What Is Your Diagnosis?

Gayle H. Jaeger California Veterinary Specialists, 25100 Hancock Ave, Ste 116, Murrieta, CA 92562.

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 DVM, MSpVM, DACVS
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Edward Maher California Veterinary Specialists, 25100 Hancock Ave, Ste 116, Murrieta, CA 92562.

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 DVM, DACVIM, DABVP
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Tana Simmons California Veterinary Specialists, 25100 Hancock Ave, Ste 116, Murrieta, CA 92562.

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 DVM

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History

A 4-year-old 31-kg (68.2-lb) sexually intact female German Shepherd Dog was evaluated for acute lethargy and anorexia. The dog was laterally recumbent and stuporous. Abnormalities detected on physical examination included pale mucous membranes, increased capillary refill time, dehydration, tachycardia, and tachypnea with increased respiratory effort. Marked hypotension was detected during evaluation of blood pressure. The abdomen was distended and tense, and palpation elicited signs of discomfort. Results of serum biochemical analyses indicated hyperphosphotemia (15.9 mg/dL; reference range, 2.5 to 6.8 mg/dL) and increased concentrations of BUN (130.0 mg/dL; reference range, 7.0 to 27.0 mg/dL) and creatinine (8.65 mg/dL; reference range, 0.50 to 1.80 mg/dL). Abnormalities detected on CBC included normocytic anemia (Hct, 11.5%; reference range, 37.0% to 55.0%) and neutrophilic leukocytosis (26.3 X 109 neutrophils/L [reference range, 3.3 to 12.0 X 109 neutrophils/L]; WBCs, 28.6 X 109 cells/L [reference range, 6.0 to 16.9 X 109 cells/L]). Treatment for shock, hypotension, and anemia was initiated by means of a whole blood transfusion and a 6% hetastarch solution.a A lateral survey radiograph of the abdomen was obtained (Figure 1).

Figure 1—
Figure 1—

Lateral radiographic view of the abdomen of a 4-year-old sexually intact female German Shepherd Dog evaluated for acute lethargy and anorexia.

Citation: Journal of the American Veterinary Medical Association 229, 4; 10.2460/javma.229.4.501

Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page

Radiographic Findings and Interpretation

A large, poorly marginated structure occupies most of the cranioventral portion of the abdomen (Figure 2). Multifocal pockets of gas are widely distributed throughout the structure. Detail of the abdominal organs is difficult to ascertain, suggesting the presence of peritoneal effusion. The intestinal tract is displaced caudodorsally. Differential diagnoses included regional peritonitis secondary to gastrointestinal tract perforation, gastric distension, localized infection caused by gas-forming bacteria, or splenic disease such as torsion or infarction.

Figure 2—
Figure 2—

Same radiographic view as in Figure 1. Notice that a large, poorly marginated emphysematous structure containing multifocal pockets of gas occupies most of the abdomen cranially and ventrally (arrows). The margins of the abdominal organs are difficult to ascertain, suggesting the presence of peritoneal effusion.

Citation: Journal of the American Veterinary Medical Association 229, 4; 10.2460/javma.229.4.501

Comments

Unfortunately, the cranial aspect of the abdomen including the diaphragm was not included in the lateral radiographic view. A ventrodorsal radiographic view was not obtained because of the critical condition of the dog and concerns regarding the clinical effects of stress associated with manipulation of body position.

On abdominal ultrasonographic evaluation, a large portion of the abdomen was difficult to visualize because of generalized, poorly demarcated, and intensely hyperechoic areas associated with an extensive distal reverberation artifact, suggesting the presence of diffuse intraparenchymal or free peritoneal gas.

Abdominal exploration was discussed with the owners, but the owners chose to have the dog euthanized. Necropsy revealed a large amount of serosanguinous peritoneal fluid. The spleen was large and twisted, and a large amount of emphysema was detected during palpation. Histologic examination of the spleen was consistent with hemorrhage. No growth was detected on bacterial culture of peritoneal fluid and spleen.

Splenic torsion occurs when the tail of the spleen rotates around its pedical, which is weakly tethered by gastrosplenic and splenicocolic ligaments.1,2 Torsion mechanically compresses the thin-walled splenic veins, resulting in vascular congestion. The thick-walled arteries become occluded with the formation of thromboemboli and resultant infarction.1

The pathogenesis of splenic torsion has not been determined. Approximately 20% of splenic torsions occur concurrently with gastric dilatation and volvulus.2 Splenic torsion may result from gastric dilatation and volvulus, allowing splenic hypermotility3,4 or congestive splenomegaly secondary to gastric dilatation and volvulus.2,3

Radiographic signs of splenic torsion include displacement of the gastrointestinal tract and loss of abdominal detail. The spleen can appear large and misshapen, with multifocal gas opacities within the splenic parenchyma.3,5,6 In the dog reported here, the source of the intraparenchymal gas accumulation was presumed to be non-infectious and secondary to splenic infarction. Intraparenchymal gas accumulation is secondary to oxygen released from the breakdown of oxygenated hemoglobin or carbon dioxide released from reticulocytes in necrotic tissues undergoing anaerobic metabolism.6

On ultrasonographic evaluation, splenic torsion will most often result in splenomegaly with the appearance of diffuse anechoic areas (dilated sinusoids from splenic congestion) and multiple parallel echogenic lines (severely dilated vessels) in a coarse, lacy, hypoechoic pattern.1,2,6 In the dog reported here, the parenchyma of the spleen and splenic vessels could not be evaluated ultrasonographically because of the extensive artifacts caused by intrasplenic gas. Blood flow in splenic veins is often not detected via Doppler ultrasonography.1,3,6

After diagnosis, treatment includes supportive therapy and splenectomy. Gastropexy is recommended because gastric dilatation and volvulus have been reported in 2 dogs after surgical treatment for splenic torsion.4 With surgical correction, a 79% survival rate has been reported.2,3,5

a.

Hetastarch, Gensia Sicor Pharmaceuticals, Irvine, Calif.

  • 1

    Saunders HM, Neath PJ, Brockman DJ. B-mode and Doppler ultrasound imaging of the spleen with splenic torsion: a retrospective evaluation. Vet Radiol Ultrasound 1998;39:349353.

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  • 2

    Weber NA. Chronic primary splenic torsion with peritoneal adhesions in a dog: case report and literature review. J Am Anim Hosp Assoc 2000;36:390394.

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  • 3

    Neath PJ, Brockman DJ, Saunders HM. Retrospective analysis of 19 cases of isolated torsion of the splenic pedicle in dogs. J Small Anim Pract 1997;38:387392.

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  • 4

    Millis DL, Nemzek J, Riggs C, et al. Gastric dilatationvolvulus after splenic torsion in two dogs. J Am Vet Med Assoc 1995;207:314315.

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  • 5

    Stickle RL. Radiographic signs of isolated splenic torsion in dogs: eight cases (1980–1987). J Am Vet Med Assoc 1989;194:103106.

  • 6

    Barzilai M, Schlag-Eisenberg D, Peled N, et al. Noninfectious gas accumulation in an infarcted spleen. Dig Surg 2000;17:402404.

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