A 12-year-old female spayed Borzoi dog weighing 25.5 kg was referred for heart failure. The dog had a history of weakness, anorexia, and diarrhea for 4 days. On initial presentation to the referring veterinarian, the patient was 5% dehydrated and had an irregularly irregular heart rhythm. A complete blood count (CBC) was normal and chemistry revealed elevated alanine aminotransferase (ALT) of 828 U/L (reference interval 10-100 U/L) and mild hyperbilirubinemia of 8.6 micromol/L (reference interval 1.7-10.3 micromol/L).
At presentation to the referral hospital, the dog was mildly febrile (39.2 C). Physical examination abnormalities included increased respiratory effort with increased bronchovesicular sounds bilaterally, decreased lung sounds ventrally, organomegaly, sinus tachycardia with pulse deficits, and a grade II/VI left systolic murmur. An initial indirect systolic blood pressure measured using a Doppler flow detector (Doppler Flow Detector Model 811-B; Parks Medical Electronics Inc., Aloha, OR, USA) was 110 mmHg and pulse oximetry (SurgiVet  3 Parameter Advisor  Vital Signs Monitor; SurgiVet-Smiths Medical, Dublin, OH, USA) was 94%. The patient was placed on continuous electrocardiogram (SurgiVet  3 Parameter Advisor  Vital Signs Monitor; SurgiVet-Smiths Medical) monitoring which showed persistent atrial premature complexes (APCs) and ventricular premature complexes (VPCs) but no sustained tachyarrhythmia.
A repeat CBC (IDEXX Procyte Dx  Hematology Analyzer; IDEXX Laboratories Inc., Westbrook, ME, USA) was normal and chemistry (IDEXX Catalyst Dx  Chemistry Analyzer; IDEXX Laboratories Inc.) revealed severe elevation of ALT >1,000 U/L (reference interval 10-100 U/L) and mild hyperbilirubinemia of 20.5 micromol/L (reference interval 0.0-15.4 micromol/L). A coagulation profile revealed normal prothrombin time (IDEXX Coag Dx  Analyzer; IDEXX Laboratories Inc.) and mild prolongation of activated partial thromboplastin time (IDEXX Coag Dx  Analyzer; IDEXX Laboratories Inc.) of 120 seconds (reference interval 72.0-102 seconds).
Thoracic and abdominal focused assessment with sonography for trauma identified a large volume of pleural effusion bilaterally, mild peritoneal effusion, and a heterogeneous mass effect in the area of the right lateral liver lobe. Left-sided thoracocentesis yielded 700 mL of serosanguineous fluid with a packed cell volume (PCV) of 13% and total solids of 30 g/L. The patient was breathing comfortably after thoracocentesis and a right-sided thoracocentesis was not performed. Treatment included Clavamox (Zoetis, Florham Park, NJ, USA) 13.75 mg/kg per oral (PO) every 12 hours (q12h) empirically, and intravenous (IV) Lactated Ringer's solution (LRS) (Abbot Laboratories, Chicago, IL, USA) at 2.5 mL/kg/hr, while awaiting fluid analysis and cytology. Fluid analysis reported an exudative fluid with a total protein of 35 g/L and 14x109 cells/L. Cytology of the fluid revealed scattered nondegenerate neutrophils, vacuolated macrophages, and rare mesothelial cells. No intracellular or extracellular microorganisms were noted, and enrofloxacin (Bayer HealthCare LLC, Shawnee Mission, KS, USA) 5 mg/kg IV every 24 hours (q24h) was added.
The following day, the patient appeared to have increased respiratory effort and an additional 1,300 mL of serosanguineous fluid was removed via left-sided thoracocentesis. Recheck of ALT, total bilirubin, albumin, PCV, and total solids revealed an improving ALT of 509 U/L (reference interval 10-100 U/L), normal total bilirubin of 29.1 micromol/L (reference interval 0.0-8.6 micromol/L), decreasing albumin of 19 g/L (reference interval 22-39 g/L), and total solids of 48 g/L, with a normal PCV of 39%. A complete abdominal ultrasound revealed less (unable to sample) peritoneal effusion with dilated hepatic veins and mild enlargement of the right liver lobe with hyperechoic mesentery (Figure 1). There was decreased blood flow to the right liver lobe using color flow Doppler evaluation. A right liver lobe torsion (LLT) was suspected. An echocardiogram and computed tomography (CT) were performed prior to surgery to rule out other causes for the pleural effusion.
The echocardiogram revealed mild dilation of the left ventricle with mild mitral and tricuspid regurgitation and a fractional shortening of 32%. There were no significant underlying cardiac abnormalities nor a structural heart disease to account for the pleural effusion or arrhythmia. There were no thoracic or cardiac masses identified or evidence of pericardial effusion. No treatment was warranted based on echocardiogram, and the APCs and VPCs were likely from underlying systemic disease.
The bicavitary CT revealed moderate bilateral pleural effusion and a single pulmonary bullae measuring 0.7 cm within the dorsolateral aspect of the left caudal lung lobe. The peritoneal effusion had resolved and there was a nonenhancing avascular soft-tissue mass (11.6x9.8x5.7 cm) with some ring enhancement adjacent to the right limb of the pancreas and caudal to the gallbladder (Figure 2). No cause for pleural effusion was identified.
An exploratory laparotomy was performed. The patient was premedicated with hydromorphone (Hospira Inc., Lake Forest, IL, USA) 0.1 mg/kg IV and diazepam (Hospira Inc.) 0.25 mg/kg IV, and induced with etomidate (Amidate; Hospira Inc.) 1 mg/kg IV. Anesthesia was maintained with isoflurane (Isoflo; Abbot Laboratories) in 100% oxygen using positive pressure ventilation, and LRS was administered at 10 mL/kg/hr perioperatively.
A standard celiotomy was performed; the caudate liver lobe was noted to be dark purple/black in color and swollen with some omental adhesions, and torsed 180 degrees. A liver lobectomy was performed using a thoracoabdominal 55 stapler (Thoracoabdominal  55 stapler; Covidien, Mansfield, MA, USA) with 3.5 mm staples. Medium sized hemoclips and gel foam were used to achieve hemostasis. No other abnormalities were noted within the abdomen. The abdomen was closed with 0 polydioxanone (PDS) for linea alba, 2-0 PDS for subcutaneous layering, and surgical staples for skin closure. Bilateral chest tubes (Argyle trocar catheter 28fr x16''; Covidien) were placed intraoperatively. Postoperative care included LRS 5 mL/kg/hr, hydroxyethyl starch (HESpan; B. Braun Medical Inc., Bethlehem, PA, USA) 1 mL/kg/hr, hydromorphone 0.1 mg/kg IV every 6 hours, metoclopramide (Reglan; Hospira Inc.) 2 mg/kg/day at a continuous rate infusion, doxycycline (APP Pharmaceuticals LLC, Schaumburg, IL, USA) 5 mg/kg IV q12h, and enrofloxacin 5 mg/kg IV q24h.
A recheck CBC and chemistry on day 1 postoperatively revealed worsening leukocytosis, with a white blood cell count of 27.7x109 cells/L (reference interval 5.7x109-16x109 cells/L), and neutrophilia with 25.8x109 cells/L (reference interval 3.0x109-11.5x109 cells/L). The chemistry revealed a worsening hypoalbuminemia of 7 g/L (reference interval 22-39 g/L) and total protein of 37 g/L (reference interval 52-82 g/L), and improving ALT of 185 U/L (reference interval 10-100 U/L). Hydroxyethyl starch was increased to 1.5 mL/kg/hr given the hypoalbuminemia.
That evening, the patient had two episodes of sustained ventricular tachycardia (VT) (heart rate of 200-230 beats/min), which responded to lidocaine hydrochloride (Hospira Inc.) 2 mg/kg IV bolus, and sotalol hydrochloride (Sandoz Inc., Princeton, NJ, USA) 1.5 mg/kg PO q12h was added. The patient continued to have VPCs, but there were no recurrence of the VT during the remainder of the patient's stay.
On day 2 postoperatively, the patient improved and transitioned from hydromorphone to buprenorphine (Reckitt Benckiser Pharmaceutical Inc., Richmond, VA, USA) 0.01 mg/kg. The chest tube was mildly productive immediately postoperatively (3.5 mL/kg/hr). Fluid production gradually decreased to 1.0 mL/kg/hr and chest tubes were pulled later that day.
The following day, mirtazapine (Apotex Inc., Toronto, Canada) 0.6 mg/kg PO q24h was added, and the patient began eating and was subsequently discharged on sotalol hydrochloride 2 mg/kg PO q12h, tramadol hydrochloride (Amneal Pharmaceuticals, Hauppage, NY, USA) 2 mg/kg PO every 8 hours, doxycycline 5 mg/kg PO q12h, and mirtazapine 0.6 mg/kg PO q24h. Given the history of chronic inflammation within the pleural cavity, prednisone (HIKMA Pharmaceuticals, Amman, Jordan) was initiated at 1 mg/kg q24h PO at a tapering dose for 14 days.
No growth resulted from the aerobic and anaerobic bacterial cultures of the pleural fluid. Resected liver lobe histopathology revealed congestion and hemorrhage with severe segmental ischemic necrosis with peripheral fibroplasia and neovascularization. The focus of necrosis and rarefaction was encapsulated by dense fibrous connective tissue supporting chronicity. There was no evidence of bacteria, neoplasia, or parasitic or fungal organisms.
At follow-up on day 7 postoperatively, the patient was reported to be doing well. Recheck CBC and chemistry revealed improving leukocytosis of 21.8x109 cells/L (reference interval: 5.7x109-16.3x109 cells/L), normal ALT, and mild elevation of alkaline phosphatase of 288 U/L (reference interval 10-150 U/L).
On day 15 postoperatively, an echocardiogram revealed myxomatous mitral valve degeneration with mild mitral regurgitation, no evidence of tricuspid disease, and complete resolution of the pleural effusion. Recheck electrocardiogram revealed occasional supraventricular and ventricular arrhythmias, but no sustained arrhythmias. Sotalol was continued with no change in the dose.
The owners and patient were relocating abroad and the plan was to follow-up with a cardiologist in England in 1 month. Therefore, further follow-up was not possible. The last communication with the family was 3 weeks postoperatively and clinically the patient was doing well. The patient received a high standard of veterinary care and all diagnostics and treatments performed were consented by the owners.