Early intervention in acute renal failure
BMJ 2006; 333 doi: https://doi.org/10.1136/bmj.38945.596215.80 (Published 24 August 2006) Cite this as: BMJ 2006;333:406All rapid responses
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EDITOR - We read with interest the editorial by Dr. Bennett-Jones
that highlighted the importance of a prompt approach to treating
hypovolaemia with intravenous fluids as the only reliable means of renal
protection1. However, there was no comment on the composition of the
fluid. This may be very important, particularly in clinical situations
where large volumes of fluid are administered during resuscitation, and
may well affect the degree of renal protection and subsequent outcome.
The commonest fluid chosen for resuscitation is often 0.9% sodium
chloride, often called normal saline (NS), which frequently causes
hyperchloraemic metabolic acidosis (HCMA)2. Although some clinicians argue
that HCMA does not cause direct harm, it may result in the incorrect
treatment of the acidosis. Unfortunately, there are relatively few
clinical studies comparing NS with balanced electrolyte solutions (such as
Hartmann’s solution or Ringer’s lactate), yet although they are small,
they nearly all suggest that NS is not the optimal fluid for the majority
of patients. It has been known for many years that hyperchloraemia causes
renal artery vasoconstriction and a progressive fall in glomerular
filtration rate3. In a comparison of NS with a balanced electrolyte
solution in human volunteers, NS was associated with significantly more
abdominal discomfort and a slower time to urination4. In a recent study of
patients undergoing renal transplantation who were randomised to NS or
lactated Ringer’s solution, those who received NS had significantly more
hyperkalaemia and acidosis5.
Increasing awareness of the ‘Stewart hypothesis’ has led to new ways
of managing acid-base balance. We would argue that it is preferable to
avoid the iatrogenic problem of saline-induced HCMA and its associated
morbidity, and choose a balanced electrolyte solution for basic initial
fluid resuscitation.
1. Bennett-Jones DN. Early intervention in acute renal failure. BMJ
2006;333:406- 407.
2. Kellum JA. Saline-induced hyperchloremic metabolic acidosis. Crit
Care Med 2002;31:259–261.
3. Wilcox CS. Regulation of renal blood flow by plasma Chloride. J
Clin Invest 1983;71:726-735.
4. Williams EL, Hildebrand KL, McCormick SA, Bedel MJ. The effect of
intravenous lactated Ringer's solution versus 0.9% sodium chloride
solution on serum osmolality in human volunteers. Anesth Analg 1999;88:999
-1003.
5. O’Malley CM, Frumento RJ, Hardy MA, Benvenisty TE, Mercer JS,
Bennett-Guerrero E. A randomised, double blind comparison of lactated
ringers solution and 0.9% NaCl during renal transplantation. Anesth Analg
2005;100:1515–1524.
Competing interests:
None declared
Competing interests: No competing interests
I read with interest the editorial by Dr. Bennett-Jones relating to
the use of loop diuretics in acute renal failure (BMJ 2006; 333: 406-407).
I also read with interest the Rapid Response by Gillbe and Evans.
Unfortunately, despite my initial intention to post a rapid response along
similar lines, I left it "under the blotter" too long and have only posted
now.
Our points, however, are similar: intensivists may well be
anaesthetists but not necessarily so. All three of central Manchester’s
intensive care units have non-anaesthetic consultant staff and this
represents an increasing trend locally and nationally.
This point may seem superficial but for patients and relatives at
their most vulnerable clarity remains important.
Steve Jones MD MRCP FRCSEd FCEM
Competing interests:
None declared
Competing interests: No competing interests
In his editorial on early intervention in acute renal failure David N
Bennett-Jones points out that clinical trials of patients with acute renal
failure (ARF) have been difficult because the care of such patients is
split between nephrologists and anaethetists [1]
This statement implies a detrimental lack of collaboration between
these specialists in the management of ARF in the intensive care unit
(ICU). This is particularly worrying because it is happening at a time
when the epidemiology of ARF is changing, often presenting first to the
intensivist in the context of multiple organ failure rather than to the
nephrologist as single organ failure [2]. Moreover patients with ARF are
increasingly elderly with extensive co-morbidity [3].
Nephrologists and intensivists require a detailed knowledge of an
enormous medical literature to optimally manage these patients, this is
unlikely to be achieved by either specialist working in isolation of the
other.
In our opinion the optimal management of ARF in the ICU demands close
co-operation between nephrologists and intensivists. Such calls are not
new, as long ago as 1998 leading experts were even arguing for a new
specialty of critical care nephrology [4].
In the United Kingdom we have a very long way to go before we could
even contemplate such a suggestion, as there are no formal links between
the professional societies of nephrology and intensive care medicine.
Mutual misunderstanding between these specialities can easily arise,
even David N Bennett-Jones in this editorial fails to appreciate that not
all practitioners of intensive care medicine are anaethetists.
Specialty training represents an obvious route to improve this
situation but unfortunately despite the fact that some 25% of all
admissions to the ICU develop ARF [5] there is no compulsion on nephrology
or intensive care medicine trainees to complete SpR posts in the other
specialty.
It should be remembered that patients with ARF are at high risk of
death [6] and in our opinion such patients deserve close collaboration
between the specialties that are most able to help them
[1]. Bennett-Jones DN. Early intervention in acute renal failure. BMJ
2006;332:406-7
[2]. Liano F, Junco E, Pascual J, Madero R, Verde E and the Madrid
Acute Renal Failure Study Group. The spectrum of acute renal failure in
the intensive care unit compared with that seen in other settings. Kidney
Int 1998; 53: S16-S24
[3]. Metcalfe W, Simpson M, Kahn IH, Prescott GJ, Simpson K, Smith
WCS et al. Acute renal failure requiring renal replacement therapy:
incidence and outcome. Q J Med 2002; 95: 579-583
[4]. Ronco C, Bellomo R, Feriani M, LaGreca G. Critical care
nephrology: The time has come. Kidney Int 1998; 53: S1-S2
[5]. de Mendonca A, Vincent JL, Suter PM, Moreno R, Dearden NM,
Antonelli M et al. Acute renal failure in the ICU; Risk factors and
outcome evaluated by the SOFA score. Intensive Care Med 2000; 26:915-21
[6]. Bagshaw SM, Laupland KB, Doig CJ, Mortis G, Fick GH, Mucenski M
et al. prognosis for long term survival and renal recovery in critically
ill patients with severe acute renal failure: A population based study.
Crit Care 2005; 9:700-9
Competing interests:
None declared
Competing interests: No competing interests
We read with interest the editorial by Dr. Bennett-Jones (BMJ 2006;
333: 406-407) relating to the use of loop diuretics in acute renal failure
(ARF). Whilst we welcome his conclusions relating to clinical practice,
we would contest his assertion that prompt initiation of continuous renal
replacement therapy is provided by anaesthetists in the intensive care
unit. Thus, training in the management of ARF forms part of the
competency-based training programme in intensive care medicine (ICM)
overseen by the Intercollegiate Board for Training in ICM, established in
the early 1990s. ICM achieved specialty recognition throughout the EU in
2000. In the UK, a Diploma in ICM attracted 22 candidates in 2006.
Whilst specialist training positions in ICM are open to trainees from
anaesthesia, they are also taken up increasingly by those in medical and
surgical primary specialties.
Whilst intensivists may well be anaesthetists, the reverse is not
necessarily true!
Charles Gillbe FRCA
Chair, Intercollegiate Board for Training in Intensive Care Medicine
Timothy Evans FRCP FRCA
Chair, Royal College of Physicians of London Critical Care Committee
Competing interests:
None declared
Competing interests: No competing interests
In his editorial on early intervention in acute renal failure, David
Bennett-Jones emphasises the importance of prompt administration of
intravenous fluids [1]. Determination of the appropriate rate of fluid
administration must include an estimate of the degree of intravascular
volume depletion at the start of therapy, with most aggressive volume
expansion targeted at patients with the greatest deficits. To determine
whether this simple principle is followed in practice, we audited
intravenous fluid prescriptions for 114 consecutive acute surgical
admissions to three UK centres (one teaching hospital and two district
general hospitals).
Elevation of the blood urea:creatinine ratio is commonly used as a
quantitative reference standard for the diagnosis of hypovolaemia [2], and
similar elevations may be seen in patients with reduced effective
intravascular volume secondary to sepsis [3]. We therefore compared the
initial rate of intravenous fluid administration for each patient with
their urea:creatinine ratio on admission. Patients with chronic renal
failure or upper gastrointestinal haemorrhage, or who were taking drugs
known to affect this ratio, were excluded from the analysis.
Across all admissions, the volume of fluid prescribed over the first
hour of treatment ranged from 83 to 1250mls. There was a very low degree
of correlation between rate of administration and urea:creatinine ratio,
with a correlation coefficient for the complete data set of only 0.23 (95%
confidence interval: 0.05 to 0.40). This indicates that just 5.3% of the
variation in rate of fluid administration can be explained by an
association with urea:creatinine ratio (and hence degree of intravascular
volume depletion).
The most likely explanation for this finding is a failure by the
admitting doctors to appropriately diagnose and treat hypovolaemia. In UK
hospitals, fluid prescription is typically left to the most junior members
of medical and surgical teams, amongst whom inadequate knowledge is common
[4]. There is a clear need for improvement in training and practice in
this area, and courses such as ALERT (Acute Life-threatening Events –
Recognition and Treatment) may be a good start [5].
The authors would like to thank Nicola Alder, Medical Statistician at
the Centre for Statistics in Medicine, Oxford, for her help with data
analysis.
References:
[1] Bennett-Jones DN. Early intervention in acute renal failure. BMJ
2006;333:406-7.
[2] McGee S, Abernethy WB, Simel DL. Is This Patient Hypovolaemic?
JAMA 1999;281:1022-9.
[3] Robinson BE, Weber H. Dehydration Despite Drinking: Beyond the
BUN/Creatinine Ratio. J Am Med Dir Assoc 2004;5(2 Suppl):S68-71.
[4] Lobo DN, Dube MG, Neal KR, Simpson J, Rowlands BJ, Allison SP.
Problems with solutions: drowning in the brine of an inadequate knowledge
base. Clinical Nutrition 2001;20(2):125-30.
[5] Smith GB, Osgood VM, Crane S, ALERT Course Development Group.
ALERT – a multiprofessional training course in the care of the acutely ill
adult patient. Resuscitation 2002;52:281-6.
Competing interests:
None declared
Competing interests: No competing interests
EDITOR—The article by David Bennett-Jones accurately reviews the
management of acute renal failure and the lack of benefit from frusemide1.
However, in describing the essential determination of fluid status in such
patients the article is deficient and fails to draw upon the admittedly
limited
evidence base for assessing hypovolaemia2. This is particularly apposite
given the preceding editorial by Sharon Strauss highlighting the
importance
of evidence in diagnostic accuracy3.
The editorial by Bennett-Jones suggests ‘Doctors should take a
pragmatic
and prompt approach to intravenous fluid replacement, based on the
patient's blood pressure, capillary refill time, and venous filling’ 1. I
would
suggest that assessment of fluid status needs to be much broader and
incorporate a full history of any fluid gains and losses from the patient,
relatives, nurses, fluid balance charts, prescription charts, anaesthetic
records
and daily weights. The patient should be assessed for symptoms of
hypovolaemia which can include postural dizziness, thirst, dry mouth,
reduced urine output, feeling cold, shivering, shortness of breath and
altered
mental status. Furthermore in examining the patient, of central importance
are blood pressure, a postural fall in blood pressure, tachycardia (or
rarely
bradycardia with severe hypovolaemia) and postural changes in pulse rate,
whilst capillary refill time is not of proven diagnostic value in adults2.
Other
signs that should be sought are the level of jugular venous pressure,
pallor,
peripheral perfusion, the dryness of mucous membranes and the presence of
pulmonary and peripheral oedema. If doubt about volume status remains
central venous pressure monitoring should be considered.
This careful assessment of fluid status is vital prior to the
instruction ‘Give
intravenous fluids, not loop diuretics’1 to avoid patients developing
dangerous pulmonary oedema, particularly since in some studies fluid
loading in the intensive care setting has been associated with a higher
incidence of acute renal failure4.
1. Bennett-Jones DN Early intervention in acute renal failure. BMJ
2006;333:
406-407
2. McGee S, Abernethy WB, Simel DL. Is this patient hypovolemic? JAMA
1999 281: 1022–1029
3. Bridging the gaps in evidence based diagnosis. Straus SE, BMJ
2006 333:
405-406
4. Van Biesen W, Yegenaga I, Vanholder R, Verbeke F, Hoste E,
Colardyn F and
Lameire N. Relationship between fluid status and its management on acute
renal failure (ARF) in intensive care unit (ICU) patients with sepsis: a
prospective analysis. J Nephrol 2005 18:54-60
Competing interests:
None declared
Competing interests: No competing interests
Getting the Fluid into the Patient - practical problems with intravenous fluid managment
EDITOR – Matheson (Evidence of inadequate fluid treatment in UK
hospitals - BMJ letters 9th September 2006) highlights a problem of
inadequate fluid prescription in surgical patients.(1) In an audit of
preoperative fluid management of hip fracture patients at Royal Alexandra
Hospital, Paisley, in 2004 we found hypovolaemia to be similarly under-
treated, but rather than inadequate prescription, we found inadequacy in
the administration of fluids. 54 consecutive patients were studied: their
notes were examined for fluid prescription and these were compared with
fluid balance charts to see what fluid each patient actually received from
admission up until entry to the anaesthetic room. Patients were written up
for on average 111 ml/hr of crystalloid (range of 83-500 ml/hr) but the
average rate of fluid actually administered during preoperative fasting
was only 53 mls/hr (range of 0-107 ml/hr). In all cases patients received
less fluid than they were prescribed, over half received less than half
what they were prescribed, and 3 out of the 54 patients did not receive
any intravenous fluid at all. Following delays or interruptions to fluid
infusions there was no evidence that rate of subsequent fluid
administration was ever increased to compensate for the short-fall, and
thus the tendency was always for patients to fall behind with their
fluids.
Good fluid management, which should be fairly straightforward, turns
out to be a complicated business. As well as getting the initial
prescription for fluid replacement right, junior doctors must ensure
adequate, well-positioned intravenous access and be prepared to return
when necessary if problems arise with cannulas. Managing intravenous
infusions is demanding of nursing time too, especially if infusion pumps
are not available for all patients. The particular problem highlighted by
our audit was that no member of staff, nursing or medical, appeared to
take responsibility for updating fluid prescriptions after delays or
interruptions in infusions.
The benefits of adequate fluid resuscitation in this group of
patients have been well documented(2), but we still don’t seem to be
getting it right. The practicalities of managing intravenous infusions
require a high degree of inter-professional communication and co-
operation. Perhaps a more flexible approach to prescribing fluids that
would allow nurses to increase flow rates where appropriate would help.
Other practical ideas might include improving cannulation skills among
medical staff and training more nurses to cannulate. Certainly, more
infusions pumps would help. And perhaps a dispelling of the myth, common
among medical and nursing staff alike, that intravenous fluid (like high
flow oxygen) is highly dangerous for frail and elderly patients and to be
used sparingly at all times. Although cases of fluid overload do
occasionally occur, it is far more common to find dehydration in this
group of patients(3) with the attendant complications of intra-operative
cardiovascular instability and post-operative renal failure.
References:
(1) Matheson NJ, Irani SR, Irani A Evidence of inadequate fluid
treatment in UK hospitals BMJ 2006; 333: 551 (9th September)
(2) Venn R, Steele A, Richardson P, Poloniecki J, Grounds M, Newman
P. Randomized controlled trial to investigate influence of the fluid
challenge on duration of hospital stay and perioperative morbidity in
patients with hip fractures. British Journal of Anaesthesia 2002; 88:
65–71.
(3) A study of the initial fluid resuscitation and pain management of
patients with fractured , neck of femur
[Abstracts: Abstracts from the Age Anaesthesia Association Annual Meeting
in Grange over Sands, Cumbria, on 10 May 2002] Levy, N.
Competing interests:
None declared
Competing interests: No competing interests