hypoaritmia

7/27/2019 hypoaritmia

1/3

1999;318;1363-1364BMJNick Lane and Kathryn AllenHyponatraemia after orthopaedic surgery

http://bmj.com/cgi/content/full/318/7195/1363Updated information and services can be found at:

These include:

References

http://bmj.com/cgi/content/full/318/7195/1363#otherarticles9 online articles that cite this article can be accessed at:http://bmj.com/cgi/content/full/318/7195/1363#BIBLThis article cites 8 articles, 2 of which can be accessed free at:

Rapid responses

http://bmj.com/cgi/eletter-submit/318/7195/1363You can respond to this article at:http://bmj.com/cgi/content/full/318/7195/1363#responsesfree at:

29 rapid responses have been posted to this article, which you can access for

serviceEmail alerting

the top left of the articleReceive free email alerts when new articles cite this article - sign up in the box at

Topic collections

(1277 articles)Other nutrition and metabolism

(347 articles)Orthopaedic and Trauma Surgery(112 articles)General Surgery

Articles on similar topics can be found in the following collections

Notes

To order reprints follow the "Request Permissions" link in the navigation box

http://resources.bmj.com/bmj/subscribersgo to:BMJTo subscribe to

on 24 September 2007bmj.comDownloaded from
http://bmj.com/cgi/content/full/318/7195/1363http://bmj.com/cgi/content/full/318/7195/1363http://bmj.com/cgi/content/full/318/7195/1363http://bmj.com/cgi/content/full/318/7195/1363#otherarticleshttp://bmj.com/cgi/content/full/318/7195/1363#otherarticleshttp://bmj.com/cgi/content/full/318/7195/1363#BIBLhttp://bmj.com/cgi/content/full/318/7195/1363#BIBLhttp://bmj.com/cgi/eletter-submit/318/7195/1363http://bmj.com/cgi/eletter-submit/318/7195/1363http://bmj.com/cgi/eletter-submit/318/7195/1363http://bmj.com/cgi/content/full/318/7195/1363#responseshttp://bmj.com/cgi/content/full/318/7195/1363#responseshttp://bmj.com/cgi/collection/others_nutrition_and_metabolismhttp://bmj.com/cgi/collection/others_nutrition_and_metabolismhttp://bmj.com/cgi/collection/orthopaedic_and_trauma_surgeryhttp://bmj.com/cgi/collection/others_nutrition_and_metabolismhttp://bmj.com/cgi/collection/orthopaedic_and_trauma_surgeryhttp://bmj.com/cgi/collection/orthopaedic_and_trauma_surgeryhttp://bmj.com/cgi/collection/orthopaedic_and_trauma_surgeryhttp://bmj.com/cgi/collection/general_surgeryhttp://resources.bmj.com/bmj/subscribershttp://resources.bmj.com/bmj/subscribershttp://resources.bmj.com/bmj/subscribershttp://resources.bmj.com/bmj/subscribershttp://bmj.com/http://bmj.com/http://bmj.com/http://resources.bmj.com/bmj/subscribershttp://bmj.com/cgi/collection/others_nutrition_and_metabolismhttp://bmj.com/cgi/collection/orthopaedic_and_trauma_surgeryhttp://bmj.com/cgi/collection/general_surgeryhttp://bmj.com/cgi/eletter-submit/318/7195/1363http://bmj.com/cgi/content/full/318/7195/1363#responseshttp://bmj.com/cgi/content/full/318/7195/1363#otherarticleshttp://bmj.com/cgi/content/full/318/7195/1363#BIBLhttp://bmj.com/cgi/content/full/318/7195/1363


2/3

Hyponatraemia after orthopaedic surgeryIgnorance of the effects of hyponatraemia after surgery is widespreadanddamaging

Iatrogenic injury is an unfortunate reversal of thephysicians role. To cause the death or brain dam-age of a patient has to be the physicians worst

transgression, particularly if the causes are well known,simple, and reversible. Each is true of acute postopera-tive hyponatraemia, but, despite repeated warnings, thecondition remains common. According to a recentestimate based on prospective and retrospectivestudies, 20% of women who develop symptomatichyponatraemia die or suffer serious brain damage,totalling 10 000-15 0000 cases every year in the UnitedStates and Western Europe.1

An elderly female friend of ours is a classicexample. Some months ago she underwent a routineknee replacement operation. Before the operation herblood sodium concentration was 134 mmol/lborderline hyponatraemiaattributable to her longterm use of thiazide diuretics. After the operation shevomited frequently and received 6 litres of 5% dextrosesaline over two days before passing into a coma. Herblood sodium concentration measured on the second

day after surgery was 115 mmol/l, but electrolytedisturbance was disregarded by the orthopaedicdoctors as a potential cause of coma until the medicalteam were called the next day. Sodium concentrationswere restored to 134 mmol/l over five days, leaving ourfriend with mildbut permanentcognitive impair-ment. The hospital concerned apologises unreserv-edly but confessed ignorance about the risks ofhyponatraemia after joint replacement surgery.

Although the literature is full of similar examples,too many orthopaedic surgeons seem unaware of thedangers of hyponatraemia or its characteristic neuro-logical symptoms. Perhaps the reason lies partly in thescatter of relevant publications: most of the articles are

published in journals dedicated to neurology, urology,and acute care; only a handful of reports refer specifi-cally to orthopaedic surgery24; and neither the RoyalCollege of Surgeons nor the British OrthopaedicAssociation publishes guidelines. Many articles focuson tightly defined issues, such as the associationbetween thiazide diuretics and hyponatraemia,2 to theexclusion of a more general overview. As a result, fourfundamental problems have arisen: clinicians fail torecognise patients at high risk of hyponatraemia; disre-gard the dangers of routine infusions of hypotonicfluids; confuse early symptoms of hyponatraemia withpostoperative sequelae; and attribute the serious

neurological symptoms of hyponatraemic encepha-lopathy to other conditions such as stroke.

Postoperative hyponatraemia is provoked by surgi-cal stress, which causes a syndrome of inappropriateantidiuretic hormone in almost everyone, oftenpromoting water retention for several days. 5 6 Womenare more affected than men, as a result of their smallerfluid volume and other sex related hormonal factors.5

Premenopausal women and children are prone tobrain damage at sodium concentrations as high as128 mmol/l. Postmenopausal women do not usuallybecome symptomatic until sodium concentrationshave fallen below 120 mmol/l, although normal symp-toms can occur at higher levels if the rate of change israpid.57 Importantly, normal ageing impairs fluidhomoeostasis and therefore increases the risk of majorperturbations in sodium and water balance, especiallysevere hyponatraemia.7 The risk of hyponatraemiaamong elderly people is compounded by chronicdiseases and long term medications. In particular,many women requiring orthopaedic surgery also take

thiazide diuretics to control hypertension.

2

Thiazidesare well known to induce mild hyponatraemia andhave been linked to the rapid onset of serious post-operative complications.2 3

Women at risk of hyponatraemia are imperilled byroutine infusions of isotonic dextrose. Patients recover-ing from surgery metabolise glucose almost immedi-ately, so isotonic dextrose infusions are in effecthypotonic. Since the 1950s numerous reports havelinked hypotonic infusions with death or permanentbrain damage in postoperative patients.1 Recentauthoritative reviews warn against routine infusions ofdextrose,1 6 8 even stating explicitly: the rationale forusing hypotonic fluids in postoperative patients is diffi-cult to discern and has no place in the modern practice

of medicine.1

Volumes as low as 3-4 litres over twodays may cause convulsions, respiratory arrest, perma-nent brain damage, and death in women who werehealthy before admission.5 8 Most of these cases gounrecognised and are ascribed to conditions such asstroke, arteriovenous malformation, subarachnoidhaemorrhage, or herpes encephalopathy, even whenblood sodium concentrations are known.8

Early symptoms of hyponatraemia (such asweakness, nausea, vomiting, and headache) can bedistinguished from postoperative sequelae on thebasis of sodium concentrations. Timing also helpsdiscrimination: many patients tolerate surgery without

Saturday 22 May 1999

BMJ

BMJ 1999;318:13634

1363BMJ VOLUME 318 22 MAY 1999 www.bmj.com

http://bmj.com/http://bmj.com/http://bmj.com/http://bmj.com/


3/3

complications, being able to talk, walk, and eat beforesymptoms of hyponatraemic encephalopathy develop.1

Treatment is simple and should be prompt: the risk ofnot treating acute cerebral oedema far exceeds thesmall risk of osmotic demyelination from treatment.1 6

Fluid infusions should be restricted to normal orhypertonic saline and sodium concentrations moni-tored every two hours.1 5 6 The aim is to raise serumsodium by 1-2 mmol/l per hour (depending on the

severity of neurological symptoms) until symptomsresolve.1 6 A loop diuretic such as frusemide (furosem-

ide) may be used to enhance free water excretion andhasten the restoration of normal sodium concentra-tions. 1 6 Iatrogenic hyponatraemia is inexcusable. It istime that doctors woke up to the risks.

Nick Lane Honorary research fellow

University Department of Surgery, Royal Free and University CollegeMedical School, London NW3 2QG ([email protected])

Kathryn Allen Honorary research associate

Department of Neurochemistry, Institute of Neurology, LondonWC1N 3BG

1 Fraser CL,ArieffAI. Epidemiology,pathophysiology and managementofhyponatremic encephalopathy. Am J Med1997;102:67-77.

2 Malin JW, Kolstad K, Hozack WJ, Rothman RH. Thiazide-inducedhyponatremia in the postoperative total joint r eplacement patient. Ortho-

pedics1997;20:681-3.3 Tolias CM. Severe hyponatraemia in elderly patients: cause for concern.

Ann R Coll Surg Engl 1995;77:346-8.4 Hornick P,AllenP.Acute hyponatraemiafollowing totalhip replacement.

Br J Clin Pract 1990;44:776-7.

5 Ayus JC, Arieff AI. Brain damage and postoperative hyponatremia: therole of gender. Neurology 1996;46:323-8.

6 Kumar S,Berl T. Sodium. Electrolyte quintet. Lancet1998;352:220-8.7 Miller M. Hyponatremia: age-related risk factors and therapy decisions.

Geriatrics1998;53:32-42.8 Arieff AI. Hyponatremia, convulsions, respiratory arrest, and permanent

brain damage after elective surgery in healthy women. N Engl J Med1986;314:1529-35.

Dietary management of hepatic encephalopathy

Too many myths persist

Myths are difficult to dispel and may delay goodevidence based clinical practice. This isillustrated well by a paper in this weeks issue

on the dietary management of hepatic encephalopathyin patients with cirrhosis (p 1391).1 Protein restriction insymptomatic patients with hepatic encephalopathy hasbeen the cornerstone of treatment since the 1950s,2 yetthere is no evidence that it has any clinical benefit.

Hepatic encephalopathy is a syndrome of impairedmental status and abnormal neuromuscular functionwhich results from major failure of liver function.Important factors contributing to it are the degree of

hepatocellular failure, portosystemic shunting, andexogenous factors such as sepsis and varicealbleeding.3 The pathogenesis of the syndrome is stilluncertain, although current hypotheses includeimpaired hepatic detoxification of ammonia absorbedfrom the gut4 and an increase in aromatic amines,which are precursors for false transmitters in thebrainfor example, octopamineand which alter thebalance between neuronal excitation and neuronalinhibition.5 Furthermore, increased expression ofbenzodiazepine receptors in hepatocellular failuresuggests that the -aminobutyric acid-benzodiazepineinhibitory neurotransmitter system may be implicatedin the development of hepatic encephalopathy.6

Protein restriction as a treatment convenientlybegan with 20 g protein/day and, with clinical recovery,10 g increments were introduced every 3-5 days, as tol-erated by the patient, to a limit of 0.8-1.0 g/kg bodyweight3; this was considered sufficient to achieve apositive nitrogen balance. This practice continuesdespite evidence showing that patients with stablecirrhosis have a higher protein requirement than nor-mal, around 1.2 g/kg dry body weight to remain inpositive balance.7

Protein energy malnutrition, defined by anthropo-metric criteria, may occur in 20-60% of patients withcirrhosis depending on the severity of the liver disease.8

It is a common finding, with causative factors whichinclude anorexia, nausea, malabsorption, and a hyper-metabolic state. Intake may be further reduced by useof unpalatable low protein diets, already restricted insodium and fluid.

In 1997 the European Society for Parenteral andEnteral Nutrition published consensus guidelinesrecommending that the daily protein intake in patientswith liver disease should, if possible, be around 1.0-1.5 g/kg depending on the degree of hepaticdecompensation.7 The guidelines also recommendedthat in patients who were intolerant of dietary protein

0.5 g protein/kg should be used transiently and thatthe remainder of their requirements should beachieved by giving branched chain amino acids.9 How-ever, not all studies agree on the use of branched chainamino acids.10 Furthermore, aggressive enteral nutri-tional support of patients with alcoholic liver diseaseaccelerates improvement without exacerbating hepaticencephalopathy.11 Taking smaller meals more oftenand eating a late evening meal also improve nitrogenbalance without exacerbating hepatic encepha-lopathy.12 This may also be achieved with vegetableprotein as opposed to animal proteins.13

The dilemma for the clinician arises in patientswith acute hepatic encephalopathy, where increasing

protein intake may worsen the condition in 35% ofpatients.4 Use of branched chain amino acids mayimprove nitrogen balance but without producing anyclinical improvement in the encephalopathy.9 How-ever, there is no consensus about the rate at whichdietary protein should be reintroduced and at whatclinical stage this is appropriatethe key points for theclinician.

Soulsby and Morgan provide recent evidence ofperpetuation of the myth of protein restriction inpatients with encephalopathy and, perhaps morealarmingly, that this therapy is used in patients with cir-rhosis who have no neuropsychiatric impairment.1 We

Editorials

Papersp 1391

BMJ 1999;318:13645

1364 BMJ VOLUME 318 22 MAY 1999 www.bmj.com

http://bmj.com/http://bmj.com/http://bmj.com/http://bmj.com/

Documents

hypoaritmia