A 60-year-old with metastatic prostate cancer requiring a suprapubic catheter and bilateral nephrostomy tubes is brought in for bleeding from his left nephrostomy. No recent chemotherapy or radiation. Blood intermittently drains from his suprapubic catheter, but it has never done so from the left nephrostomy.
Malignant retroperitoneal nodes partially obstructing bilateral ureters? Glancing at the tubes, I sense we are not looking at much quantity in life. We should instead target quality.
Normal pulse and respiratory rates and a blood pressure of 127/72 mm Hg. But he appears fatigued.
Volume status. Lower extremities have 3+ pitting up to his inguinal ligament. His scrotum is grossly edematous. Resisting the temptation to call him hypervolemic, I consider this. All edema whittles down to only a few pathologic forces: elevated venous hydrostatic pressure from increased volume, obstruction, or poor right heart function; decreased oncotic pressure from loss of albumin or red cells; capillary leak from inflammation or neoplasia; lymphatic insufficiency; or impaired turnover of the extracellular matrix in hypothyroidism.
Today I lean toward veins. In someone requiring bilateral nephrostomies for ureteral obstruction who now presents with anasarca of the scrotal internal iliac tributaries as well as the external iliac extremity tributaries, I must consider that the march of neoplasia has engulfed his IVC.
His suprapubic catheter is clean and dry. The urinary bag has 200 mls of dark bloody fluid. His son reassures us that this amount of bleeding is a daily occurrence.
Abdomen is soft, but scattered inguinal lymphadenopathy is a window into something invisible. I feel deeply for a pulsating mass. Retroperitoneal nodes caked over the aorta will transmit pulsations to the palpating hand. More evidence for the rostral malignant march. By placing palms on either side of the pulsation, masses atop the aorta will bounce straight at your hands and up into the sky. An aneurysm will jolt your hands apart.
The nephrostomy sites are dry and secure. The right tube has cloudy urine, the left has the same dark bloody output as his suprapubic, about 200 mls in this bag as well. Better old and dark than bright and red.
He moves slowly because of pain when leaning forward. Light percussion of the midline back reproduces this pain. Vertebral metastases?
Breath sounds are coarse. No work of breathing. Heart sounds are regular, normal valve closure, and a nonradiating 2/6 ejection murmur at his aortic area. No palpable supraclavicular or suprasternal nodes. Malignant ascension has yet to reach this point. Upper extremities move freely and are not edematous.
Cervical and submandibular triangles are benign, mucous membranes dry. I pull his conjunctiva down. Very pale. His neck flexes easily without limitation, and his mentation is normal. He feels warm. Oral temperature is 101.6°F. Cultures are drawn and antibiotics started. I am betting on the urine because of multiple sites where the urothelial lining is breached. I suppose rectal microbes are another possibility in prostatic malignancy.
Hgb returns at 5.9. The remainder of his labs do not suggest hemolysis. Without much blood in either bag, we have to take a trip...
...to the theater. Unlike bile, pancreatic juice, succus entericus, or feces, blood is not a major irritant of the peritoneal lining. So the physical exam for hemoperitoneum can be misleading. Sitting in the audience you use bedside ultrasound to see what's happening on stage: no fluid in either upper quadrant or the rectovesicular area.
Backstage? Behind the actors stands a curtain, and behind it, the retroperitoneum. Just below the stage sits the orchestra. Allow the curtain to reflect anteriorly and run along the stage floor toward you as it hits the ground, covering the orchestra. The orchestra is now the true pelvis. It houses the bladder, uterus or prostate, and distal rectum among vasculature and a dense web of neural fibers.
It is not in the true pelvis if we declare “free fluid in the pelvis” on ultrasound. Rather it is above the inferior-most portion of the curtain reflecting between the stage and orchestra. It is still intraperitoneal fluid.
The true pelvis and retroperitoneum are confluent. Lumbar nerves, iliopsoas fibers, ureters, and great vessels run the length backstage and then reflect anteriorly under the curtain into the orchestra to meet pelvic organs or continue to emerge through specified portals into the lower extremities, soft tissue of the inguinal region or perineum. This is where his cancer started and advances superiorly. Could he be bleeding there? You are an audience member with ultrasound in hand; you would not necessarily know.
We are called back to the bedside because his heart rate jumped to 170. He is rigoring, tachypneic, and slightly confused. His son is worried. Sudden onset could mean dysrhythmia.
Quantified on the monitor, it appears regular. A steady finger on his pulse, I find the quality of each beat is also rhythmic and consistent. I doubt this is atrial fibrillation. I think a re-entrant rhythm involving his AV node or a re-entrant rhythm involving the right atrium. The former is AVNRT, the latter atrial flutter.
We give 12 mg of adenosine and have our answer. His ventricular response slows, but no break in the rhythm, no sawtooth or fibrillatory baseline, just sinus tachycardia. In a few seconds he is back at 174.
Not a dysrhythmia. The sinus node is reacting to something. Packed red cells flow through peripheral lines and a subclavian cordis. I recheck his urinary bags, and they have not accumulated any new blood.
Has the dam broken backstage? I doubt it. His mentation and pulses are too good for this degree of hypotension to be solely hemorrhagic. I am betting on vasodilation with bounding radial and dorsalis pulses at the moment his blood pressure cycles 70/40. Antibiotic-mediated bacterial lysis liberating intracellular endotoxin resulting in loss of arteriolar tone.
I reach for the ultrasound again to be sure. No cardiac tamponade and still no intraperitoneal fluid. I peek backstage: noncollapsing proximal, retrohepatic IVC with measurably distended hepatic veins. The IVC above the level of malignant invasion is still a reliable measure of volume status. Persistent hypotension from hemorrhagic shock would not have an IVC like this. No doubt he needed the volume from blood lost in days past, but at this moment the main player is distributive, and the stand-in is hemorrhage.
His pulse levels at 100, and his BP rises to 88/56 with blood, saline, and norepinephrine. His mentation clears, rigors disappear, and tachypnea resolves. He was alert and interactive. A CT scan showed malignancy creeping through the orchestra and backstage personnel, but no retroperitoneal hematoma and no arterial blush. Serial lactate measurements trended below 1.
He must have been very volume-depleted on presentation. Vasogenic edema from IVC encasement was not representative of his circulating intravascular volume. His brachial artery tone looked good when quantified at 127/72 on arrival, but it was composed mostly of clamped down arterioles rather than healthy forward flow. His fatigued face told the real story. Now at 88/56 after volume resuscitation and a low-dose pressor, he converses with his son, and his smile reminds me of the benefits to targeting quality over quantity.
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