Urothorax Associated with Uroperitoneum in a Dog Without Diaphragmatic Disruption

Introduction

Pleural effusions develop in cases of increased hydrostatic pressure, decreased plasma oncotic pressure, decreased pressure in the pleural space, increased pleural permeability, thoracic duct rupture, and in cases of diaphragmatic defects.¹ Several cases of pleural effusion associated with peritoneal fluid accumulation have been reported. Uroabdomen/urinoma, acute pancreatitis, bile peritonitis, and ascites associated with either ovarian tumors or hepatic cirrhosis have all been incriminated for the development of pleural effusions.^2–7 In those cases, the fluid can reach the thoracic cavity directly through an anatomical defect in the diaphragm or it can be transferred via the diaphragmatic lymphatics.⁸ Urothorax (or urinothorax) is a rarely described condition of pleural transudate characterized by the presence of urine in the pleural space. In this report, a case of a posttraumatic urothorax associated with uroperitoneum without detectable diaphragmatic disruption is described for the first time in a dog.

Case Report

A 2 yr old male cross-breed dog weighing 11 kg was referred to the Companion Animal Clinic of the Aristotle University of Thessaloniki with tachypnea, labored and shallow respirations, and suspected peritoneal effusion. The dog had a 2 day history of stranguria and hematuria after a road traffic accident. Physical examination revealed a heart rate of 140 beats/min, normal femoral pulse quality, and congested mucous membranes with a capillary refill time of <1 sec. Thoracic auscultation disclosed the lung sounds to be absent ventrally bilaterally. The abdomen was distended and painful on palpation. Serum biochemical analysis showed increased creatinine^a (450.8mmol/L; reference range, 61.8–114.9 mmol/L), blood urea nitrogen (BUN, 58.9 mmol/L; reference range, 3.5–13.5 mmol/L), and potassium (6.3 mmol/L; reference range, 3.7–5.9 mmol/L) concentrations. A complete blood cell count revealed neutrophilic leukocytosis^b (48.96 × 10⁹/L; reference range, 6.0–17.0 × 10⁹/L). The dog initially received a 20 mL/kg bolus of 0.9% normal saline IV and O₂ via a face mask (1.5 L/min) and was transferred to the intensive care unit (ICU). An indwelling urinary catheter was placed to monitor urine output.

Thoracic (Figure 1) and abdominal radiographs revealed the presence of pleural and abdominal effusion with no evidence of a diaphragmatic rupture. Those findings were confirmed by ultrasonography. Positive-contrast retrograde urethrography was performed, which proved extravasation of the contrast medium^c from the urethra into the perineal soft tissues and abdominal cavity (Figure 2). Thus, a diagnosis of urethral rupture was established.

View Figure

• Download as Powerpoint
• Download Figure

View Figure

• Download as Powerpoint
• Download Figure

After the dog returned to the ICU, serosanguineous fluid was obtained by needle thoracocentesis and abdominocentesis. Biochemical analysis of the thoracic and peritoneal fluid showed high concentrations of creatinine (875.1 and 1547.0 mmol/L, respectively). When those values were compared to serum concentrations, the tentative diagnosis of uroperitoneum and urothorax was confirmed. Removal of 350 mL of fluid from the thoracic cavity, 190 mL from the left hemithorax, and 160 mL from the right hemithorax via needle thoracocentesis significantly alleviated the dyspnea. Fluid treatment (0.9% normal saline) via a central jugular vein catheter^d was adjusted to maintain a central venous pressure of 3–9 cm water. O₂ (0.5 L/min) was delivered via a nasal catheter. Urine drainage from the peritoneal cavity was achieved through a peritoneal lavage catheter^e, which was placed after infiltration with lidocaine^f (2 mg/kg) of the skin, subcutaneous tissues, and rectus abdominis muscle. Antimicrobial therapy including marbofloxacin^g (2 mg/kg IV q 24 hr) and clindamycin^h (10 mg/kg IV q 12 hr) was instituted. Analgesia was provided with a fentanylⁱ infusion at a rate of 0.1 μg/kg/min. Maropitant^j (1 mg/kg subcutaneously q 24 hr) and ranitidine^k (2 mg/Kg IV q 12h) were also administered because of two vomiting episodes. The patient's clinical condition improved over the next few hours (heart rate was 100 beats/min, mucous membranes were pink, capillary refill time was <2 sec). Indirect arterial blood pressure measurement indicated a systolic arterial pressure of 100–110 mm Hg and a mean arterial pressure of 70–90 mm Hg. Two successive measurements of BUN (performed 6 and 12 hr after the initial admission of the dog) showed a progressive decrease (44.7 and 23.2 mmol/L, respectively). During the first day of hospitalization in the ICU, 1200 mL of urine was collected through the peritoneal lavage catheter and 75 mL through the urinary catheter. Although not dyspneic, the dog remained tachypneic during the first day.

On the next day, after all biochemical parameters had been normalized (i.e., creatinine, 123.7 mmol/L; BUN, 4.2 mmol/L; and potassium, 4.1 mmol/L), the dog underwent a prepubic urethrostomy. The patient was premedicated with dexmedetomidine^l (2 μg/kg IV). General anesthesia was induced with propofol^m (2 mg/kg) and maintained with isofluraneⁿ (2%) in O₂ (2 L/min) through a semiclosed circle rebreathing system. Intraoperative analgesia was provided with fentanyl (0.1 μg/kg/min), and normal saline solution was infused at a rate of 10 mL/kg/hr. After urethrostomy, a Foley catheter^o was placed in the urethra to facilitate the initial healing of the urethrostomy and to monitor the urine output. The ventral midline incision was extended cranially towards the sternum, and the diaphragm was found to be intact. Surgery was completed uneventfully, a chest tube^p was placed in the left hemithorax for drainage of the pleural fluid, the peritoneal catheter was removed, and the dog was readmitted in the ICU for recovery. After surgery, the fentanyl infusion was discontinued and morphine^q (0.1 mg/kg q 4–6 hr) was initiated for analgesia.

The dog had an uneventful recovery. Within the first 5 hr of surgery, before the tube became nonproductive, 255 mL of fluid was aspirated from the chest tube. Biochemical analysis of the aspirated fluid showed decreased creatinine levels (167.9 mmol/L). The next day, survey thoracic radiographs confirmed the absence of fluid in the pleural cavity, and the chest tube was removed. No respiratory problems were observed after the chest tube removal. Urine output was also normal within the first 2 days of postoperative hospitalization; therefore, the Foley catheter was removed. Urine dribbling and straining to urinate were observed after the catheter removal; thus, a soft texture catheter^r was used (q 6 hr) to empty the bladder. Four days after the initial admission, the dog had fully recovered and was discharged from the clinic after 8 days.

At the time of follow up, 10 mo after surgery, the owner reported that the dog was free of clinical signs.

Discussion

Pleural effusion associated with uroabdomen has been reported as a complication of urinary tract obstruction or disease, malignancy, medical intervention, and surgical or blunt trauma.⁹ In small animals, uroperitoneum is frequently associated with abdominal and pelvic trauma.¹⁰ In a retrospective study, vehicular trauma was identified as the most common cause of urethral rupture in dogs.¹¹

The diagnosis of uroperitoneum is based on the analysis of the abdominal fluid. In dogs, the presence of two out of the three following criteria confirm diagnosis of uroperitoneum (1) an abdominal fluid creatinine concentration of at least four times the normal peripheral blood concentration; (2) an abdominal fluid/peripheral blood creatinine concentration ratio >2:1; and (3) an abdominal fluid/peripheral blood potassium concentration ratio >1.4:1.¹² Measurement of urea is not considered a useful tool in the diagnosis of uroperitoneum because it rapidly equilibrates with the peripheral blood. Urea has a small molecular weight and reaches equilibrium within 45 hr of a traumatic event concerning the urinary tract.¹² In the patient described herein, no measurement of urea in the abdominal fluid was made because the dog was referred to the clinic 2 days after the accident. Positive-contrast radiography is the method of choice for identification of the site of the urinary tract rupture. Depending on the site of the lesion (i.e., upper or lower urinary tract), either excretory urography or retrograde urethrocystography is preferred.¹³ In the patient described in this report, a retrograde urethrography was performed to localize the site of the lesion. The diagnosis was based on an abdominal fluid/peripheral blood creatinine concentration ratio of 3.43:1. The abdominal fluid creatinine concentration was 13.4× the normal peripheral blood creatinine concentration.

Urothorax is a rare condition in small animals. Up to now, only one canine and one feline case have been described in the literature.^2,14 In both reported cases, the movement of urine from the abdominal to thoracic cavity took place through a disruption of the diaphragm, contrary to the case described herein in which the diaphragm was found to be intact. A case of urothorax secondary to uroperitoneum, with no diaphragmatic defect, has been reported in an newly born foal with a urinary bladder rupture.¹⁵ In cases of urothorax, the pleural fluid usually meets Light's criteria for transudate based on the protein and lactate dehydrogenase levels.¹⁶ Nevertheless, in cases of categorization of the fluid as an exudate, due to either high lactate dehydrogenase or protein concentrations, the suspected diagnosis of urothorax should not be excluded and other characteristics should be considered.^16–18 In most cases, the fluid has low pH and glucose; however, the diagnosis is confirmed when the pleural fluid/serum creatinine ratio is >1, with most cases having values >10.¹⁷ In this case, the diagnosis of urothorax was based on a pleural fluid/serum creatinine ratio of 1.94.

Urothorax results from the movement of urine from the peritoneal cavity to the pleural space. The urine may reach the thoracic cavity directly through a diaphragmatic defect or via the diaphragmatic lymphatics.⁸ In the present report, no visible defects of the diaphragm were found either by radiography or during surgery. In the case reported herein, it is most likely that the urothorax was the result of urine migration through the diaphragmatic lymphatic vessels. In dogs, transdiaphragmatic migration of fluid from the peritoneal cavity has first been reported by Lemon and Higgins (1929), who demonstrated the presence of two descending transdiaphragmatic lymphatic vessels that communicate with lymph nodes in the region of the kidney.¹⁹ A one-way movement of fluid from the peritoneal to the thoracic cavity has been described in cases of ascites and hydrothorax due to ovarian tumors.⁶ In rodents, the reduction of fluid migration from the peritoneal to the pleural space following lymphatic blockage with heavy concentration graphite also emphasizes the importance of the lymphatics as a link between the two cavities.²⁰

Cases of pleural effusion that (based on the biochemical analysis of the fluid) were associated directly with peritoneal fluid accumulation have been documented. The absence of diaphragmatic defects in published reports of biliary and urine pleural effusions suggests a nondirect passage and a similar mechanism of extension of the fluid, whether it is bile or urine, from the peritoneal to the pleural space.^5,15

Conclusion

Urothorax should be considered in animals with pleural effusion and a history of abdominal trauma with involvement of the urinary tract. The diagnosis is based on a high pleural fluid/serum creatinine ratio and treatment of the primary cause usually results in resolution of the pleural effusion. To the authors' knowledge, this is the first reported case of urothorax associated with uroperitoneum with no detectable defects of the diaphragm in a dog.