Acute hypoxemic respiratory failure as a manifestation of urinothorax

THE CASE

A 75-year-old man with a history of tobacco-related emphysema, BPH, and osteoarthritis presented to the emergency department (ED) with a complaint of progressive exertional dyspnea and oliguria of 3 days' duration. The patient had been seen in the ED 1 week earlier for atypical chest pain on the right side. A chest radiograph at that time was clear, and 2-dimensional echocardiography indicated an ejection fraction of 55%.

The patient had previously had a right total knee arthroplasty. He had stopped taking tamsulosin about 3 months earlier because his primary care physician told him his prostate examination findings were "fine."

On arrival to the ED, he was afebrile; pulse oximetry indicated an oxygen saturation of 78% on room air. The patient had a respiratory rate of 32 breaths per minute, heart rate of 106 beats per minute, and blood pressure of 148/84 mm Hg. His heart sounds were regular without evidence of a murmur. His breath sounds were markedly diminished in the middle to lower lung fields. Inspiratory rales were absent on auscultation.

The patient had no pretibial or pedal edema. He was placed initially on a nonrebreathing mask, and a chest radiograph was ordered. A Foley catheter was placed, and more than 1100 mL of yellow/clear urine was drained from the catheter. His oxygen saturation improved to 94%, but he remained tachypneic with increased work of breathing.

Noninvasive positive pressure ventilation (NPPV) was initiated, with an inspiratory pressure of 12 cm H₂O and an expiratory pressure of 6 cm H₂O. The patient showed marked improvement in his work of breathing and resolution of the tachypnea.

The chest radiograph revealed a large right-sided pleural effusion with haziness in the left costophrenic angle, suggesting a left-sided effusion (Figure 1). There was minimal pulmonary vascular congestion. He was sent to the ICU. Renal ultrasonography showed that the kidneys were well visualized and unremarkable with respect to size; bilateral hydronephrosis was seen (Figure 2).

Urology consultation suggested that the urinary retention was secondary to the patient's BPH. A CT scan revealed bilateral hydronephrosis without nephrolithiasis or tumor; the large right-sided effusion was clearly seen (Figure 3). A decision to perform a diagnostic and therapeutic thoracentesis was made.

On thoracentesis, 1400 mL of yellow/clear fluid was removed from the right hemithorax without complication. The pleural fluid characteristics were consistent with a transudative effusion, with a pleural fluid pH of 7.2. The pleu- ral fluid creatinine level was 3.1 mg/dL, and the serum creatinine level was 1.0 mg/dL (the ratio of the pleural fluid creatinine to serum creatinine was 3.1). The blood urea nitrogen (BUN) level in the pleural fluid was 34 mg/dL, and the serum BUN level was 21 mg/dL. The results of cytologic examination of the pleural fluid were negative for malignancy.

NPPV was discontinued within 6 hours after the thoracentesis. A follow-up chest radiograph at 72 hours was clear of any effusions. Echocardiography revealed an ejection fraction of 60% without any significant left- or right-sided ventricular enlargement. The patient's Foley catheter was removed, and treatment with tamsulosin was resumed.

Because of his high postvoid residual levels, the patient was instructed on how to perform self- straight catheterizations before discharge. The results of outpatient cystoscopy were essentially unremarkable. A 2-week follow-up chest radiograph remained clear and free of any effusions (Figure 4). The patient remained compliant with the medications that were prescribed on discharge.

DISCUSSION

Urinothorax is defined as the presence of urine in the pleural space, commonly associated with a form of obstructive uropathy, with resolution of the effusion once the obstruction has been removed. Urine leakage from the urinary tract may give rise to urinoma, a retroperitoneal collection of fluid, which may lead to the urinothorax. It is most commonly ipsilateral to the obstructed urinary tract with rapid accumulation of fluid.¹

Respiratory symptoms, such as dyspnea and cough, may or may not be present. Fewer than 100 cases have been reported in the literature since the first description by Corriere in 1968.² This may be the result of a low index of suspicion.

In the present case, the patient had obstructive urinothorax with bilateral hydronephrosis secondary to his uncontrolled BPH. As a result, hypoxemic respiratory insufficiency ensued, requiring NPPV. Underlying cardiac disease was excluded as a contributing factor, since preadmission echocardiography revealed no left ventricular dysfunction or hypertrophy. To our knowledge, this is the first case of urinothorax associated with hypoxemic respiratory insufficiency requiring NPPV.

Etiology and pathophysiology

Urinothorax may stem from multiple causes and has been reported in association with malignancy, renal cysts, nephrolithiasis, blunt trauma, surgical ureteral manipulation, posterior urethral valves, renal transplantation, ileal conduit with ureteral obstruction, renal calculi lithotripsy, and extrinsic compression by a gravid uterus. Traumatic urinothorax is usually associated with an iatrogenic event such as surgical injury, blunt trauma, attempted percutaneous nephrostomy tubes, or renal biopsy.² In the absence of trauma, however, unilateral obstruction at the ureteral or renal level does not cause urinothorax with preserved contralateral kidney function.²

Garcia-Pachon and Romero³ have noted that only obstruction of both ureters or an obstruction located at the level of the urethra or bladder can cause the diversion of urine and lead to urinothorax. Reported cases of obstructive urinothorax have been associated with prostate disease, hydronephrosis, bladder cancer, urethral valves, urethral perforation, and gravid uterus.²

A few theories have been suggested to explain how urine extends into the pleural cavity. Friedland and associates⁴ suggested that urine from a ruptured collecting system directly enters the retroperitoneal space and then reaches the pleural space by direct leakage into the mediastinum or drain- age via the lymphatic ducts. The urine may reach the pleural cavity through anatomical defects in the diaphragm, similar to the development of hydrothorax in patients who are on peritoneal dialysis.⁵ Lemon and Higgins⁶ demonstrated lymphatic connections between the pleural space, the diaphragm, and lymph nodes of kidneys in their study of dogs in which injected graphite was removed via diaphragmatic and retrosternal lymphatics through normal or paralyzed diaphragm.

Diagnosis

The diagnosis of urinothorax requires a high index of suspicion. The pleural fluid may have certain biochemical characteristics, such as low glucose level,⁷ low pH,⁸ and transudative features. Urinothorax is the only noted cause of low-pH effusions, according to Miller and colleagues⁸ in 1988.

The diagnosis of urinothorax can also be confirmed by measuring the creatinine level in the pleural fluid, which is greater than the level in serum. Stark and associates⁷ found that the ratio of pleural fluid creatinine to serum creatinine was greater than 1 in patients with urinothorax. However, more recent studies have shown that this ratio may be elevated in other instances, such as empyema, with the highest reported value of 4.11 in a study by Gutierrez and colleagues.⁹

Protein levels are usually low, and lactate dehydrogenase values may be elevated, which may incorrectly classify the effusion as being exudative. A newly proposed biochemical marker, an elevated carcinoembryonic antigen,² may also be useful in establishing the diagnosis; however, study data are still inconclusive. In a case report by Ralston and Wilkinson,¹ the diagnosis of urinothorax was identified by technetium-99m DPTA renal imaging without the aid of a thoracentesis fluid analysis. A thoracentesis may not always be warranted, as was the case in that study, since there was prompt resolution of the pleural fluid following nephrostomy tube placement.

Treatment

Current treatment guidelines depend on correcting the underlying cause, whether obstructive or traumatic. In the present case, the cause of the urinothorax was obstructive and related to untreated BPH. Thoracentesis was both therapeutic and diagnostic. Treatment with tamsulosin was restarted, and self-straight catheterization functioned as a bridge until the patient's BPH resolved. There was no recurrence of fluid in the pleural cavity 2 weeks after discharge. Previous case reports have also reported spontaneous resolution of urinothorax once the urologic obstruction was removed.

References:

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