May I955 STAPLETON: Fluid Balance in Intestinal Obstruction in Infancy and Childhood 227

ones during the post-operative period; the writerhas seen serious trouble from this cause.

Acute appendicitis with peritonitis. The straight-forward case of appendicitis diagnosed early doesnot require any intravenous fluids. Once severeperitoneal irritation has occurred,. there is anincreased danger of paralytic ileus developing.In treating such cases intestinal suction is used.The volume of fluid aspirated must be replacedby the intravenous route, giving the solution ofsodium and potassium chloride described earlier.

In summary, fluid balance can be maintained

in intestinal obstruction in children without manylaboratory investigations, so long as the measure-ments of the volumes of fluid removed by suction,lost at operation, and given intravenously aremade accurately.

BIBLIOGRAPHYDODD, K., and RAPOPORT, S. (I950), ' Mitchell-Nelson Text-

book of Pediatrics,' sth edition, p. 20z; W. B. SaundersCompany.

GROSS, R. E., and FERGUSON, C. C. (I952), Surg. Gynaec. &Obstet., 95, 631.

KEMPTON, J. J. (195g), Brit. med. J., i, 1140.LEE, C. M. (I951), Ann. Surg., I34, io66.

FLUID BALANCE IN INTESTINALOBSTRUCTIONBy L. P. LE QUENE, F.R.C.S.

Department of Surgical Studies, Middlesex Hospital, London, W.I

The last 20 years have seen a great improve-ment in the results of treatment of patients withacute intestinal obstruction. In the main thisimprovement is due to an increasing understandingof the importance of the two basic pathologicaleffects of obstruction, namely, intestinal disten-sion, and the loss from the body of large quantitiesof fluid and electrolytes. It is now well recog-nized that in the treatment of intestinal obstructionthe relief of this distension and the replacementof fluid losses play as great a part in the successfuloutcome of the case as the release of the obstruc-tion itself. In many cases the management of thepatient's water and electrolyte equilibrium willpose very complex problems, and in all cases anexact analysis of the exchanges taking place willrequire intricate biochemical calculations, butthese considerations must not be allowed toobscure the fact that the great majority of thesecases can be successfully handled by attention toa few simple concepts.The Nature of the Fluid LossesThe crux of the problem of the maintenance of

fluid and electrolyte equilibrium in patients withintestinal obstruction consists in the assessmentand replacement of the abnormal losses whichoccur from the alimentary tract. These abnormallosses consist of the secretions into the intestinalcanal, which accumulate proximal to the obstruc-tion and are to a varying extent vomited up, or

TABLE I

Source Volume

Saliva .. .. .. . 1500 ccs.Gastric secretion .. .... 2500 ccs.Bile .. .. .. .. .. 500 ccs.Pancreatic juice .. .. 700 ccs.Secretion of intestinal mucosa .. 3000 ccs.

Total .. .. .. .. .. 8200 ccs.

Normal Plasma Vol . . .. 3500 ccs.

The normal volume of digestive juices secreted per24 hours, by an adult. (From Gamble, 1950.)

removed by intestinal suction. Certain salientfacts about these secretions must be borne inmind. First, the total volume of fluid secretedinto the alimentary tract each 24 hours amountsto over 8 litres (Table i). When it is remem-bered that the normal circulating plasma volumeis only 3 litres, it is apparent that losses from theintestine can readily and rapidly lead to a danger-ously large fluid deficit. Secondly, such lossesconsist not of water but of a solution of electrolyteswhich, though varying in composition in eachsecretion, is in all of them essentially isotonicwith the plasma electrolytes. Fig. x shows thecomposition of these secretions in their pureform, but as lost from the body in intestinalobstruction they are, of course, diluted to avariable extent by ingested water, and Table 2

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228 POSTGRADUATE MEDICAL JOURNAL May I955

HCQ

CI

"'c'-"'": ';

BLOOD GASTRIC GASTRIC PANCREATIC HEPATIC DUCT JEJUNALPLASMA JUICE MUCUS JUICE BILE SECRETIONS

FIG. i.-Composition of the intestinal secretions in their pure form (from Gamble, I950).

TABLE 2

Source Na m.eqiv./L. K m.eqiv./L. C1 m.eqiv./L.Stomach .. .. .. 60.4 9.2 84.0

(9 to ii6) (0.5 to 32.5) (7.8 to I54.5)Small Bowel (M-A Suction) .. 11.3 4.6 104.2

(82 to I47.9) (2.3 to 8.o) (43 to I37)Ileostomy (Recent) .. .. 129.4 I1.2 16.2

(105.4 to I43.7) (5-9 to 29.3) (90 to I36.4)Ileostomy (Adapted) .. .. 46 3.0 21.4Caecostomy .. .. .. 52.5 7-9 42.5Formed Stool .. .. .. < o < I < 5Bile .. .. .. .. .. I48.9 4.98 ioo.6

(I3I to 164) (2.6 to 12) (89 to 117.6)Pancreatic Juice .. .. . 4I.1 4.6 76.6

(II3 to 153) (2.6 to 7.4) (54.1 to 95.2)(From Lockwood and Randall, 1949)

TABLE SHOWING THE ELECTROLYTE LOSSES IN FLUIDS FROM VARIOUS PARTSOF THE ALIMENTARY TRACT

The upper figure is an average, whilst those in brackets show the range of observed values.

shows the composition of the losses from thevarious portions of the alimentary tract as theyoccur in clinical practice: even under these cir-cumstances the fluids, particularly a mixture ofgastric and intestinal juices, are nearly isotonic andso must be replaced, not by water or dextrosesolutions, but by an appropriate electrolyte solu-tion. Thirdly, it is important to remember thatthese intestinal fluids contain potassium in a con-centration up to three times that in the plasma,so that their loss from the body can cause a rela-tively large potassium deficit which may wellrequire replacement.

The Effect of Losses from the AlimentaryTractAs a result of the loss from the body of these

intestinal fluids and also because of the interferencewith the normal intake caused by the obstruction,there will develop a combined deficit of water andsalt (sodium). The clinical picture will thereforecontain the features of both these deficits, but inorder to recognize the significant features of thismixed state it is necessary to consider separatelythe fundamentally differing effects of water deple-tion and salt depletion. Initially water depletioncauses hypertonicity in the extracellular space,

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May 1955 LE QUESNE: Fluid Balance in Intestinal Obstruction 229

o\

i/ 0

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: * 0 0* °e - -

INTRACELLULAR ENTRACELLULARDEHYDRATION DEHYDRATION

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FIG. 2.-Diagrammatic representation of the difference between water and salt depletion. The bodywater is represented as a tank, divided into the smaller extracellular space and larger intracellularspace: the dots represent the ions in solution. Water loss initially causes extracellular hypertonicity;to compensate for this there is a shift of water out of the cells, resulting in intracellular dehydration.Salt loss initially causes extracellular hypotonicity; this is compensated for partly by a shift of waterinto the cells, but mainly by a renal excretion of water, leading to extracellular dehydration. (Repro-duced from the author's ' Fluid Balance in Surgical Practice,' by kind permission of Messrs. Lloyd-Luke (Medical Books), Ltd., London.)

leading to a shift of water out of the intracellularspace and so resulting in intracellular dehydration:by contrast, salt (sodium) depletion causesinitially an extracellular hypotonicity, leading toan excretion of water by the kidneys in an effortto restore extracellular tonicity, and so resulting inextracellular dehydration (see Fig.2). This extra-cellular dehydration does not result in equal con-traction of the two portions of the extracellularspace, namely, the interstitial space and theplasma space, as at first the osmotic force of theplasma proteins maintains the plasma volume atthe expense of the interstitial space; but as thecondition progresses this mechanism eventuallybreaks down, resulting in a contracting plasmavolume and finally peripheral circulatory failure.

These differences in the type of dehydrationcaused are reflected in the different clinical andbiochemical effects of the two losses (see Fig. 3).

The predominant clinical feature of water deple-tion is increasing thirst, and there are no strikingphysical signs: as would be expected the urine issparse, with a raised specific gravity (above I.oio)and a high salt content; as the brunt of the lossfalls on the intracellular space there are nosignificant changes in the blood chemistry untillate in the condition, when there will be a steadyrise in the haemoglobin, plasma protein and plasmaelectrolyte concentrations, the only exception tothis being the blood urea concentration whichwill rise steadily from the start owing to theinadequate urine output. In salt depletion thirstis noticeably absent, but as the condition pro-gresses the patient becomes increasingly lethargicand nauseated, with postural giddiness andeventually extreme weakness. In the early stagesthe important physical findings are dryness of theskin and mouth with diminishing skin elasticity,

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230 POSTGRADUATE MEDICAL JOURNAL May 1955

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FIG. 3.-The tank represents the extracellular space, divided into its two component portions, the larger interstitialspace and smaller intravascular (or plasma) space. The dots represent the ions in solution and the circles theplasma proteins. The containers to either side represent the urine output. In water depletion there is a scantyurine output of high specific gravity and electrolyte (chloride) content; late in the condition there is a rise in boththe plasma protein and plasma electrolyte figures. In salt depletion the urine output is copious of a low gravity,but the most significant finding is a lowered or completely absent electrolyte (chloride) content. In the earlystages of salt depletion the brunt of the loss falls on the interstitial space, but later the plasma volume falls markedly:the plasma protein concentration rises steadily throughout the condition, but only late is there a significant fall inthe plasma electrolyte figures. (Reproduced by kind permission of the editors of the Proceedings of the RoyalSociety of Medicine.)

and later as the blood volume begins to fall therewill be postural hypotension progressing to thecomplete picture of peripheral circulatory failure.Provided there is no associated water depletion theurine volume will be within normal limits untillate on, of a low specific gravity, but with adiminished or absent chloride content (normal,> 3om.eq/l.). The most significant blood findingsare a steadily rising haemoglobin and plasmaprotein concentration, and it is only late in thecondition that the plasma electrolyte concentra-tions fall; it cannot be too strongly emphasizedthat a large deficit of sodium and/or chloride canreadily exist with normal plasma levels of theseions. As in water depletion, the blood urea willshow a steady rise, particularly late in the conditionwhen there is an interference with renal function.Two other effects of the loss of intestinal fluids

require note. As already mentioned, in some ofthe intestinal secretions the concentrations ofsodium and chloride are not equal, so that lossesof these fluids can lead to disproportionate deficitsof either sodium or chloride, resulting in an acid-base disturbance. In most cases of intestinalobstruction the fluid lost is a mixture of thevarious secretions containing essentially equivalentamounts of sodium and chloride (Table 2), so that

the problem does not arise, and even in the fewcases in which an acid-base disturbance does com-plicate the picture it rarely requires specific treat-ment. A further complication is provided by thedeficit of potassium which may arise as a resultof severe losses from the alimentary tract. Themain effect of this deficit is to lead to markeddepression of muscular activity resulting in themuscular hypotonus, the paralytic ileus, thelowered plasma K level, and the E.C.G. changeswhich together form the important diagnosticfeatures of the condition. It is now apparentthat in many cases of obstruction the recognitionand replacement of such a potassium deficiency isof great importance, but nevertheless in all casesthe problem of overriding importance is thecorrect replacement of the salt and water deficitand this must always receive prior attention.

The Aims of TreatmentIn nearly every case of intestinal obstruction it

is necessary to give the patient his fluids intra-venously or by some other parenteral route. Theaim of this treatment is twofold, to provide thepatient with the normal daily requirements ofwater and electrolytes, and in addition to replacequantitatively the abnormal fluid loss from the

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LE QUESNE: Fluid Balance in Intestinal Obstruction

intestines. The administration of a reasonablebasic daily intake is the first requirement in thetreatment of patients with fluid and electrolytedisturbances. This basic intake is designed toreplace the normal loss of water and electrolytesfrom the skin and lungs, and from the kidneys asurine. Such requirements are met by an intakeof 3 litres of water containing 4-5 g. of NaCl per24 hours. This can be given quite simply intra-venously by giving each 24 hours 21 litres of5 per cent. dextrose and 0.5 litre of normal saline,and provided there are no abnormal losses thisallows of a urine output of about I,500-1,700 ml.per 24 hours, of a specific gravity below I.oIo,and with a chloride concentration of about40 m.eq/l. Under normal circumstances thereis much to be said for adding some potassium tothe basic intake, but this should only be donewhen there is a good urine output. In most casesof intestinal obstruction, at least in the earlystages, the urine output is sparse so that such anaddition is not permissible, and accordingly it iswiser to omit potassium from the basic intake inthese cases, and to give it when indicated as partof the quantitative replacement of abnormal losses.It cannot be stressed too strongly that the regularadministration of a sensible, daily intake is theessential first step in the management of fluiddisturbances arising in intestinal obstruction.Additional fluids will be required to replace theabnormal loss from the intestines, but suchreplacement is useless unless superimposed upona regular, rational provision for the losses bynormal routes.

The Replacement of Abnormal LossesIn the replacement of the abnormal losses from

the alimentary tract two distinctly different prob-lems arise. When a patient with intestinalobstruction comes under treatment he is likely tohave an established deficit of water and electrolytes,due mainly to losses into and from the alimentarytract and partly to an inadequate or absent basicintake since the start of the illness. Once treat-ment has been started there should be no furtherdeficit owing to an inadequate basic intake, butthe abnormal losses may well continue for severaldays. These 'observed losses' which occurwhilst the patient is under treatment can to agreat extent be measured, and their replacementis comparatively simple. But the ' pre-existinglosses' cannot be measured, so that their assess-ment and replacement creates a much moredifficult problem. In clinical practice the replace-ment of both these losses must go on simul-taneously, but they involve such different niethodsthat they must be considered separately.The first step in the replacement of pre-existing

losses is to arrive at an estimate of their size andtype. There is no one single test which will givethis information, which can only be obtained bya careful clinical and biochemical examination ofthe patient. The object of this examination is todetect the stigmata of water and salt depletiondescribed previously, and to dissect out from thewhole picture the evidence indicative of one orboth of these deficits. In this process care mustbe taken not to get overwhelmed in a mass ofdetailed and possibly conflicting information andit is important to concentrate upon the essentialsigns. In the clinical examination the signs ofsalt depletion should be carefully looked for, andit must not be forgotten that in itself this deficit,when marked, can cause peripheral circulatoryfailure. In the urine the finding of a specificgravity above .I015, provided there is no sugarpresent, is practically diagnostic of water deple-tion, and a chloride concentration below 2o m.eq/l.is equally strong evidence of salt depletion (butsee below for effect of operation on these findings).The most important observations on the blood arethe estimation of the haemoglobin and/or plasmaprotein concentrations, which will be raised in saltdepletion, and of the blood urea which is a verysensitive index of depletion as it is raised by bothsalt and water deficits. In assessing the signifi-cance of the haemoglobin figure the possibility ofa co-existent anaemia must be remembered. Ingeneral, plasma electrolyte concentrations needonly be estimated in complicated cases, and itmust be clearly recognized that large deficits ofboth salt and water can exist with normal plasmaelectrolyte concentrations. On the basis of thehistory and the findings just reviewed it will bepossible to decide on the type of deficit present orpredominating, and some estimate of the size canusually be made. In reaching this last figure,which can only be approximate, it is useful toremember that when the signs of depletion areobvious the deficit amounts to about 5 per cent.of the body-weight, so that under these circum-stances an average-sized man (70 kg.: II stone)will be short of at least 4 litres of fluid, of whichat least half will be an extracellular deficit requiringreplacement by saline.Once an estimate of the size of the pre-existing

deficit has been arrived at the requisite amount of5 per cent. dextrose and normal saline should beadded to the basic intake over the ensuing 24-48hours. Every case must be considered as atherapeutic trial, and it is only by the repetitionof the initial examinations and tests that theadequacy of the treatment can be judged andfurther additions made as indicated. The processof replenishment may be considered completewhen there are no longer any clinical signs of

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POSTGRADUATE MEDICAL JOURNAL

depletion, when the urine volume is normal, witha chloride concentration in excess of 40 m.eq/l.and a specific gravity below I.o0o, and when theblood chemistry is steady within normal levels.The replacement of observed losses is a much

simpler problem. All abnormal losses from thealimentary tract must be accurately measured andthen replaced volume for volume with normalsaline. In view of the fact that the intestinallosses are somewhat hypotonic this method ofreplacement is likely to give somewhat too muchsalt, so that if in any 24-hour period the abnormallosses exceed 2 litres, the fifth i-litre bottle ofreplacement fluid should consist of glucose notsaline. In practice it is most convenient to makethese adjustments to cover observed losses every12 hours, adding to the intake for the ensuing12-hour period an amount of saline equal to theabnormal losses during the previous 12 hours.Thus every 12 hours the intake for the next periodis calculated by adding to the basic intake (a) anyfluid required to replace a pre-existing deficit,(b) any fluid required to replace observed losses,and the adequacy of the intake can be accuratelychecked by observations on the urine volume,etc., as explained in the last paragraph.Potassium Depletion

Patients with intestinal obstruction are liable todevelop potassium depletion for two reasons: (a) thelosses from the alimentary tract contain potassiumin a concentration up to three times that in theplasma (Table 2), and (b) there is a constant lossof potassium from the kidneys, which do not con-serve this ion very zealously, even when the intakeis zero; further, if the patient has to undergo anoperation the loss in the urine will be greatlyincreased by the potassium diuresis which alwaysoccurs in the first 48 hours post-operatively.Experience in the past has shown that themajority of patients with intestinal obstructionwill recover without any attention being paid tothis potassium deficit, but in the minority it cer-tainly can and does give rise to serious trouble.Accordingly, it is wise to be constantly aware ofthis possibility and whenever possible to administerpotassium before a serious deficit has developed.

Potassium depletion should always be suspectedin any patient who has abnormal losses over aperiod of days during which the intake of this ionis negligible or zero. Clinically the diagnosiswill be suggested by muscular weakness andhypotonia, and the development of a chronic ileus,and it can be confirmed either by the presence ofcharacteristic E.C.G. changes (for a description ofthese changes see Lewis, Somerville and LeQuesne, 1954), or by a lowering of the serum Klevel. The normal serum K concentration is

3.9-4.5 m.eq/l., and findings below 3.5 m.eq/l. arehighly suggestive of a deficit. Whenever possiblepotassium salts should be given by mouth, andthey should not be given intravenously in the:presence of a marked deficit of water or salt, orto any patient who has an inadequate urine output(less than I,ooo ml. per 24 hours) or poor renalfunction. Accordingly, in the treatment of pre-existing losses the first requirement is the replace-ment of the salt-and-water deficit, and it is onl:when this has been done that the potassium deficitshould be sought for and treated if required. Inthe replacement of observed losses it is onlynecessary to add potassium to the replacementfluid if the losses continue for over 48 hours, orare in excess of 2 litres in any given 24-hourperiod, though again this addition must only bemade if the urine output is adequate. Apart fromthose already mentioned, certain other pre-cautions should be taken when giving potassiumsalts intravenously. The total daily dosage shouldnot exceed 80 m.eq., the concentration in whichthey are given should not exceed 40 m.eq/l., andthe rate of administration should not be in excessof 20 m.eq/hr. As regards the actual solutionsused, considerable experience has shown the fol-lowing two simple formulae to be most useful:(I) NaCl 2.25 g. per litre, KCI 3.0 g. per litre(K 40 m.eq/l., Na 40 m.eq/l., C1. 80 m.eq/l.), and(2) KC1 3.0 g. per litre (K 40 m.eo/l., Cl 40m.eq/l.). Of these two, the first is particularlyuseful, and can be used with great advantage inthe volume for volume replacement of observedlosses, and in many cases we have given 2 litresof this solution per 24 hours with no trouble,though it is wise to control such treatment withdaily serum K estimations until considerableexperience has been obtained.

The Effect of OperationThe management of fluid and electrolyte

balance in patients with intestinal obstruction isdistinctly complicated if, as in many cases, anoperation must be carried out. Such an operationwill be followed by the usual metabolic responsewhich follows all surgical operations. The mostimportant features of this response may be sum-marized as follows: (a) For 24-48 hours there isan impaired ability to excrete water, accompaniedby a diminished urine flow of raised specificgravity and electrolyte concentration; and (b) forup to 4-5 days after a major operation there is animpaired ability to excrete salt; after the initialinterference with water excretion has passed offthis is manifested by a markedly lowered concen-tration of electrolytes in the urine. As a result ofthese manifestations of the metabolic response toa surgical operation many of the features which

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May 1955 LE QUESNE: Fluid Balance in Intestinal Obstruction 233

are usually used as guides in the management of afluid and electrolyte deficit temporarily lose theircustomary significance, especially the relationshipbetween fluid intake and urine output, the urinespecific gravity and the urine chloride concentra-tion. Thus, usually the finding of a low urineoutput of high specific gravity is indicative ofwater shortage, but such findings 24 hours afterrelease of a strangulated hernia would carry nosuch significance as they would most likely, undersuch circumstances, be no more than a manifesta-tion of the patient's normal response to an opera-tion. Further, if these findings are interpreted asindicating water shortage and the intake is in-creased, serious trouble may ensue, for, as aresult of the temporarily impaired ability toexcrete water, any excess water will not beexcreted but will be retained in the body. Similarconsiderations apply with respect to the urinechloride concentration after operation.As a result of these changes certain precautions

should be taken in the post-operative period.First, during the first 24-36 hours after operationthe basic intake of water should be restricted to 2litres per 24 hours. Secondly, during this period theonly reliable guides to management offluid disturb-ances are the clinical condition of the patient anda careful recording of the intake and output bythe various routes. Thirdly, owing to the dangerof overloading, deficits of salt and water shouldbe replaced cautiously. Fourthly, in the absenceof imperative indications potassium salts shouldnot be given intravenously during the first 36hours after operation, owing to the low urineoutput during this period. Lastly, these con-siderations emphasize the importance, wheneverpossible, of replacing pre-existing deficits beforeoperation. Quite apart from the undesirability ofsubmitting a patient to surgery whilst still depleted

of water and electrolytes, the process of replenish-ment is much easier before than after operation.ConclusionThe management of many cases of intestinal

obstruction will entail consideration of manyfactors not discussed in this brief article. Thus,in cases complicated by strangulation of bowel, itmay well be necessary to give blood, plasma or aplasma substitute. Again, the actual technicalproblem of administering fluids intravenously overseveral days may require the use of special tech-niques, such as the passage of a polyethylenecatheter up into one of the great veins. Or thepatient may have diabetes mellitus or somekidney disease, which in themselves disturb thenormal metabolism of water and electrolytes.However, such considerations must not beallowed to distract attention from the main pur-poses of treatment, namely, the administration ofa rational basic intake, the assessment and replace-ment of pre-existing losses, and the measurementand volume-for-volume replacement of observedlosses. In general all this can be achieved andcontrolled by quite simple clinical and biochemicalmethods, of which none exceeds in importance thekeeping of accurate intake and output records-well designed and accurately maintained fluidbalance charts form an essential background totreatment in all cases, and in many they provideall the information that is required for successfultreatment.

BIBLIOGRAPHYGAMBLE, J. L. (I95o), 'Chemical Anatomy Physiology and

Pathology of Extracellular Fluid,' Cambridge, Mass. (HarvardUniversity Press).

LEWIS, A. A. G., SOMERVILLE, W., and LE QUESNE, L. P.(I954), Arch. Middx. Hosp., 4, io6.

LOCKWOOD, J. S., and RANDALL, H. T. (I949), Bull. N.Y.Acad. Med., 25, 228.

RUTHIN CASTLE, NORTH WALESA Clinic for the diagnosis and treatment of Internal Diseases (except Mental or Infectious Diseases). The

Clinic is provided with a staff of doctors, technicians and nurses.The surroundings are beautiful. The climate is mild. There is central heating throughout. The annual

rainfall is 30.5 inches, that is, less than the average for England.The Fees are inclusive and vary according to the room occupied.

For particulars apply to THE SECRETARY, Ruthin Castle, North Wales.Telegrams: Castle. Ruthin. Telephone: Ruthin 6

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