He wouldn't stop writhing. A little disconcerting, I thought, but not atypical for ureterolithiasis.
The 25-year-old had no past medical history and a story of relatively rapid onset right flank pain. He was quite uncomfortable.
Tachycardic and tachypneic with a soft anterior abdominal exam, he twists and turns on the cot, never satisfied in one position. Sweating and pale, he appears like any other patient with renal colic.
Except it wasn't colic. It wasn't episodic. It never let up. Intermittent migration of calculi scraping through the ureter and accompanied by an occasional ureteral spasm, the pain of ureterolithiasis is usually colicky. So I ask him again, hoping his history will conform to my preconception of his illness.
“Is your pain intermittent? Does it come and go?”
“No,” he muttered, “It hurts. Can I have something for the pain?”
“Yes, we have ordered Motrin and morphine. But tell me again, how long has the pain been going on? Does it ever let up? Even a bit?”
I am reaching.
“No. It never lets up.”
He wouldn't give in. No matter how I ask, I cannot get him to obey the written rule.
OK, so I concede that it is constant. But ureterolithiasis can produce constant pain if a stone is nicely wedged within the ureter and there is moderate proximal hydroureter and hydronephrosis, with no distal migration of the calculus. No respite from symptoms in that case, I suppose.
So my leading diagnosis was just that: a nonmobile, probably large, ureteral calculus that failed to migrate or induce episodes of ureteral spasm.
“We need your urine. We need to test it for blood. You probably have a kidney stone.”
Our nurse asks a few times, but for whatever reason, he doesn't produce. I just wanted confirmation of what I already knew was going on. I wanted diagnostic closure.
In the meantime, he receives NSAIDs, IV narcotics, and saline.
Ultrasound. Because most stones pass spontaneously, I don't feel the need to perform a noncontrast CT but instead corroborate my diagnosis with a bedside ultrasound demonstrating hydronephrosis. The problem comes when my ultrasound, like my patient, refuses to conform. There is no hydronephrosis.
But can't ureterolithiasis produce pain, sometimes constant and without proximal hydronephrosis, from a very small nonmobile stone somehow wedged into the distal ureter? I suppose it is possible. I felt myself teetering far out on a ledge of strained logic. Yes, possible, but with this degree of discomfort and no hydronephrosis, I wondered, “Is it probable?”
Medical School. A common phrase I heard was that half of what we learn in medical school will one day be proven false. The written word is fallible, and we just do not know yet where the errors lay. I am not sure who decided that 50 percent was the magical fraction of nontruth, but I do know a set of information that is not subject to this rule.
The Anatomy. It is 100 percent true. The only medical school text never to be discarded. It has been true for thousands of years before we knew anything about it, and it will be true for the entirety of our careers and beyond. What better tool to deconstruct our patient's diagnosis? He may choose not to conform to the written word; that word is not necessarily truth. But about the anatomy, I am sure. His illness must abide by it.
He presented with pain below the costal margin and between the anterior and posterior axillary lines. By anatomic definition, he presented with flank pain. With no superficial inflammatory response, it did not seem to be in the overlying epidermis, dermis, or subcutaneous tissue. Below lies the fascia and muscle of the external and internal obliques. No induration or tenderness on exam, and he certainly moved a lot for a patient with a muscle strain or, worse, fasciitis or myositis of his oblique musculature.
So we move deeper and find ourselves in the right upper quadrant of the peritoneal cavity. Right lobe of the liver, gallbladder, portal triad, the first and second portions of the duodenum, and the colonic flexure sit before us. Yet his anterior abdominal exam was entirely soft. No evidence for peritoneal irritation when you pushed and displaced it posteriorly against the underlying anatomy.
Just laterally lies the ascending colon. It is the best anatomic correlate to the flank. It runs up the very area where our patient claims his pain originates. So the colon must be suspect. But with a benign abdominal exam, I am not concerned with the anterior part of the colon. It is the posterior aspect, the area tethered as the retroperitoneum, an area where a posteriorly directed inflammatory or ischemic process could be contained, producing flank pain without irritation of the anterior abdominal wall.
I unkindly jab my fingers into this man's midaxillary line below the costal margin, exploring the limits of the flank and the anatomic correlate to the ascending colon. He does not seem to mind. No particular pain. He continues to writhe in agony regardless of where I push or prod.
As you head north, the ascending colon reflects medially at the hepatic flexure, becoming the transverse colon. Just above this area lies the right kidney. Contained in the retroperitoneum and covered by Gerota's fascia, it rarely produces an abdominal exam of concern because it is sequestered from the anterior abdominal wall.
But you can palpate it. Placing the ultrasound at the posterior axillary line to visualize a non-hydronephrotic kidney, I push in on the inferior pole of the organ. And this, unlike anything else I had done, disturbs him. He continues to writhe, but ultrasound-assisted palpation of the inferior renal pole reveals tenderness.
The problem is renal in origin but not related to a distended collecting system. As far as I can tell, he has no hydronephrosis. The excretory arm of the organ is functional.
Does he have pyelonephritis? Bacterial proliferation in the renal pyramids, calyces, and pelvis? Possibly, but I have not seen many patients with an inflamed kidney writhing around like this. What else is there?
Kocher maneuver. This surgical technique involves opening the retroperitoneal tissue just to the patient's right of his duodenum, and reflecting it medially. What you see is the inferior vena cava. As you move laterally, you see the right renal vein and posterior to this the right renal artery. With a normal excretory arm to the kidney and a mental Kocher maneuver, I am left looking at the nutritive and decompressing limbs of the organ.
This man needs a CT scan. But it is not the scan one would think he needed upon presentation for renal colic. He needs IV contrast. The perfusing artery and decompressing vein must light up or reveal obstruction. After mental dissection, they are the only anatomic sites left.
CT with IV contrast revealed a wedge infarction of the right kidney. The renal vein was patent, but a tributary off his renal artery must be occluded.
In situ thrombosis is uncommon. Instead, our anatomic dissection should carry us retrograde up the arterial system and aorta and to the cardiac chambers and valves in search of an embolic source. We may even squirm through a patent foramen ovale, and find ourselves in the right atrium or the peripheral venous system in a case of paradoxical embolus.
Wherever it ends, the dissection began in the emergency department. We found the right path. We started on the correct trail. The pursuit will continue as an inpatient in the hands of our internist colleagues.
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