Neil Goldsack,
respiratory specialist registrar
Chest Clinic,
North Middlesex Hospital,
London
David Howell,
Medical Research Council fellow
Richard Marshall,
Wellcome fellow
Hugh Montgomery, cardiology specialist registrar
University College and Middlesex Hospital,
London

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Emergency!

In the sixth part of our emergency series, Neil Goldsack, Hugh Montgomery, Richard Marshall, and David Howell tell you how to treat patients with oliguria

Introduction
One of the most common conditions you will meet on a daily basis as a house officer in surgery or medicine is oliguria. This is defined as the production of less than 400 ml of urine in 24 hours. This means producing at least 20 ml/hour. Remember that this is not a magic figure, and the trend in urine production is the crucial factor. A sudden stop of a good urine output is as crucial as a general decline in flow.

19th century approach to incisions, suture and anastomosis

The aetiology of oliguria can be simplified into prerenal, renal, and postrenal causes.

Aetiology of oliguria   Cause Prerenal   Hypovolaemia Blood loss Fluid sequestration - paralytic ileus Septic shock Cardiogenic shock Renal   Acute tubular necrosis Acute interstitial nephritis - for example, caused by drugs such as gentamicin Acute glomerulonephritis Postrenal   Prostatic hypertrophy Blocked urinary catheter

(1) Prerenal oliguria is characterised by a reduction in renal blood flow causing intravascular volume depletion. Therefore, anything that results in a reduction of circulating volume or prolonged hypotension (for example, cardiogenic shock) can result in prerenal failure.

(2) Intrinsic acute renal oliguria implies damage to the kidneys themselves and is usually the result of acute tubular necrosis or acute interstitial nephritis. These conditions normally reflect a systemic illness such as sepsis or multiorgan failure and have a high mortality. They can be caused by a multitude of everyday drugs such as non-steroidal anti-inflammatory drugs (aspirin, ibuprofen, etc) and aminoglycoside antibiotics (gentamicin, etc).

(3) Postrenal failure indicates an obstruction in the renal outflow tract. The commonest cause of this is a blocked urinary catheter, which affects many people and is simply relieved by a bladder washout. In addition, an inappropriately placed catheter can result in a similar problem. However, obstructions in the collecting system, ureters, and bladder outlet need to be considered.

Management and exam approach to oliguric patient
(1) Oliguria is a medical emergency that can kill if not treated quickly. Therefore, go and see this patient immediately.

 

Conditions that kill patients with acute renal failure Hyperkalaemia (K+>7.0)   Fluid overload   Profound acidosis (pH)

(2) On arrival, assess the need for urgent resuscitation. This will give an immediate answer as to how sick the patient is. If the patient is extremely breathless, pale, clammy, and shut down peripherally with an unrecordable blood pressure you know that there is a serious cause for their oliguria - call a senior doctor for help immediately.

(3) If the patient is not seriously unwell then commence high flow oxygen, position a pulse oximeter, and perform an electrocardiogram.

(4) Establish venous access if this has not been done yet and take routine blood samples (an urgent estimation of the potassium concentration is essential in every patient).

(5) Calculate the fluid balance. This can be done by a combination of a quick history and a clinical examination.

(a) Take a brief history. Divide the specific questions relating to causes of pre-renal, renal, and postrenal oliguria as discussed above. Look at the fluid input and output chart. Never forget to take a full drug history. Remember that a single dose of a non-steroidal anti-inflammatory in a susceptible patient can cause catastrophic renal impairment.

(b) Aim the examination to assess the patient's fluid balance. By picking up the patient's hand and assessing its warmth you will know if their circulation is shut down or not. A cold, poorly perfused hand suggests that a patient is fluid depleted.

(c) Look at and feel the skin and check the turgidity. Carefully examine the mucous membranes and tongue. Dry mucous membranes are a clear sign of prerenal failure.

(d) If you do nothing else to the oliguric patient, remember that the most accurate and useful bedside test is taking a postural blood pressure. A significant postural drop is a fantastic and accurate way of assessing diminished intravascular volume.

(e) The jugular venous pressure is another area that frightens doctors and is a poorly used clinical sign. The best way to get better is by practising. By examining every normal jugular venous pressure you will soon be able to read the abnormal ones.

(f) Fully examine the rest of the other systems, taking particular note of any peripheral or pulmonary oedema. Any sign of oedema means that the patient is overloaded with salt and water and will have a high total concentration of sodium in the body. This does not mean, however, that a patient is definitely intravascularly overloaded. You must confirm this with the rest of the clinical examination - the postural blood pressure, jugular venous pressure, and assessment of mucous membranes. The patient may well need fluid replacement rather than a diuresis. Remember, just because a patient has peripheral oedema doesn't mean that they need frusemide (furosemide).

(h) Another good tip to remember during examination is that you can give the patient a fluid challenge without giving him or her any more volume. The patient's legs contain circulating volume, and by lifting one or both at the same time and holding them up you can give the fluid challenge. Immediately repeat your basic vital signs again - take a postural blood pressure, jugular venous pressure, and reassess. The signs will change according to the patient's volume status; the patient with intravascular volume depletion will have a lessened postural drop after the fluid challenge.

(6) Analysing arterial blood gases in any oliguric patient is very useful. Not only does it tell you their arterial partial pressures of oxygen and carbon dioxide but also their acid-base status. It is commonly forgotten that acidotic patients with renal failure can be extremely breathless, without any respiratory or cardiac pathology to account for it. They are simply blowing off carbon dioxide to compensate for their gross systemic acidosis.

(7) The only accurate way to monitor urine output is with a urinary catheter. If the patient is sick, place one early and measure urine outputs hourly. Get the nurses to set up an accurate fluid balance chart and daily weight chart.

(8) Always get the nurses to do a dipstick test on the urine. In glomerulonephritis there will be haematuria and red cell casts. Also send the urine for Na+ analysis. In prerenal failure the urinary Na+ concentration is usually 10 mmol/l and in established renal failure is usually >20 mmol/l.

Treatment
(a) If patients have prerenal failure (falling jugular venous pressure, postural hypotension, dry mucous membranes) they require fluids. These can be given through a plasma expanding agent such as Gelofusin (500 ml over 15 minutes). Watch the urine output very carefully after this. If patients fail to pass urine in the hour after the procedure you should discuss this with a senior doctor. If they respond well then you can prescribe normal saline over the next few hours. However, keep a close eye on their urine output.

(b) If the patient has an intrinsic renal problem (without signs of pre- or postrenal impairment) then this will need more intensive management. These patients are usually well filled (rising jugular venous pressure, no postural drop in blood pressure). Management of these patients requires expert help. Call your registrar or the renal team. Patients will need to have a central line inserted and be given renally active drugs such as dopamine. If their condition deteriorates and they become grossly overloaded with fluid, hyperkalaemic, or acidotic they may require dialysis.

(c) Postrenal failure is usually overcome by simple measures such as catheter insertion or flushing a blocked catheter. If you're in doubt the urologists should be able to help. Similarly, if you are unable to pass a catheter you should call the urologists as repeated attempts may result in urethral damage.

 

Special occasions (1) Postoperative patients will have a high concentration of antidiuretic hormone in their plasma. This obviously will cause oliguria but is only a diagnosis of exclusion. You must exclude all other causes first, such as blood loss and ileus. (2)   Jaundiced patient have exquisitely sensitive kidneys. Keep them hydrated, as hepatorenal syndrome may develop, which has a very high mortality. (3)   Never forget that contrast agents can cause renal damage, so make sure you keep these patients well hydrated. (4)   A sudden loss of urine usually implies obstruction. (5)   Remember not to be fooled by oedematous patients: if their serum albumin concentration is low fluid leaks out into the tissues, leaving them intravascularly depleted. (6)   It is also important to remember that patients with chronic renal failure on haemodialysis may pass no urine whatsoever, which is entirely normal for this group of patients. (7)   Never forget that contrast agents used in angiograms etc. are profoundly nephrotoxic in a sensitive person. Make sure any patient going for an investigation with contrast is well hydrated before the procedure.

Summary
On completion of the full history and examination you should now be in a good position to implement any basic management change, order relevant investigations and seek extra help if required. Remember the basic framework while contemplating your next step. Think of the prerenal, renal, and postrenal causes and rule them out accordingly. Order relevant investigations using the usual breakdown - urine, blood, radiography. An ultrasound scan is crucial if you expect an obstruction.

 

Things to be aware of (1) Don't treat all patients the same. Watch out for patients at risk - elderly people, those with impaired renal function, and those with jaundice. (2)   Do not treat oliguria flippantly. Oliguria can herald renal failure and therefore is an emergency requiring a quick response. (3)   Do not simply treat oliguria with blindly administered diuretics. Assess the patient accurately before commencing any treatment. (4)   Most doctors can remember a case where a haemodialysis patient had been given massive doses of diuretics when what they needed was dialysis. As a result the patient ends up deaf as a toxic effect of the frusemide (furosemide).

Essentially the management of oliguric patients is simple if the above framework is applied, and you should not run into any problems. But always remember to seek help early if you are at all confused.

It is well known that fluid balance is one of the areas that are least well managed by doctors and nurses. Random prescriptions of 3 litres of crystalloid and potassium are written up daily by house officers for patients and backed up by - usually inaccurate - charts. Fortunately, the human body is usually able to tolerate large volumes of fluid taken inappropriately as the kidneys respond by producing more urine. This is why members of the rugby team after each drinking 10 pints of beer after a game don't get admitted en masse with pulmonary oedema. However, we will not discuss the management of the hangover in this article. Unwell patients are a different matter, and fluid balance can be critical, with overzealous prescriptions of fluid possibly being fatal.