Ep 129: A 68-Year-Old with Lower Abdominal Pain

This episode talks about acute kidney injury, its complications, potential etiologies, and therapy.

See more on this topic on AccessMedicine

Transcript

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[Ms. Heidhausen] This is Katerina Heidhausen, executive editor of Harrison's Principles of Internal Medicine. Harrison's Podclass is brought to you by McGraw Hill's AccessMedicine, the online medical resource that delivers the latest content from the best minds in medicine. And now, on to the episode. 

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[Dr. Handy] Hi, everyone. Welcome back to Harrison's Podclass. We're your co-hosts. I'm Dr. Cathy Handy. 

[Dr. Wiener] And I'm Dr. Charlie Wiener and we're joining you from the Johns Hopkins School of Medicine. 

[Dr. Handy] Welcome to episode 129: a 68-year-old with lower abdominal pain. 

[Dr. Wiener] Cathy, today we have a two-part question, but let's start with the case. So a 68-year-old man presents to the emergency department with severe lower abdominal pain and confusion. His spouse, who's there with him, tells you that these symptoms have worsened over the last three to four days and that he's not had either a bowel movement or urinated in the last two days that she knows of. His past medical history is only notable for hyperlipidemia and presumed prostatic hypertrophy. His medications are atorvastatin, alfuzosin, and finasteride. On physical examination, his vitals are normal except for a heart rate of 105. He's confused and only oriented to his self. There are no focal neurologic deficits, but he does have asterixis. His abdomen is diffusely distended and is tender over the bladder. You get laboratory studies, and they reveal a normal CBC, but his chem panel is notable for a sodium of 130, a potassium of 5.8, a chloride of 90, bicarbonate of 15, BUN of 110, and creatinine of 3.5. 

[Dr. Handy] All right, so he's pretty sick, and let's unpack this for a little bit. Since our patient has no prior renal history that we know of, I would say, he has acute kidney injury and the notable elevations are in his potassium of 5.8, the anion gap, and then the BUN of 110. Given the labs and his mental status with the asterixis, he would be considered uremic. 

[Dr. Wiener] Wait, uremia can cause asterixis? 

[Dr. Handy] Absolutely, we usually think about it with hepatic encephalopathy, but essentially, any encephalopathy, including uremic encephalopathy, will cause asterixis. Remember that asterixis is simply the inability to maintain a sustained muscle contraction. We typically look for it at the wrist, but it's also easily elicited by flexing the foot at the ankle. 

[Dr. Wiener] Okay, well let's get to the first part of the question 'cause it's going to ask what do you want to do next? So the question says, which of the following tests will be diagnostic? Option A. is an abdominal liver CT scan; option B. is a bedside bladder ultrasound; option C. is an electrocardiogram; option D. is a renal ultrasound; and option. E is urine microscopy for red blood cell casts. 

[Dr. Handy] So he is likely going to need all the tests that you mentioned, but only one will really be diagnostic in this case, and that's the simple bedside ultrasound of the bladder. The history of not urinating with severe abdominal pain and tenderness and distension on exam makes me most suspicious for bladder outlet obstruction. He does need an EKG with his hyperkalemia, but that will not be diagnostic. And he may wind up getting a renal ultrasound to look for hydronephrosis, which I'm sure he has; but again, the enlarged bladder tells you where the obstruction is. Everyone with acute kidney injury should have urine microscopy, but I don't think he has any RBC casts due to glomerulonephritis. 

[Dr. Wiener] The enlarged bladder would also explain his localized pain, right? 

[Dr. Handy] Absolutely. 

[Dr. Wiener] Well, the answer is B. the bedside ultrasound, which shows a massive urine-filled bladder. A Foley catheter is placed with difficulty, which immediately drains over 2 liters of urine. 

[Dr. Handy] And that should be therapeutic as well. 

[Dr. Wiener] Yeah, his abdomen feels better, but he's still very confused and he still has the asterixis. And that gets us to our next question. Which of the following statements regarding his condition is true? A. he is likely to develop hypernatremia. B. he's likely to remain anuric for days. C. he likely has a complication of his medication. D. he needs urgent dialysis. And E. his renal function is unlikely to recover. 

[Dr. Handy] Well, let's take a pathophysiologic approach. So by placing the Foley catheter and decompressing the bladder, we've isolated the problem to beyond the ureters. He may have a totally atonic bladder, but given his history of BPH, it's reasonable to assume that his anatomy is no longer amenable to medical therapy. He was on alfuzosin, an alpha blocker, which relaxes the smooth muscle in the prostate and bladder, and he was also on finasteride, a 5-alpha reductase inhibitor, which shrinks the prostate. Both of those medications are useful in BPH and would not be expected to cause his symptoms. 

[Dr. Wiener] Okay, so C. is not correct. This is not likely a result of his medications. 

[Dr. Handy] No, the medication should have the opposite effect and should actually be improving his urinary flow, but it is possible that his BPH is getting worse or he has some other prostate pathology that's now making the urinary symptoms worse. 

[Dr. Wiener] Okay. Well, how about the other choices then? 

[Dr. Handy] So B. and E. are related. Obstruction of urine flow from the bladder results in an increase in hydrostatic pressures in the ureters and distension of the renal collecting system. This causes elevated intratubular pressures and tubular dysfunction. In the first days of obstruction, the dilation of the poorly compliant collecting system may be minimal but as the increased hydrostatic pressure is expressed in the urinary space of the glomeruli over time, further filtration decreases or stops completely. The result is acute kidney injury and potentially, as in this case, azotemia. 

[Dr. Wiener] So what happens when you relieve the pressure by bypassing the obstruction? 

[Dr. Handy] Well, that's the good news. Usually, once the pressure is relieved, the glomeruli regain filtering function and you're left with reversible tubular dysfunction. The improvement in renal function will depend on the state of the kidneys before the acute insult, the duration of the acute obstruction, and whether or not irreversible renal injury has occurred. In most cases, urine flow resumes and renal function improves, although possibly not to baseline. 

[Dr. Wiener] Okay, so now we know that B. and E. are not true because we said that he should not be anuric for days and it is not from the medication. Does he need urgent hemodialysis? 

[Dr. Handy] That's not going to be an absolute answer, but rather a judgment call. Based on his mental status, he is uremic so you could make the case for urgent hemodialysis, but that would require placing a central line. His EKG did not show signs of severe hyperkalemia, so I think you could safely monitor closely his response to relief of the obstruction. It is possible that his renal function could improve over the next day or so, so you may avoid urgent dialysis. So I'm not going to call option D. correct. 

[Dr. Wiener] Okay, so we've ruled out the others, and it sounds like option A. is true, he is likely to develop hypernatremia. Tell me about that. 

[Dr. Handy] Relief of bilateral complete obstruction commonly results in polyuria, which may be massive. The urine is usually hypotonic and may contain large amounts of sodium chloride, potassium, phosphate, and magnesium. The natriuresis is due in part to the correction of extracellular volume expansion, the increase in natriuretic factors accumulated during the period of renal failure, and depressed salt and water reabsorption when urine flow is re-established. Additionally, the retained urea is excreted with improved GFR, and that results in osmotic diuresis that increases the volume of hypotonic urine. The tubular injury may also cause transient nephrogenic diabetes insipidus. So all of these together put the patient at risk of hypernatremia. Fortunately, when extracellular volume and composition return to normal, the diuresis usually abates spontaneously. 

[Dr. Wiener] But it probably is worth monitoring his sodium at least for the first period of time when he starts improving, right? 

[Dr. Handy] Yeah, that would be a typical follow-up course for him. 

[Dr. Wiener] Great. So the teaching points of this case are that urinary outlet obstruction due to causes such as prosthetic hypertrophy may cause bilateral hydronephrosis, acute kidney injury, and even uremia. Relief of the obstruction usually results in improved renal function and often a post-obstructive diuresis which may cause hypernatremia. 

[Dr. Handy] And you can check out questions like this in the Harrison's Self-Review book. And if you want more information, you can go to Harrison's chapter on urinary tract obstruction. Visit the show notes for links to helpful resources, including related chapters and review questions from Harrison's. And thank you so much for listening. If you enjoyed this episode, please leave us a review so we can reach more listeners just like you. 

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