“Drink plenty of fluids”: a systematic review of evidence for this recommendation in acute respiratory infections
BMJ 2004; 328 doi: https://doi.org/10.1136/bmj.38028.627593.BE (Published 26 February 2004) Cite this as: BMJ 2004;328:499All rapid responses
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We read with interest this report by Guppy et al. However, their
final comment that “we should be cautious about universally recommending
increased fluids to patients, especially those with infections of the
lower respiratory tract” should perhaps be further qualified.
Firstly, the studies used to support their comment relate mainly to
paediatric patients where the observed risk of hyponatraemia was >30%.
It cannot be assumed that the same applies in adult patients. Indeed,
Fine et al in cohorts of 14,199 and 38,039 adult patients with community
acquired pneumonia (CAP) reported hyponatraemia (Na < 130 mmol/l) in
only 7.7% and 6.5% respectively.[1]
Secondly, as hyponatraemia is a recognised poor prognostic factor in
CAP [1](this is indicated by the authors as well), most patients with
hyponatraemia would have disease severe enough to warrant hospital
referral. This is reflected in the extremely low incidence of
hyponatraemia in adults with CAP treated in the community -0.7% of 944 out
-patients compared to 6.1% of 1343 in-patients in the large prospective
Pneumonia PORT cohort study.[1]
Therefore, we believe the risks to adults with CAP treated in the
community from hyponatraemia are not as high as suggested by the authors.
Patients with severe CAP need hospital referral. In these patients,
hyponatraemia will be detected from ‘routine blood tests’ performed to
assess disease severity. A powerful marker of prognosis is a raised urea
which occurs in >20% of hospitalised adults with CAP [1], mostly as a
result of dehydration. In these patients, fluid replacement is essential.
References:
1. Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify
low-risk patients with community- acquired pneumonia. New England Journal
of Medicine 1997;336(4):243-250.
Competing interests:
None declared
Competing interests: No competing interests
We read with interest Guppy et al’s recent paper [1] as we have
concerns that routinely advising patients to increase their fluid intake,
especially in the elderly and after some procedures, can have serious
consequences. Post operative urological patients are often routinely
advised to drink plenty of fluids to keep a urinary catheter flushed. It
is not unusual for these patients to drink an extra 5 litres of water per
day in addition to their normal fluid intake. A recent case has
highlighted to us that older patients don’t always handle this extra
volume well, which is consistent with age related renal changes [2].
Polydipsia can lead to severe hyponatraemia with serious consequences,
including death, even in apparently healthy individuals with normal renal
function [3 - 5].
References
1.Guppy MPB, Mickan SM, Del Mar CB. “Drink plenty of fluids": a
systematic review of evidence for this recommendation in acute respiratory
infections. BMJ 2004; 328:499-500.
2. Andreucci VE, Russo D, Cianciaruso B, Andreucci M. Some sodium,
potassium and water changes in the elderly and their treatment. Nephrol
Dial Transplant 1996; 11 Suppl 9: 9-17.
3. Gardner JW. Death by water intoxication. Mil Med 2003 ; 168(3):432
-434.
4. Issa MM, Pruthi RS, McNamara DE, Terris MK. An unusual
complication following uroflometry: water intoxication resulting in
hyponatremia and seizure.Urol Int1997;59(2):129-130.
5. Sjoblom E, Hojer J, Ludwigs U, Pirskanen R. Fatal hyponatraemic
brain oedema due to common gastroenteritis with accidental water
intoxication. Intensive Care Med 1997 ;23(12):1289.
Competing interests:
None declared
Competing interests: No competing interests
Editor- The article by Guppy, Mickan and Del Mar as a systematic
review of
evidence for the effects of fluid intake on the course of acute
respiratory
infections has been interpreted in the press as a warning against fluid
intake
whilst suffering from acute upper respiratory tract infections such as
common
cold or flu. Headlines in newspapers and the inter-net warn that the ‘age
old
advice on fluids for colds’ is now disputed by research out of Australia.
The
authors have mischievously taken an old folk-lore on fluids and colds and
presented evidence on severe lower respiratory infections in infants to
make a
case that intake of fluids may be harmful. The press and public have got
the
wrong message because of the confusion in the article. The saying “Drink
plenty of fluids” is generally accepted to refer to common colds and is
not
normally associated with acutely ill and hospitalised infants. By linking
these
two together the authors have created a scare story, but they have not
addressed the main issue of the folk-lore. There are no controlled
clinical
trials in the literature to support any beneficial effect of maintaining
fluid
intake whilst suffering from an acute upper respiratory tract infection,
but
neither is there any evidence that indicates that this remedy is harmful
in any
way when applied as intended to colds and flu.
Competing interests:
RE and MJ conduct sponsored
clinical trials for the
pharmaceutical industry on
common cold medicines at the
Common Cold Centre.
Competing interests: No competing interests
Guppy et al report that they had found "two prospective prevalence
studies [which had] reported hyponatraemia at rates of 31% and 45% for
children with moderate to severe pneumonia. None of these children showed
clinical signs of dehydration. Symptoms associated with hyponatraemia were
not reported, but four children with a serum sodium below 125 mmol/l died
during one study" (1).
The fall in tissue pH that may develop either regionally or
systemically in acute illnesses and severe exercise, because of unreversed
ATP hydrolysis, is accompanied by a rise in ionised [Ca++] and may cause
intracellular calcium overload which if excessive is toxic to cells. This
may be accompanied by a rise in intracellular [Na+] because the sodium
pump is inhibited by an extracellular acidosis because protons are
buffered intracellularly in exchange for potassium. The hyponatraemia
might be compounded by activation of the Na(+)-Ca(2+) exchanger (2).
Activation of pH regulatory mechanisms, including Na+/H+ exchange, may
also compound the severity of the hyponatraemia to a degree limited by
its stimulation of Na+/ K+-ATPase activity (3).
These changes could account for the hyponatraemia seen in the
children with respiratory infections, and its association with poor
outcomes. They might also account for the antidiuretic hormone secretion
that increases in proportion with the extent of lung parenchymal
involvement. In fetal sheep normocapnic hypoxia releases vasopressin and
hypercapnia/acidemia augments the response to hypoxia (4).
Fluid intake, particularly if excessive, may compound the severity of
these changes in patients with acute respiratory infections in the same
manner that it does in marathon runners (5). The fluid intake could have
an adverse effect by causing oedema and increasing the diffusional
distances for the transport of oxygen, nutrients and metabolic by-
products between capillaries and cells. They might also make matters worse
be decreasing the a-v pressure gradient in capillaries by increasing
venous outflow pressure. Some degree of dehydration may have the reverse
effects and increase capillary flow rates as observed in the electronic
discussion of Noakes' paper. Keeping patients "dry" rather than "wet"
improves outcome patients in haemorrhagic shock.
Shock, defined as the presence of an impairment of tissue energetics
evident from the presence of a gastric intramucosal acidosis, was
undoubtedly present in those children with respiratory infections who
died. In which case the translocation of endotoxin, and its release of
cytokines, may have been another compounding factor as proposed in
marathon runners.
1. Michelle P B Guppy, Sharon M Mickan, and Chris B Del Mar
"Drink plenty of fluids": a systematic review of evidence for this
recommendation in acute respiratory infections
BMJ 2004; 328: 499-500
2. Tomes DJ, Agrawal SK. Role of Na(+)-Ca(2+) exchanger after
traumatic or hypoxic/ischemic injury to spinal cord white matter.
Spine J. 2002 Jan-Feb;2(1):35-40.
3. Harvitt DM, Bonanno JA. pH dependence of corneal oxygen
consumption.
Invest Ophthalmol Vis Sci. 1998 Dec;39(13):2778-81.
4. Raff H, Kane CW, Wood CE. Arginine vasopressin responses to
hypoxia and hypercapnia in late-gestation fetal sheep.
Am J Physiol. 1991 Jun;260(6 Pt 2):R1077-81.
5. Noakes TD. Overconsumption of fluids by athletes
BMJ 2003; 327: 113-114
Competing interests:
None declared
Competing interests: No competing interests
I am not convinced that drinking fluid is harmful to all patients
with respiratory infection (RTI).
It is not correct to think that
increased antidiuretic hormone (ADH) secretion in lower respiratory tract
infection (LRTI) is a common phenomenon. Hyponatraemia is a well known
complication of LRTI but it is not common. Furthermore, it is difficult to
prove that the incidence or the death of the LRTI related hyponatraemia
cases were associated with increased water intake or not.
I believed that
hyponatraemia could still occur even with normal fluid intake. Fluid
restriction may not be helpful to all LRTI. It can be even harmful if we
restricted fluid too much to the extent of causing dehyration.
I did not
think that the data the authors found could be extrapolate to patients
with upper respiratory infection (URTI) because there was no definite
evidence.
In Hong Kong, the newspaper had quoted the study and said
"plenty of fluid in flu can be harmful"! I worried the community might
have misconception about the finding of the study.
Competing interests:
None declared
Competing interests: No competing interests
Each year during the heat early spring and summer, my e-mail is
flooded with reports from endurance athletes who drink too much fluid,
take too few electrolytes, or consume too much carbohydrates for energy
during a hyperthermic prolonged endurance event.
Proportionate to the
increase in temperature and humidity above 60 degrees F. and 60%
respectively in relationship to the athlete's exposure to training-induced
adaptations are the reports of dilutional hyponatremia. The endurance
athlete requires approximately 10-14 days training in exposure to similar
heat and humidity as imposed during an event that lasts 3-6 hours in
length at an exercise pace of 75-85% VO2 Maximum Heart Rate. If 10-14 days
of adaptation to heat and humidity is accomplished, the athlete is also
advised to consume from 24-28 fluid ounces liquid with 0.3-0.7 g sodium
and no more than 280 calories from carbohydrates each hour divided dose to
prevent dilutional hyponatremia.
If the adaptation training exposure is not completed, the fluids,
electrolytes, and carbohydrate caloric replenishment formula may lead to
severe dehydration, tempting the athlete to consume too much fluids above
1 liter per hour, leading to dilutional hyponatremia. It is observed that
the athletes who consume in excess of 1 liter fluid per hour in prolonged
endurance events are most likely to experience the symptomatic malaise
observed in 1st-stage hyponatremia.
Competing interests:
None declared
Competing interests: No competing interests
I worry that the authors of the recent article “Drink plenty of
fluids": a systematic review of evidence for this recommendation in acute
respiratory infections” have left readers with recommendations and
implications that are not supported by the data they have reviewed. Upper
respiratory tract infections (URTI's) and episodes of bronchitis are very
common and presumably outnumber episodes of pneumonia by a factor of more
than 100. The only data they give to show excess fluid may potentially be
harmful in acute respiratory infections is from studies with moderate to
severe pneumonia. While they give a number of theoretical reasons why
antidiuretic hormone may be increased in respiratory infections, most of
those mechanisms would not be relevant in conditions where pneumonia was
not present. Their article would have been better entitled “Drink plenty
of fluids": a systematic review of evidence for this recommendation in
moderate to severe pneumonia”.
The title of their article has implication for all respiratory
infections including URTIs I however do not believe the data they have
reviewed should be used to extrapolate for conditions other than moderate
to severe pneumonia (and with these latter cases one would hope close
medical or hospital supervision was taking place and so hyponatraemia
could be avoided). We need to ensure that we do not leave the community
with the implication that this advice applies to the much more common
URTIs. As they state in the first paragraph of their paper it appears self
-evident that there are many benefits in keeping patients with less
serious respiratory tract infections well hydrated. They have presented no
data to show that this “common sense” approach should not continue to be
the case.
Competing interests:
None declared
Competing interests: No competing interests
SHOULD WE RESTRICT FLUIDS IN RESPIRATORY INFECTIONS– NO PROOF YET.
The article “Drink plenty of fluids “ a systematic review of evidence
for this recommendation in acute respiratory infections” is misleading.
The authors also have not reviewed the studies available in adults and
animal models of pneumonias. The authors observe “giving increased fluids
to patient with respiratory infection may cause harm”, and comment that
“fluid restriction may be appropriate management.” They base their
recommendation on frequent occurrence of hyponatraemia in lower
respiratory infections and higher risk of death in those with severe form
of hyponatremia. Implicit in the above recommendation is the assumption
that hyponatraemia caused deaths. With the current evidence this
assumption is not tenable; a cause and effect relationship can not be
assigned between hyponatraemia and death. It is equally possible that
hyponatraemia was a marker of severe illness. In all the four patients who
died, hyponatraemia was present at admission, and had nothing to do with
fluids that they received.1 These patients had more severe disease, a
point that was emphasized in the original paper.1 Indeed, hyponatraemia
occurs more frequently in all kinds of seriously ill patients irrespective
of the primary diagnosis.2
Hyponatraemia in patients with pneumonia and bronchiolitis has been
attributed to impaired water excretion3-5. However, fluid restriction
across the board in all the patients with respiratory infection may not be
justified as about two thirds of patient with pneumonia or bronchiolitis
do not have hyponatremia Why should they be given restricted fluids?
Moreover, in all the patients hyponatraemia may not be because of water
retention. An important mechanism of hyponatraemia in critically ill
patients is translocation of sodium from extracellular to intracellular
space, and leakage of intracellular solutes, so called ‘sick cell
syndrome. In a recent study in critically ill adults an accumulation of
non-diffusible osmotically active solutes in plasma, measured was
increased `osmolar gap’, was observed in more than 50% of hyponatraemic
patients.6 In experimental model of sepsis Hannon and Boston showed
significant intracellular shift of sodium and suggested that hyponatraemia
and hypo-osmolality in sepsis was caused by intracellular shift of sodium
and dilution of extracellular space as a result of water retention.7 We
found a significant increase in RBC sodium and impaired sodium-potassium
pump coinciding with hyponatraemia in septicemic children.8 In another
study we found that intracellular (RBC) sodium was significantly increased
in hyponatraemic patients with pneumonia while it was normal in
hyponatraemic patients having acute diarrhoeal illness (unpublished data).
None of these arguments is directed towards advocating liberal fluid
therapy in lower respiratory infections. Plasma volume expansion resulted
in increased extravascular lung water in a canine model of pneumococcal
lobar pneumonia9 and increased the extent of pneumonia in a canine model
of acute Pseudomonas pneumonia.10 If one is inclined to use fluid
restriction, perhaps it should be confined to hyponatremic patients and
that too after correcting hypoxemia. A study published in 1970 had shown
that an expansion of plasma volume in acute phase of pneumonia in elderly
patients improved cardiac output and decreased arteriovenous oxygen
difference.11 However, one cannot be categorical on either side. One
should take a balanced approach till such time that randomised controlled
studies answer the question.
References
1. Dhawan A, Narang A, Singhi S. Hyponatremia and the inappropriate
ADH syndrome in pneumonia. Annals of Tropical Paediatr 1992; 12: 455-62.
2. Singhi S, Prasad SV, Chugh KS. Hyponatremia in sick children: A marker
of serious illness. Indian Pediatric 1994; 31: 19-25.
3. Dreyfuss D, Leviel F, Paillard M, Rahmani J and Coste F. Acute
infectious pneumonia is accompanied by a latent vasopressin-dependent
impairment of renal water excretion. Am Rev Respir Dis 1988;138:583-589.
4. Gozal D, Andrew A. Water, electrolyte and endocrine homeostasis in
infant with bronchiolitis. Pediatr. Res. 1990;27:204-209.
5. Podder U. Singhi S, Ganguli NK, Sialy R. Water and electrolyte
homeostasis in acute bronchiolitis. Indian Pediatr. 1995;32:59-65.
6. Guglielminotti J, Pernet P, Maury E, Alzieu M, Vanbourdolle M, Guidet
B, et al. Osmolar gap hyponatremia in critically ill patients: Evidence
for sick cell syndrome? Crit Care Med 2002; 30: 1051-1055.
7. Hannon RJ and Boston VE. Fluid and ion redistribution in skeletal
muscle in an animal sepsis model. J Pediatr Surgery, 1990;25:599-603.
8. Suri M, Kumar L, Kaur G, Singhi S and Prasad R. Electrolyte
disturbances due to ouabain sensitive sodium potassium pump in
erythrocytes of children with sepsis. Indian J Med Res 1997;105:67?71.
9. Hanly P, Light RB. Plasma volume expansion and PEEP in a canine
model of acute Pseudomonas pneumonia. Lung 1989; 167: 285-99.
10. Cooligan T, Light RB, Wood LD, Mink SN. Plasma volume expansion in
canine pneumococcal pneumonia. Its effect on respiratory gas exchange and
pneumonia size. Am Rev Respir Dis. 1982; 126: 86-91.
Competing interests:
None declared
Competing interests: No competing interests