What Is Your Diagnosis?

Mary Sarah Bergh Department of Clinical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104-6044.

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Deborah C. Silverstein Department of Clinical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104-6044.

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History

A 5-month-old 3.3-kg (7.3-lb) sexually intact male Maltese was evaluated because it had collapsed and was dyspneic. According to the owner, the dog had been clinically normal in the morning, but in the evening, the dog was found recumbent and had tachypnea. The dog had not been vaccinated.

On physical examination, the dog was recumbent, had signs of depression but was responsive, was moderately dehydrated, and had white mucous membranes. The dog's heart rate was 170 to 190 beats/min (reference range, 80 to 120 beats/min), and the pulses were bounding. The dog was tachypneic (respiratory rate, 54 breaths/min; reference range, 10 to 30 breaths/min) and had mild increase in respiratory effort. Lung sounds were dull, but worse on the left side of the thorax. The oxygen saturation as measured by pulse oximetry was 96% (reference range, 93% to 100%).

The dog's PCV (13%; reference range, 37% to 55%) and the total solids concentration (4.3 g/dL; reference range, 5.5 to 7.5 g/dL) were low. Results of serum biochemical analyses indicated that the concentrations of lactate (6.9 mmol/L; reference range, 0.6 to 2.5 mmol/L), BUN (54 mg/dL; reference range, 5 to 30 mg/dL), and sodium (136 mmol/L; reference range, 140 to 153 mmol/L) were high. The prothrombin time and partial thromboplastin time were severely prolonged (both > 100 seconds; reference ranges for fresh citrated blood,a prothrombin time, 12 to 16 seconds and partial thromboplastin time, 54 to 94 seconds). Ultrasonography of the thorax with a 5-MHz curvilinear probe in an intercostal approach in both sagittal and transverse planes revealed bilateral mild to moderate hypoechoic pleural effusion surrounding the lung lobes. The dog received a transfusion of packed RBCs and fresh frozen plasma. The PCV increased to 25%, and coagulation times were within reference ranges; however, the dog's oxygen saturation decreased to 86%, and lung sounds were dull on auscultation of the left hemithorax. Supplemental oxygen (fraction of inspired oxygen, 50%) was administered. Radiographs of the thorax were obtained (Figure 1).

Figure 1—
Figure 1—

Right lateral (A), left lateral (B), and ventrodorsal (C) radiographic views of a 5-month-old dog evaluated because it had collapsed and was dyspneic.

Citation: Journal of the American Veterinary Medical Association 228, 8; 10.2460/javma.228.8.1193

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

Radiographic Findings and Interpretation

A homogeneous soft tissue opacity can be seen in the left hemithorax, and minimally aerated left lung lobes can be seen on the ventrodorsal radiographic view (Figure 2). Slight lateral malpositioning, or alternatively, a right mediastinal shift can also be seen. The diaphragmatic borders cannot be completely seen. Differential diagnoses included diaphragmatic hernia; pleural or thoracic wall mass or cyst; abscess; fluid or blood in the left hemithorax with collapse of the left lung lobes; and severe pulmonary consolidation attributable to pneumonia, hemorrhage, or edema.

Figure 2—
Figure 2—

Same ventrodorsal radiographic view as in Figure 1. Notice the soft tissue opacity (white arrows) and compression of the lungs in the left hemithorax. The mediastinum is displaced to the right (black arrows).

Citation: Journal of the American Veterinary Medical Association 228, 8; 10.2460/javma.228.8.1193

Comments

Color flow Doppler ultrasonography of the thorax performed the next morning with an L10-5 MHz linear array probe in an intercostal approach in sagittal and transverse planes revealed a large, mottled, nonvascular, hypoechoic soft tissue structure encompassing a large portion of the left hemithorax and causing compression of the left lung lobes, which were seen as vascularized hyperechoic structures that could inflate only to the border of the mass (Figure 3). A minimal amount of hypoechoic pleural effusion was detected in the left hemithorax surrounding the lung lobes.

Figure 3—
Figure 3—

Transverse ultrasonographic image of the left hemithorax of the dog in Figure 1. A nonvascular, mottled structure (white arrows) is evident between the body wall and the hyperechoic, minimally inflated left lung lobes (black arrows).

Citation: Journal of the American Veterinary Medical Association 228, 8; 10.2460/javma.228.8.1193

The clinical signs and results of initial diagnostic evaluation were consistent with rodenticide toxicosis. Pleural effusion detected ultrasonographically was likely hemorrhage secondary to rodenticide-induced coagulopathy. Interestingly, the thoracic hemorrhage solidified into a blood clot after treatment with fresh frozen plasma and gave the radiographic appearance of a soft-tissue mass that compressed the lung lobes. By use of ultrasonography, the architecture of the mass and the absence of blood flow made it possible to rule out a diaphragmatic hernia, cystic structure, or other vascularized mass. The dog was treated initially with vitamin K1 administered SC followed by vitamin K administered orally for 4 weeks. The dog recovered without complications. Results of the rodenticide toxicity screen received several days after the initial evaluation indicated that the concentration of brodifacoum was 45 ppb (45 μg/L; clinical signs may develop at the detection limit of 0.01 ppm [0.01 μg/mL]).

Brodifacoum is a second generation anticoagulant rodenticide that inhibits vitamin K 2,3-epoxide reductase, preventing cycling of the inactive (oxidized) and the active (reduced) vitamin K in the liver.1 Activation of clotting factors II, VII, IX, and X requires the reduced form of vitamin K for carboxylation. Effective clotting is reduced when these factors are depleted and clinical signs develop; factor VII has the shortest half-life at 6.2 hours.2 The mean ± SD half-life of brodifacoum in serum is 6 ± 4 days, and serum concentrations may be detectable until 28 days after initiation of treatment.3

a.

Coagulation Analyzer 2000, Synbiotics Europe, Lyon, France.

  • 1

    Chua JD, Friedenberg WR. Superwarfarin poisoning. Arch Intern Med 1998;158:19291932.

  • 2

    Sheafor SE, Couto CG. Anticoagulant rodenticide toxicity in 21 dogs. J Am Anim Hosp Assoc 1999;35:3846.

  • 3

    Woody BJ, Murphy MJ, Ray AC, et al. Coagulopathic effects and therapy of brodifacoum toxicosis in dogs. J Vet Intern Med 1992;6:2328.

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