Today I want to have a final rant for 2008!
The rant is about the sometimes observed 'knee jerk reaction' that one sees by inexperienced physicians when the patient's urine output is low and furosemide is given to 'make the patient pee'.
Low urine output means assessment of the cause rather than just pumping diuretic into the patient which may makes matters far worse.
For example, low urine output might mean the patient has a urinary tract obstruction (post-renal), hypoperfusion from hypovolaemia (pre-renal) or intrinsic renal failure from an insult (e.g. ATN).
When one assesses this problem, take further history from the patient. They may tell you that they have trouble passing urine and / or a painful lower abdomen or distension suggestive of urinary tract outflow obstruction. On the other hand, it may be more clear whereby bleeding may have already been diagnosed e.g. upper GI haemorrhage. The patient might be taking nephrotoxic drugs, have sepsis or a local glomerulonephritis. The causes of pre -, intra-, and post-renal impairment are too many to discuss on this blog.
However, in patients who have low urine output, suffice it to say that the physical examination is of prime importance in addition to looking at the sequential laboratory studies, to identify the cause and follow the progression or improvement respectively.
When one examines the patient, start generally and then focus on the individual systems.
- Does the patient look ill? Confused? Sweaty?
- Then look at the hands! Check for those splinter haemorrhages as endocarditis can cause renal failure. Assess for encephalopathy by checking for flap (asterixis) -renal failure can cause flap the same as for liver failure and CO2 retention.
- Check the pulse - is there a tachycardia?
- Assess the fingers. Are they cold suggestive of vasoconstriction?
- Check the blood pressure - is there hypotension?
- Check the skin turgor on the dorsum of the hand / arm / inner thigh? Think to yourself, could this be dehydration?
- Feel for axillary sweaty - this is lost in dehydration
- Look at the conjunctivae to assess for anaemia - patient could be in a hypovolaemic state from bleeding
- Check the tongue & mucosa for dryness - a sign of possible dehydration
- Check the JVP - is it raised ? (could be a sign of CHF) or is there guttering (sign of hypovolaemia).
- Check the respiratory rate and rhythm - Is there Kussmul respiration / Air hunger -- can be seen in metabolic acidosis (renal failure), bleeding etc
- Listen to the chest - is there a focus of infection? Are there effusions / crepitations of heart failure?
- Listen to the heart for murmurs, added sounds
- Inspect the abdomen - is there a focus of infection? Are there signs of liver disease ? (liver failure can result in renal failure - hepatorenal syndrome)
- Are the renal angles tender ? (pyelonephritis / pyonephrosis)
- Can you feel a distended bladder in the lower abdomen? It is dull to percussion and when pressed and the patient may say they want to pass urine.
- Are there any abdominal bruits? Might suggest renal artery stenosis or a dissection if there is a compatible history
- Is there pitting oedema of the lower limbs? Might suggest liver disease, nephrotic syndrome, cardiac failure, venous obstruction, lymphatic obstruction or a low protein state.
- Look at the urine in the catheter bag (if one has been placed already) - measure the total amount since it was last checked. Look at the colour - is it dark suggestive of concentrated urine (hypovolaemia) or straw coloured in the euvolaemic state. Is it orange - bilirubin or red - bloody?
- Consider a rectal examination to look for GI bleeding and / or an enlarged prostate gland and / or malignancy.
The above features can help you to understand whether the patient is hypovolaemic, euvolaemic or hypervolaemic and a clue of the potential cause.
A patient with a hypovolaemic state (cold hands/feet, tachycardia, decreased skin turgor, hypotension, no axillary sweating, low JVP, dry tongue, dark small volume urine) should be given fluid to replenish the circulation and NOT diuretics! The reason for the decreased urine output is a result of ADH release and upregulation of the renin-angiotensin-aldosterone (RAS) system to retain water to maintain the circulation. Using a diuretic can result in worsening renal failure at the detriment of the patient. Yes, the frusemide splurge may make the doctor and nurses feel better that the patient is passing some more urine but the worst will be yet to come with the incipient renal failure.
A patient with an hypervolaemic state e.g. CHF, can have a low urine output as a result of vasoconstriction because of low cardiac output. Frank Starling forces denote that when the myocardium is overstretched (as in systolic heart failure), the muscles contracts less. Hence, to maintain blood pressure, the peripheral resistance increases which can reduce kidney perfusion and cause reduced urine output. Moreover, such patients also can have a high RAS activity worsening matters. In this situation, blocking angiotensin 2 production or activity (ACE-I / ARB) and aldosterone (with spironolactone) plus off-loading the circulation with a loop diuretic are the mainstay of conservative therapy. In this situation, it can improve the urine output quite appropriately.
A hypervolaemic state is demonstrated by symptoms and / or signs of CHF, liver disease, nephrosis etc. One might see a raised JVP, normal skin turgor, oedema around the eyes (nephrosis usually), pitting oedema of the extremities, abdominal ascites etc.
In a euvolaemic state, none of the adverse features seen in either the hypovolaemic or hypervolaemic states should be seen. One should also consider other causes such as:
- Drugs: e.g. morphine (causes release of ADH and direct urinary retention)
- Endocrine: SIADH
- Metabolic: hypoxaemia (increases ADH secretion)
- Misc: Pain and nausea (both increase ADH secretion)
- Urological: outflow obstruction e.g. prostatic hypertrophy with acute retention, bilateral ureteric obstruction from malignancy
Please refer to a standard textbook for the extensive list of causes. The above are merely examples to consider.
Hence, when assessing a basic thing such as urine output, we come back to basics. History and physical examination.
Looking at the laboratory studies can tell us further information e.g. worsening BUN and creatinine levels. Such lab results with an examination consistent with hypovolaemia tells us that the patient needs more fluid and not diuretics.
Normal laboratory studies but an examination consistent with hypovolaemia and low urine output should still prompt us to give more fluid.
On the other hand, a hypervolaemic patient may have laboratory studies indicating liver disease, cardiac failure (raised BNP) etc. These can guide us to a more precise diagnosis. Sometimes, such patients have existing renal dysfunction and so the cautious and judicious use of loop diuretics can be considered.
Remember that in acute renal failure, a meta-analysis of 9 studies in adults with ensuing or actual acute renal failure showed no benefit with the use of frusemide and in fact, caused ototoxicity (BMJ 2006;333:420-3)
If you are concerned about causing heart failure (a topic I have touched upon several times in the past) a fluid challenge of 250ml 5% dextrose can be given stat. One can then reassess the circulation for blood pressure, rise in the JVP (or CVP), pulmonary crepitations and improvement of urine output.
If urinary retention is considered, a renal tract ultrasound is quick, non-invasive and provides valuable information. Please don't jump for the contrast CT as contrast nephropathy can ensue.
Examination of the urine may reveal white cells, red cells, casts etc, that can point you towards an intrinsic renal problem rather than pre- or post- renal cause.
So, in summary, please fully assess your patients. Don't go for the easy option of giving frusemide to increase the urine output as you may just end up with a worse problem ! Get out of the habit of knee jerk frusemide and use the grey matter you have been given instead.