A 7-year-old 23-kg (50.6-lb) spayed female Border Collie was evaluated by the emergency service of the Veterinary Teaching Hospital at North Carolina State University College of Veterinary Medicine for respiratory distress secondary to bilateral pneumothorax. The dog had a history of positive heartworm test results 2 years previously, and although no adulticide treatment was given, the dog had been receiving monthly administration of heartworm preventative^a since the owner adopted it 18 months ago. The dog had no history of trauma. Earlier that day, the owner noticed that the dog vomited its morning meal and began to have marked respiratory distress and concurrent signs of anxiety. The dog was taken to the referring veterinarian, and a dorsoventral radiographic image of the thorax revealed bilateral pneumothorax. The referring veterinarian performed a left-sided thoracocentesis, and removed 2 L of air; however, negative pressure could not be achieved. The dog was referred for ongoing further diagnostic evaluation and management.

Upon arrival at the hospital, the dog was bright, alert, and responsive. The HR was 120 beats/min with normal pulses, and no murmur was auscultated. The dog was panting, and on thoracic auscultation, lung sounds were considered quieter than normal bilaterally in the dorsal fields. The remainder of the physical examination was unremarkable. A catheter was placed in the right cephalic vein, and a sample of venous blood was obtained for assessment of PCV, total protein concentration, CBC, serum biochemical analysis, and a heartworm antigen ELISA.^b The only abnormality found on CBC was mild leukocytosis (12.84 × 10³ cells/μL; reference range, 4.39 × 10³ cells/μL to 11.61 × 10³ cells/μL) characterized by mild neutrophilia (11.042 × 10³ cells/μL; reference range, 2.84 × 10³ cells/μL to 9.11 × 10³ cells/μL). Serum biochemical analysis revealed mildly increased albumin concentration (4.3 g/dL; reference range, 3.0 to 3.9 g/dL) and alanine transaminase activity (114 U/L; reference range, 12 to 54 U/L). Results of the heartworm test were positive and indicated a high serum antigen concentration. The dog was sedated with butorphanol (0.3 mg/kg [0.14 mg/lb], IV) and acepromazine (0.02 mg/kg [0.009 mg/lb], IV), and two 14-gauge fenestrated polyurethane catheters^c were inserted, one on each hemithorax. Initially, 195 mL of air was aspirated from the right hemithorax and 470 mL of air was aspirated from the left hemithorax. The dog was connected to a continuous chest tube drainage system^d for overnight management. Thoracic radiographs were obtained and showed continued evidence of bilateral pneumothorax; however, pneumothorax was noted as considerably improved, compared with its appearance on the radiograph from the referring veterinarian.

The dog was anesthetized the next day for diagnostic imaging via helical computed tomography. On preanesthetic evaluation, the dog was bright, alert, and responsive, and the dog's physical status was classified as a 3 (a patient with severe systemic disease), according to the scheme adopted by the American Society of Anesthesiologists.¹ The dog was premedicated with acepromazine (0.01 mg/kg [0.005 mg/lb], IV) and buprenorphine (0.01 mg/kg, IV), and anesthesia was induced with propofol (3.6 mg/kg [1.64 mg/lb]). Anesthesia was maintained with isoflurane (1% to 2%) in oxygen, and the dog was allowed to breathe spontaneously. The total anesthetic time was 1 hour 20 minutes, during which time HR, respiratory rate, systolic arterial pressure, MAP, diastolic arterial pressure, Spo₂, end-tidal CO₂ concentration, and rectal temperature were monitored and remained within clinically acceptable limits. The computed tomographic scan revealed continued mild bilateral pneumothorax as well as possible pulmonary blebs in the medial aspect of the cranial lung lobes. Anesthetic recovery was unremarkable, and the dog was returned to the intensive care unit for continued monitoring.

The dog was anesthetized again the following day for a thoracic exploration via a median sternotomy. On preanesthetic evaluation, the dog was again bright, alert, and responsive; however, it was noted that the right-sided chest tube was no longer functional. Breath sounds could be auscultated throughout all lung fields bilaterally. The dog's physical status was again classified as a 3, according to the scheme adopted by the American Society of Anesthesiologists.¹ The dog was premedicated with hydromorphone (0.1 mg/kg [0.05 mg/lb], IV), and anesthesia was induced with propofol (4.4 mg/kg [2.0 mg/lb]). Anesthesia was maintained with isoflurane (1.5% to 3.5%) and a continuous rate infusion of fentanyl (0.3 to 0.5 μg/kg/min [0.14 to 0.23 μg/lb/min]). A 20-gauge catheter was placed in the dorsal pedal artery, and direct arterial blood pressure monitoring was performed. The patient was mechanically ventilated on a positive pressure ventilator,^e and anesthesia was unremarkable for the initial 3 hours. A median sternotomy was performed, and the lung lobes were visually inspected for leakage or the presence of bullae or blebs. Although no bleb or bulla was found and no bubbles were observed after sequential immersion of the lung lobes, the right caudal lobe was noted to appear abnormal. The most peripheral portion appeared discolored (pale pink), and a clear line of demarcation was observed. Positive pressure could not deploy alveoli in this area, although the rest of the lung lobes were fully inflated (maximum inflation pressure, 20 cm HO). In the absence of any other finding, it was hypothesized that this abnormal portion of the lung could represent an area of suspicious potential leakage. At this time, the dog's HR was 70 beats/min and MAP was 85 mm Hg. A right lung lobectomy was performed by stapling and removal of the right caudal lung lobe near the hilus with a stapling device.^f A worm segment was observed both on the remaining stump of the lung lobe and on the cut surface of the lobe as it was placed into formalin.

At this time, the dog became acutely tachycardic (HR, 180 beats/min) and hypotensive (MAP, 38 mm Hg). The anesthetist began initial treatment for presumed bleeding and summoned an anesthesiologist. A 15 mL/kg (6.8 mL/lb) bolus of lactated Ringer's solution was administered with no change in either HR or MAP. The thorax was evaluated for potential bleeding, but none was found. Administration of crystalloid fluids was continued at bolus rate for a total of 22 mL/kg (10 mL/lb), and phenylephrine (2.0 μg/kg [0.9 μg/lb], IV) was administered. There was a minimal response to the phenylephrine, with the HR decreasing to 150 beats/min and MAP increasing to 45 mm Hg; therefore, the phenylephrine dose was repeated. The second dose produced no change in HR; however, MAP increased to 62 mm Hg. At this time, the anesthesiologist, who had not been in the room at the time the lung lobe was removed, questioned the surgeon as to whether anything unusual had occurred and was informed about the worm. Diphenhydramine (1 mg/kg [0.45 mg/lb], IV) and dexamethasone sodium phosphate (0.15 mg/kg [0.07 mg/lb], IV) were administered, resulting in resolution of the tachycardia and stabilization of blood pressure. Within 10 minutes of the final drug administrations, the HR had returned to 92 beats/min and MAP had risen to 75 mm Hg. The period of anaphylaxis lasted for approximately 25 minutes, and anesthesia was unremarkable for the remaining 45 minutes of the procedure and recovery.

Following anesthetic recovery, the dog was admitted to the intensive care unit for monitoring and postoperative care. Over the subsequent 2 hours, 375 mL of blood was aspirated from the chest tubes. The PCV of the aspirated fluid was determined to be 15% at 1 hour and 40% at 2 hours with a peripheral PCV of 37%. A PT of 17 seconds (reference range, 9 to 12 seconds) and partial thromboplastin time of 84 seconds (reference range, 59 to 87 seconds) were recorded, and the dog received an auto transfusion of 100 mL of the blood recovered from the chest tube. In the face of massive blood loss, the mild increase in PT and normal partial thromboplastin time were not regarded as good indicators of the patient's current physical status, and the dog was started on a transfusion of fresh frozen plasma (190 mL total) and sent back to the surgical suite. During reexploration of the chest cavity, no major bleeding vessels were found, but suspicious areas were double ligated in the area of the internal thoracic arteries on both sides of the sternum. The lung lobectomy site was examined, and no clot or leakage was seen. The anesthesia and subsequent anesthetic recovery were unremarkable. After the second surgery, the dog made an uneventful recovery. After surgery, the chest tube was aspirated intermittently and produced moderate volumes of serosanguineous fluid. The tube was removed at 63 hours after surgery.

Histologic examination of the submitted lung lobe revealed severe atelectasis with mild peribronchiolar and perivascular lymphocytic cuffing as well as mucus, eosinophils, and macrophages in the bronchi and bronchioles. This was indicative of a low-grade inflammatory process; however, no evidence of parasitic disease was observed, likely attributable to long-term heartworm preventive treatment. A parasitological evaluation of the worm segment removed from the dog confirmed the diagnosis of infection with Dirofilaria immitis. The dog was discharged 5 days after surgery and received doxycycline (4.4 mg/kg, PO, q 12 h) for 30 days as well as continued monthly administration of heartworm preventative.^a