Urinary Retention Manifesting as Excessive Venous Ooze During Cranio-Vertebral Junction Surgery

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To JNA Readers:
The surgical correction of atlanto axial dislocation (AAD) at the cranio-vertebral joint (CVJ) requires meticulous bleeding control. This region being loaded with large venous plexuses can be flooded with venous bleed, which can affect the conduct of the surgery.1 We encountered an interesting case where during the final stages of AAD surgery, the surgical field showed unexplained and disproportionate diffuse venous ooze, which could only be arrested with extreme difficulty. Concomitantly, kinking of the urinary catheter tubing was found obstructing the urinary outflow and distending the bladder, and we hypothesize that the sudden inexplicable increase in venous bleeding could be secondary to acute urinary retention.
An 11-year-old male patient diagnosed with AAD and basilar invagination was posted for posterior fusion. His preoperative investigations including a coagulogram were unremarkable. After induction, he was turned prone over bolsters. During the initial 2 hours, when the right-sided joint was being fixed, surgical bleeding, hemodynamics, and the urine output (130 mL) remained within the normal range.
As the CVJ of the patient had a preexisting left-sided tilt (Fig. 1), the operating table had to be tilted to the right by around 20 degrees to compensate for the tilt before attempting left-sided fixation. Soon thereafter, the surgeons started noticing abnormal spontaneous slow and steady venous ooze from the surgical site. As obvious vascular injury (arterial spurts) or coagulation abnormalities were absent, the straight-neck position was ensured to exclude venous engorgement due to excessive twisting. Head and neck levels were verified and found to be above the heart’s level, and the PaCO2 reading was within acceptable limits (34 mm Hg). Also, during this stage of surgery, it was noticed that the patient had a scanty urine output (15 mL). To correct this, 500 mL of fluid challenge was also given to the patient. Meanwhile, usual methods to control the oozing such as gelfoam and cottonoid application were used, but it could not be curtailed satisfactorily and procedural losses increased significantly (1200 mL). As the hematocrit had decreased substantially and hemodynamic deterioration was setting in, along with crystalloid resuscitation, the anesthesiologists had to transfuse 1 unit of packed red blood cells. The surgeons completed the procedure with considerable difficulty, but could not secure adequate hemostasis. As the urine output had remained low (20 mL in 2 h), we proceeded to find the cause, and a close inspection revealed that during a subtle position change (table tilting), the catheter tubing had kinked and was being compressed between the patient’s groin and the edge of the bolster causing bladder distention and tenseness. Because of the sterile draping and patient position, the kink had gone unnoticed. After the straightening of the kinked portion, urine started rushing and in around 5 minutes, the patient voided 1600 mL of urine. As the urine flow resumed, the venous ooze was also observed to subside, and proper hemostasis and wound closure were achieved in response. The patient was kept intubated for elective overnight ventilation and was extubated safely on the next day. Postoperative imaging of the CVJ was found to be satisfactory.
In the absence of any plausible justification of this sudden increase in venous ooze and temporal cessation of urinary flow, we believe that catheter compression and the resultant urinary obstruction were the reasons for this unexplained bleeding observed during the latter half of the surgery. The distended bladder compressed by the bolsters increased the intraabdominal pressure. This obstructed the inferior vena caval return and augmented the epidural Bateson’s venous plexus pressure.

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