bleep.guide · Foundation Emergencies
Wednesday, 23 September 2026
Assessment of oliguria and anuria, bladder examination and catheter troubleshooting, distinguishing retention from true oliguria, and the initial investigation and management of acute kidney injury.
Foundation Emergencies · Session 3 · 23 September 2026 · Oliver Devine
Caution: live-session transcript
This is an edited version of an automated transcript of a live teaching session. It may contain transcription errors or clinical inaccuracies, and information may become out of date. Check current guidance and local protocols before using it in clinical practice.
All patient examples are hypothetical.
Okay, we'll make a start. This is session three of our Foundation Emergencies teaching: short sessions covering common things you'll encounter as foundation doctors, particularly emergency and acute problems.
Today we're doing low urine output, retention and acute kidney injury. As usual, pop your questions in the chat and we'll get to them at the end.
Imagine it's 8 pm and you're carrying the ward-cover bleep. You're called about Mr R, who's 72 and on day two after bowel surgery. He weighs 70 kg. There's nothing in his catheter bag.
He's had poor intake and vomiting for 48 hours. He takes ramipril, has recently had ibuprofen, and is receiving morphine. What are you thinking?
You ask about the observations, or look at the electronic record. The blood pressure seems okayish, the heart rate is a bit higher than you'd like, but his respiratory rate and saturations are reassuring. He's alert and afebrile. You establish that there's been no drainage since about 5 pm, and now he's got lower abdominal discomfort.
I would be thinking: has this chap got a full bladder that isn't draining? Recent surgery and morphine can contribute to retention. But he's also had poor intake and vomiting. Could he have an AKI and be producing very little urine?
A bladder scan helps separate those questions. Is there urine in the bladder that can't get out, or is very little reaching the bladder?
If it's full and there's already a catheter, check the drainage system first. Follow the whole line. Is it kinked? Is a clamp closed? Is the bag below bladder level? Is the catheter blocked or displaced? You may find that a straightforward mechanical problem explains the empty bag.1
If the bladder is small, ask why urine production is low. Perhaps he lost fluid or became hypotensive during the operation. Perhaps there's tubular injury, a drug-related problem or congestion. Venous congestion can impair kidney function too; low output doesn't always mean dehydration.2
A small bladder also doesn't exclude obstruction higher up the urinary tract. Obstruction is particularly concerning when both kidneys are affected or there's only one functioning kidney.3
With a full bladder, think about tubing, kinks, clamps, bag position and bypassing. Urine might be leaking around the catheter into a pad rather than reaching the bag. Bypassing is a clue to investigate, not proof that the catheter is working properly.
The immediate job is to establish drainage. Correct a simple external problem if you find one. If that doesn't work, get someone with the appropriate catheter skills to assess whether it needs replacing or another intervention. Don't keep making traumatic attempts, particularly if there's pain, bleeding or a history of difficult insertion.1
Then think about the underlying retention: prostate problems, constipation, recent surgery, infection and drugs, particularly opioids. In someone who already has a catheter, those possibilities don't remove the need to check that the catheter itself is patent.
You might occasionally find a very large retained volume. Record what drains, then start measuring new urine output over time. Emptying the retained urine isn't the same as the kidneys suddenly producing that volume.
After relieving substantial or longstanding obstruction, watch for excessive ongoing losses—post-obstructive diuresis. Monitor fluid balance, observations and electrolytes, and agree an individual replacement plan if losses are significant. You can otherwise trade one problem for dehydration and an electrolyte disturbance.4
Pain and clots deserve particular attention. Blood after a difficult catheterisation might reflect trauma, and clots can obstruct drainage. A washout or a three-way catheter may be needed, but this is a reason to involve an experienced colleague or urology, especially if you're unfamiliar with the procedure. Routine flushing isn't the answer to every catheter that isn't draining.5
Suppose Mr R's scan shows 620 mL. You release a kink and 650 mL drains. His discomfort improves.
That's encouraging, but now his creatinine has risen from 90 to 196 micromol/L, and his potassium is above 5.5 mmol/L. His pressure has fallen and his pulse has risen. He's still losing fluid, and when you examine him his capillary refill is delayed. His JVP appears low and his chest is clear.
Taken together, those findings suggest volume depletion and poor perfusion. A clear chest or a difficult-to-see JVP alone wouldn't establish that he's dry.
He still needs an A–E assessment, an ECG, a gas and senior review. Depending on the severity, progression and local arrangements, that may include discussion with renal. Fixing the kink has solved a drainage problem; it hasn't explained away the AKI or the potassium.36
You'll know these criteria from medical school. In adults, NICE identifies AKI by any of the following:
For Mr R, 196 divided by 90 is about 2.2 times baseline. Assuming this is an acute rise, that's stage 2 by creatinine. AKI has three stages; stage 3 is the highest. Urine-output criteria can also determine the stage.7
For a 70 kg patient, 0.5 mL/kg/hour is 35 mL/hour. But don't wait for six hours to pass before investigating a painful full bladder or assessing someone who's deteriorating. The diagnostic threshold isn't a waiting period.
And be careful with the eGFR printed beside the creatinine. It assumes a reasonably stable creatinine, so it's unreliable during a rapid change. Look at the dated creatinine results and the clinical picture.8
This is something we deal with regularly, and it's easy to slip into “they're dehydrated, give fluid, check tomorrow”. Even if the creatinine improves after rehydration, that doesn't necessarily explain the whole problem.
My recommendation is to have an initial AKI investigation set you're comfortable with. Start with the current U&Es, especially potassium and bicarbonate, and compare the creatinine with previous dated results. Send a blood count and other bloods directed by the presentation; a gas is useful in an unwell or oliguric patient. Test the urine. Then decide what further investigations the suspected cause requires.9
If the creatinine is rising rapidly, I would discuss it early rather than wait for potassium to become dangerous. Imagine a rise from 90 to 400 or 500, with potassium currently 5.4. That potassium result doesn't tell you what it will be later tonight.
Agree when to repeat the bloods, who will review them and what should trigger another call. “Bloods in the morning” isn't an adequate plan for every rapidly worsening AKI. The urgency depends on the trajectory and complications, not just the stage or a single reassuring result.
Do a urine dipstick when you identify an AKI. Blood and protein can change the whole differential. If there's no adequate explanation such as urinary infection or catheter trauma, think about nephritis and discuss it with renal.3
The dip doesn't prove glomerulonephritis, and white cells aren't a specific vasculitis marker. Interpret it alongside the history, examination and blood results.
If there's protein, quantify it. A spot albumin-to-creatinine ratio (ACR) measures albuminuria. A protein-to-creatinine ratio (PCR) measures total protein and may be useful with heavier or suspected non-albumin proteinuria. You don't automatically need both for every AKI; follow the clinical question and local renal advice.8
If nephritis is suspected, ask about fresh urine microscopy and sediment, including casts. That isn't necessarily the same request as a routine urine culture.9
Imagine Ms A, who's 34. She's had fatigue and sinus symptoms for a couple of years, and now feels unwell over a few days. Her creatinine is 540 micromol/L, from a previous baseline of 85. You were diligent and dipped her urine: blood 3+ and protein 2+.
What would you be thinking? This combination should make you consider glomerulonephritis and systemic disease, including vasculitis. The point of this talk isn't to identify the exact subtype at the bedside. It's to recognise the pattern and get the right people involved.
Now suppose she develops respiratory findings: saturations 90% on air, a falling haemoglobin and bilateral chest opacities. She hasn't coughed up blood.
That could be pulmonary–renal syndrome, including diffuse alveolar haemorrhage with glomerulonephritis. The absence of haemoptysis doesn't exclude pulmonary haemorrhage. Sinus symptoms alone aren't what makes this a pulmonary–renal syndrome; it's the new lung findings alongside the renal presentation. Infection and pulmonary oedema remain possible alternatives.10
This is an emergency. Assess and support her using A–E, and contact the senior, renal and appropriate respiratory or critical care team urgently. Send useful samples in parallel; don't wait for a complete screen before making the call.
For suspected nephritis, the first set of blood tests you discuss with renal may include:
Urine protein quantification and sediment assessment accompany the blood tests. This is a targeted investigation of a working diagnosis, rather than a blood panel that every patient with dehydration needs.
Complement can be low in some immune-complex conditions, including lupus nephritis, but a normal complement result doesn't rule out nephritis. Nor should you wait for antibody results before escalating this patient's deterioration.
It's all very well thinking about vasculitis, but there are other patterns you should recognise.
Suppose someone has had a long lie with muscle injury. Check creatine kinase—CK—and potassium, and think about rhabdomyolysis. A dip positive for blood may be detecting myoglobin rather than red cells.9
If someone has AKI, anaemia and a high calcium, particularly an older patient, think about myeloma. Send serum protein electrophoresis and serum free light chains, with immunoglobulins as part of the local work-up. Those findings raise suspicion; they don't establish the diagnosis.12
And remember that a routine dipstick mainly detects albumin. It can miss free light chains. A negative dip for protein doesn't exclude myeloma-related kidney disease.13
If the platelets and haemoglobin are low, consider whether there's haemolysis and a thrombotic microangiopathy. Ask for a blood film and haemolysis tests, and discuss urgently with haematology and renal if you suspect it. You don't need to wait for a complete collection of textbook features.9
Then there's acute interstitial nephritis. This affects the tubules and interstitium; it isn't a subtype of glomerulonephritis. Drugs such as proton pump inhibitors, antibiotics and NSAIDs can be responsible. The onset can be insidious, so look beyond medicines started yesterday. Fever, rash and eosinophilia may be absent.14
The physiology helps make sense of this. Filtration depends on the pressures across the glomerular filter and on the filter itself. Reduced perfusion, raised downstream pressure or injury to the kidney can all reduce filtration.
!Simplified glomerulus showing blood entering through the afferent arteriole, leaving through the efferent arteriole, and filtrate passing into the tubule.
Original slide illustration: glomerular filtration. A simplified teaching diagram; the arrows show directions of flow, not measured pressures or filtration rates.
Think about blood entering through the afferent arteriole and leaving through the efferent arteriole. Changing resistance on either side changes the pressure within the glomerular capillaries. That's useful when you're looking at the drug chart.
Everyone knows to look for NSAIDs in AKI, but it's worth understanding why. They inhibit cyclo-oxygenase and reduce prostaglandin production. Those prostaglandins help maintain afferent arteriolar dilatation, particularly when perfusion is threatened. Lose that support and blood flow and filtration can fall. In this patient, I would stop the ibuprofen.15
ACE inhibitors reduce angiotensin II, so there is less efferent arteriolar constriction. That can also lower glomerular filtration pressure. It's why we monitor renal function and potassium after starting them, and why a modest creatinine rise can be expected.
In someone like Mr R, with vomiting, hypotension and AKI, review temporarily withholding ramipril. That isn't the same as declaring it permanently unsuitable. A larger or persistent change in renal function needs assessment for reversible causes, and any pause needs a plan for review and restarting when appropriate.16
The other issue is drug clearance. Morphine's metabolites can accumulate when kidney function falls, causing prolonged sedation or respiratory depression. Review the analgesia and involve pharmacy or an experienced prescriber.
Oxycodone may be an alternative in some settings, but it can also accumulate and needs cautious dosing and monitoring. Alfentanil may be appropriate under specialist guidance; it isn't a routine like-for-like swap for a foundation doctor to make unaided.17
This is something I've stressed in each of these sessions: don't prescribe fluids blindly because the urine output is low.
If the bladder is small and the overall assessment suggests volume depletion with poor perfusion, a fluid challenge may be appropriate. For general adult resuscitation, NICE describes 500 mL of isotonic crystalloid over less than 15 minutes, followed by reassessment. The volume needs individualising, particularly with heart failure or a risk of overload.18
If you're following the suspected-sepsis pathway, the current initial bolus is 250 mL over 10–15 minutes, again with reassessment. That's the context we discussed in session two.19
Go back and examine the patient. Has perfusion improved? What's happened to the breathing, saturations, chest and JVP? If congestion or pulmonary oedema is developing, stop further routine boluses and get senior help. That patient may need a decongestion plan, rather than more fluid.2
Let's say Mr R has received 500 mL. His blood pressure has come up a little, his pulse has fallen, his capillary refill is improving and his chest remains clear. But there still isn't much new urine.
Don't respond by automatically prescribing another bag. Recheck the measurement and drainage, reconsider the cause, and look for complications. Is potassium rising? Is there acidosis? Is fluid accumulating?
Urine output doesn't have to recover within an hour or two of fluid treatment. Established kidney injury can take longer, and giving more fluid after perfusion has improved may simply produce overload.9
A potassium of 5.5–5.9 mmol/L is classed as mild hyperkalaemia, but the trend and clinical condition matter. At 6.0 or above, obtain an urgent ECG. Severe hyperkalaemia—6.5 or above—requires emergency treatment and expert help. A normal ECG doesn't exclude dangerous hyperkalaemia.6
IV calcium protects the heart when there are hyperkalaemic ECG changes; it doesn't lower potassium. Follow the emergency hyperkalaemia protocol for the complete treatment and monitoring plan. Don't give calcium automatically just because someone has AKI and a mildly raised potassium.6
Renal replacement therapy is considered for the whole clinical picture. Refractory hyperkalaemia, severe acidosis, pulmonary oedema or uraemic complications need urgent renal or critical care discussion. A creatinine number alone doesn't decide who needs dialysis.3
If the cause remains unclear, or there's a risk of urinary tract obstruction, arrange a renal tract ultrasound urgently—NICE specifies within 24 hours. It isn't a routine requirement for every AKI with an established cause.3
If you suspect an infected obstructed kidney, speak to urology immediately. Ultrasound should be performed within six hours, alongside urgent assessment and treatment. White cells or nitrites in urine and a high CRP may support concern about infection, but a CRP of 300 doesn't diagnose obstruction or locate the source.3
Likewise, discuss unexplained or worsening AKI, a poor treatment response or possible nephritis with renal early. Ms A's lung and kidney presentation needs an immediate call, not a routine referral left until tomorrow.
The patterns I particularly don't want you to miss are the rapid creatinine rise with blood and protein; AKI with anaemia and high calcium, even if the dip is negative for protein; and AKI after a long lie. Ask yourself what investigation would change your thinking, and who needs to know about the patient now.
How do you restore catheter patency? Are doctors expected to know how to flush a catheter?
Start with the external checks we've discussed. You may not yet have been trained to perform a washout yourself. What you do need to recognise is when there's a drainage problem that needs someone with the right skills.
Blood or clots may make a washout appropriate, but don't assume that visible sediment means you should flush every catheter. Ask a trained nurse, senior doctor or urology colleague, follow local policy, and get help if drainage cannot be restored or there's significant pain or bleeding.5
You might ask a urology registrar to show you how a three-way catheter and irrigation are set up. That's a useful supervised learning opportunity; you don't need to pretend you've already been taught it.
When is it appropriate for an F1 to insert a three-way catheter instead of a standard Foley?
Again, speak to urology or an appropriately experienced senior. A three-way catheter allows irrigation and may be needed for significant haematuria or clot retention. The decision should be based on the indication and your competence, with supervision if needed. It isn't simply the next step whenever a standard catheter stops draining.5
How would you manage oliguria with a small bladder in an older person with heart failure? Would you trial IV fluids?
The word “trial” is useful, but first establish that there is a reason to give fluid. Someone with heart failure can be volume depleted, congested, or have a mixture of problems. A small bladder doesn't settle that question.
If the assessment supports a cautious fluid challenge, you might use 250 mL, then reassess at the bedside after about 10–15 minutes, with senior input. Look at perfusion and tolerance, not just whether urine has appeared. Only repeat it if the reassessment supports doing so.92
If they're congested or developing respiratory compromise, more fluid may be harmful. And don't let “stage 1” or “stage 2” reassure you on its own: deterioration and dangerous complications can occur at any stage.
Are the sessions recorded?
Yes. We also prepare written notes because they're easier to access and review.
The topics we've discussed are covered in the Bleep Guide app, including the emergency checklists and ward-cover scenarios. Thanks very much, guys.