Williams & Wilkins; 2004:401-412.

    7. Giraudel JM, Pagès J, Guelfi J. Monoclonal gammopathies in the dog: a retrospective study of 18 cases (1986-1999) and literature review. J Am Anim Hosp Assoc 2002;38:135-147.

    8. Avery AC. Determining the significance of persistent lymphocytosis. Vet Clin North Am Small Anim Pract 2007;37:267-282.

    References »

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