GU Bedside Emergencies

Source: ICU FAQ.org

99: What if my patient stops making urine?
100: Makes too much urine?
101: Pulls his foley out?
102: Twice?
103: Develops hematuria?
104: With clots?
105: Without clots?
106: What if his BUN and creatinine are doubling every day?

GU

99: What if my patient stops making urine?

Remember all that stuff about pre-renal, intra-renal, and post-renal?

Pre-renal: ("dry") "Pre" meaning: what’s happening in the blood before the kidney gets a chance to see it. Ahead of the kidney. The patient isn’t making much urine because he’s volume depleted – there’s not much water component in his blood. Is his hematocrit 52? Sometimes patients arrrive in the MICU after being diuresed into renal failure from too much volume loss: the BUN will be high, but the creatinine will be normal or heading upwards, maybe something like 70/ 1.2, assuming that they were normal to start with. Some patients certainly look like they need aggressive diuresis – it’s usually not wrong to treat someone for CHF if that’s what seems to be the problem. Of course if it isn’t CHF, or even if it is, they may get a bit too dry. These patients’ will probably be making some urine, but very concentrated. One time you might see the pre-renal thing happen is in a patient receiving full-strength tube feeds as her only intake – this stuff is so concentrated that the patient may literally dry out and stop making much urine. Time to dilute that stuff to half strength, and run it at twice the speed. Watch the aspirates.

Intra-renal: In the kidney. If the patient has actually taken a "kidney hit", the problem will probably be something like ATN. This can take a long time to resolve – months, sometimes. Acutely, the scenario is usually a period of hypotension for one reason or another; sepsis maybe. The BUN may not rise right away, but the creatinine will bump up suddenly: 35/ 4.0 . Kidneys really hate to be underperfused – they become "insulted". ("Stupid kidneys!") It seems even easier to insult elderly kidneys that may be perfused by stenotic arteries – if your patient is a vasculopath everywhere else, e.g. coronary arteries, carotid bruits maybe – you can bet they may have renal artery stenosis. These folks’ kidneys usually see decent perfusion only at high blood pressure levels, ‘cause not a whole lot of blood gets by the stenosis – even an hour or so at a relatively low pressure may make them go into a coma. The kidneys.

Jayne: Keep the patient’s MAP above 65 to try to avoid the whole problem.

Post-renal: This is what happens when nobody flushes the foley after the urine output drops. Something is stuck in the urine path after it’s been processed by the kidney. Ureteral stone, maybe, or compression of the ureter(s) by something like lymphadenopathy, or tumor? What happens to the kidney if its drainage system is plugged? What does a renal ultrasound look for?

100: Makes too much urine?

Give a little too much lasix, did ya? Sometimes patients will do it on their own; they’ll “auto-diurese” for one reason or another – often this has to do with a patient who has high baseline blood pressure and comes in hypotensive. They may not be developing renal failure, but once their pressure gets back up into their normal range they may suddenly start to produce really large hourly volumes. You might see this in a patient who gets sedation for a short period of intubation. While the sedation is on (and the BP is relatively low) the urine output may not be so great – but when the sedation is weaned off – and especially if the patient is a bit agitated (BP up), the output may suddenly become very impressive. Other auto-diuresers: patients who are a couple of days postop may suddenly start mobilizing the five liters of Ringer’s that they got during the case.

Then there’s diabetes insipidus – this is when you (let me think about this for a second) don’t make enough ADH: anti-diuretic hormone. ADH stops you from peeing. Anti diuretic. Not enough ADH, you pee all the time, with a thirst to match. In one end, out the other. Like a siphon. Which is what “diabetes” means. Greek to me, man. Of course, you also turn into a siphon if your blood sugar is 700 for a couple of days…

SIADH is the other way: too much ADH – you don’t pee hardly at all. Got something to do with holding onto sodium.

101: Pulls his foley out?

Ow. Was the balloon up? Call urology. Better yet – don’t let this happen. (Although even with the best precautions, Houdini down the hall there may find a way.)

102: Twice?

Really ow! Where’s urology? If the urethra has been injured, the foley may have to stay in for some time – a couple of weeks?- until it heals.

103: Develops hematuria?

Are you surprised? You spoke to urology, right? Time to start a saline drip through a three-way catheter – and urology put it in, right? Don’t let it clot off…

104: With clots?

What did I just say? Are you even listening? Am I just talking to exercise my face? That’s the problem with young nurses nowadays. In my day, we had to make our own clots! In the summer! Out of snow! Uphill! Both ways! Yadda yadda! (This doesn’t work on my kids, either.)

If the clots are passing through the catheter, good! The problem is: what if they don’t? This is why it is absolutely a rule that a saline infusion through a 3-way foley must never, ever be on a pump. Gravity only. Figure it out – what if the pump kept pumping in, and nothing was coming out because a clot was covering the drainage lumen…? If you think that a three-way catheter is clotted, you can try manually flushing it with 30cc of saline, but what often happens is that the clot forms a little flapper over the openings at the tip, which will let you flush into the bladder, but closes when fluid tries to drain. You’re going to have to change that tube.

A word about scrotums. Yeah, I know. But somebody has to bring it up. (Maybe the wrong phrase?) We see a lot of patients who are very third-spaced – they have diffuse tissue edema, and the scrotum is not immune; they can really swell up. After getting really worried about one of my patients I checked with the surgeons – simple treatment: an ace wrap. Not too tight. Works like a charm. Like a jewel. Jewels. Something like that.

105: Without clots?

You can usually prevent clots from forming if you run the saline irrigant drip quickly enough – this may involve using bag after bag of saline, but that’s just what you have to do. It can be hard to measure exactly what’s going in and out – just make sure that what’s coming out every hour is more than what’s going in! Sometimes we use the little spring measures that are used with PD bags – these tell you how much is infused by the changing weight of the bag.

It’s good to have some standard to identify how bloody urine is, besides “Clots or no clots?” Over the years we’ve gotten comfortable with the “wine-shop” method: “Well, his urine is a nice chardonnay today, but it was definitely a merlot yesterday. Getting better.” Often hematuria will be bad enough to require transfusions… what is amicar?

106: What if his BUN and creatinine are doubling every day?

Bad. Foley plugged? Did she spend eight hours hypotensive – heading into ATN? She may be in for a rough month. A useful maneuver that’s come up in the past year or so: patients heading into renal failure will usually (duh!) stop making urine – but if you slap them with a big dose of diuretic while they’re still on the steep part of the failure curve – just as they’re heading into it – sometimes you can get them to change from oliguric (“not peeing much”) to non-oliguric (“peeing pretty good”) renal failure. What we do is to give some enormous dose of “synergistic diuresis” (whoa! $1.50 for that one) – something like 200mg of lasix and 500mg of diuril, one after the other. If it works, then at least the patient will get rid of water – they won’t clear much BUN, but you’ll be able to keep them out of CHF.

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