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PARALYTIC ILEUSBy L. P. LE QUESNE, D.M., F.R.C.S.

Department of Surgical Studies, The Middlesex Hospital

Established paralytic ileus, with gross distensionand severe water and electrolyte depletion, is nolonger a common post-operative complication.Nonetheless, bearing in mind those cases of frankileus that still occur, and all those patients whodevelop ' wind' to a greater or lesser extent afteroperation, it is apparent that the problem of thereturn of normal intestinal motility after operationis one that demands conscious attention. Ofgreatest importance after abdominal operations,the problem is not confined to this branch ofsurgery, for ileus may develop after operations onthe urinary system, on the female pelvic organs,and on the spine, and rarely following injury to thespine or abdominal organs or as a complicationduring the administration of certain drugs (e.g.mecamylamine hydrochloride).For many years the clinical features and patho-

logical changes in paralytic ileus have been wellrecognized, but it is only comparatively recentlythat its aetiology has been understood and that ithas been possible to plan rational prophylaxis andtreatment. To a considerable extend the confusionsurrounding the condition has stemmed from itsmisleading name. Paralytic ileus is, in fact, afunctional obstruction of the intestines, withmarked distension, usually of the entire small andlarge gut, by gas and fluid. Accordingly, the twomain questions to be faced are: (i) Why is there afunctional obstruction? (2) Why are the in-testines distended? The statement of the problemin this form is important: in the past a failure todo so has led to a number of theories whichpostulate a flaccid paralysis of the intestines, result-ing in no clearly defined way in a passive distensionof the gut. But set out in this form much of themystery is removed and replaced by two relativelyclear-cut questions.

AetiologyThe Functional Obstruction

After every abdominal operation there is aninhibition of intestinal motility which lasts for aperiod which is in general in direct proportion tothe severity of the operation. Peritonitis is accom-panied by a similar inhibition which relents as the

peritonitis clears up. These facts can be simplyverified by auscultation of the abdomen, and thereis, in addition, experimental evidence to the sameeffect. Wakim and Mann (I943) carried out ex-periments on dogs with exteriorized loops of in-testine and showed that after a laparotomy undergeneral anaesthesia there was complete abolitionof intestinal activity for at least four hours andthat normal activity did not return for 24 hours,whilst after an operation involving division andanastomosis of the intestines activity was abolishedfor 42 hours, after which peristalsis slowly returnedand regained its normal activity by the sixth day.Information about the activity of the human gutafter operation is not so complete, but Bisgard andJohnson (1939), by recording pressure changes inswallowed balloons, have shown a diminution inintestinal motility after operation, and Davis andHansen (1945) demonstrated that barium traversedthe intestine more slowly after operation than innormal circumstances. Devine (1946) has alsoshown, by the use of intestinal balloons, thatintestinal motility is inhibited after operation andthat on their return contractions are at firstirregular before the re-establishment of normalperistalsis.

This post-operative diminution in intestinalmotility is not due to an actual paralysis of the gutmusculature, but to a reflex inhibition of itsactivity. Speaking in general terms, peristalsis isan inherent property of the intestines dependentupon the intramural nerve plexuses, with theextrinsic sympathetic and para-sympathetic nervesonly exercising a controlling influence. Thus peri-stalsis can occur in a denervated loop of intestine,and in a normally innervated loop stimulation ofthe para-sympathetic supply increases peristalticactivity whilst sympathetic stimulation depressesor completely inhibits muscular contractions. Thedepression of gut motility occurring after operationis not due to any interference with the intrinsicmechanism of the intestine, but is a reflex phe-nomenon mediated via the sympathetic and can betemporarily abolished by paralysis of the sym-pathetic nerves. If a spinal anaesthetic is given to apatient during the period of absent peristalsis,

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active gut movements immediately return andflatus may be expelled. This must mean that theabsence of peristalsis is not an intrinsic condition,but is reflexly imposed on the bowel. The afferentimpulses presumably arise as a result of irritationof the peritoneum, or from emotional stimuli (ileusis more common in nervous than placid patients),or from direct irritation of the nerves, thus account-ing for the inhibition after injuries or operationson the spine and retroperitoneal structures (i.e.kidney).A period of reflex inhibition of intestinal

motility is then a normal occurrence after allabdominal operations and may occur after variousother procedures, and it is only when distension issuperadded that so-called paralytic ileus develops.It is important to remember that the ' paralytic'feature of the condition is a normal occurrenceafter many operations, so that the crucial problembecomes, why do some patients, in addition,develop distension, causing either 'wind' or, insevere cases, full-blown paralytic ileus.

The Cause of DistensionThe answer to the problem is to be found in a

consideration of the nature of the distension. Thefluid in the distended gut consists of intestinaljuices and it is the gas which forms the crux of theproblem. There are three possible ways in whichgas can accumulate in the bowel, namely, by de-composition of intestinal contents, by diffusionfrom the blood gases, and by the swallowing of air.It appears that in paralytic ileus (i.e. functionalobstruction), as in cases of organic obstruction,the last of these routes is the important one. Threelines of evidence lead to this conclusion. Perhapsthe most striking is the experimental evidence ofMcIver et al. (I926), who produced peritonitis incats by the intraperitoneal injection of faeces andthen killed them 28 hours later. As expected,autopsy showed a generalized peritonitis with dis-tension of the intestines as far down as the colon:however, if at the time of the injection of faeces thepylorus was occluded by ligature, then at autopsyno distension was found. Further evidence isprovided by analysis of the gas in the intestine incases of ileus. This shows, first, the presence ofonly small quantities of hydrogen sulphide andmethane, which would be expected in large quanti-ties if decomposition was the main source; and,secondly, that some 8o per cent. of the gas consistsof nitrogen, with rather more C02 and less 02than is present in air. These findings are preciselythose that would be expected if swallowed air isthe source of the gas. The rate at which gases areabsorbed from the intestine depends upon theirrelative tension in the blood and intestinal lumen,and the composition of air is so similar to the blood

gases that once the 02 and C02 have reachedequilibrium further absorption takes place onlyvery slowly. McIver et al. (1926) distended loopsof cats' intestines with various gases and foundthat, whereas °2 and CO2 are rapidly absorbed,nitrogen is only taken up slowly and, as would beexpected from this, that air is absorbed at approxi-mately the same rate as nitrogen.The final argument is provided by the clinical

evidence that if after operation careful steps aretaken to minimize the passage of air into theintestines, then ileus can be largely prevented.This point has been investigated by many workers.Typical results are those of Davis and Hansen(I945), who compared two groups of patientsundergoing a variety of abdominal operations, onegroup being treated by continuous gastric suctionafter operation, the other not receiving this treat-ment; they found that only io per cent. of thetreated group became distended after operation, ascompared to 29 per cent. of the controls.

This conclusion that the gas in the distendedintestines is air implies that it must have beenswallowed. At first sight inherently improbable,this is, in fact, what most probably occurs. Paine,Carlson and Wangensteen (I933) observed a seriesof patients who were treated after operation bycontinuous gastric suction. They found that on anaverage 2,000 ml. of air per day were aspiratedfrom patients undergoing appendicectomy orhernia repair, 3,000 ml. per day from those havingoperations on the biliary tract, and 3,500 ml. fromthose having gastric operations. Admittedlyobtained from patients with indwelling tubes, thesefigures nonetheless emphasize the unexpectedlylarge quantities of air which may be swallowed inthe first few days following operation.The mechanism by which this swallowing takes

place has been elucidated by Maddock and hisco-workers in two papers (Morris et al., I947;Maddock et al., 1949) which repay close study.In summary they have shown that the swallowingof air is normally prevented by the cricopharyngeusmuscle and that if during inspiration this muscle isrelaxed, then air readily passes into the oesophagus,from which it is propelled into the stomach. Thisprocess is much accentuated if at the time ofswallowing the glottis is closed. Maddock showedthat in this process, which he refers to as ' air-sucking,' the average normal oesophageal pressureof -6 cm./H20 is converted to-3 I cm./H20, andthat practised ' air-suckers ' swallowed into theirstomachs over ioo ml. of air with each suck, whilstsubjects who could not belch at will nonethelessswallowed 6o ml. of air when making an inspiratoryeffort against a closed glottis. He further showedthat subsequent belching does not remove as muchair as is swallowed, so that the repetition of these

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movements can lead to rapid distension of the.stomach.Many nervous people regularly swallow air and

belch when upset and it is a common clinicalobservation that patients complaining post-opera-tively of wind also often complain of flatulence, andsay that if only they could get the wind up theywould feel better. In fact, in their efforts to breakwind these patients simply swallow more air, andcareful observation shows that many more patientsthan is commonly realized indulge in this trickafter operation, presumably stimulated thereto bythe discomfort following surgery.

The Effects of DistensionNormally if air is swallowed or introduced into

the stomach it passes through the intestine veryrapidly. First demonstrated by Magnusson (I93I),this has since been confirmed by many workers,notably again Maddock (Maddock et al., 1949),who showed that on the average swallowed airtakes some I5 minutes to reach the caecum andthat it appears as flatus in 25 minutes. However,air swallowed after operation will enter not anormal alimentary tract, but one in which peri-stalsis is markedly inhibited; as a result its passagewill be impeded and some degree of distensionmust occur. Now distension of the intestines,especially if marked, produces a series of effectswhich tend both to exacerbate the distension andcause further inhibition of gut motility. Theseeffects may be summarized as follows: first, kink-ing of the intestine is caused, adding some degreeof mechanical obstruction; secondly, distensionof one part of the small intestine causes inhibitionof all types of movement in the rest of the gut,as a result of reflexes passing via the extrinsicnerves of the intestine (Youmans et al., 1938);thirdly, over-stretching of the gut musculaturefurther impairs its ability to contract; and,fourthly, there is an increasing interference withthe venous return from the distended loops,leading to further troubles. Thus, it causes anincreased exudation of plasma into the peritonealcavity and into the wall and lumen of the gut; itcauses an increased secretion and diminishedabsorption of intestinal juices, leading to theiraccumulation in the gut, which is so marked afeature of both organic and functional obstruction;and, finally, it threatens the viability of the dis-tended loop, again interfering with its motilityand eventually leading to necrosis and perforation.

Additional FactorsThere are several other factors which un-

doubtedly predispose to the development of ileus.Mecray, Barden and Ravdin (I937) have shownthat in hypoprotinaemic dogs the gastric emptying

time is delayed and that there is oedema of the gutwall, which may well interfere with its motility,and it is possible that protein deficiency explainsthe clinical observation that patients in a poornutritional state are particularly prone to the con-dition. It is also possible that vitamin deficienciesmay interfere with gut motility, Jacques (I951)suggesting that a deficiency of pantothenic acidmay be ofimportance and claiming excellent resultsfrom its administration in cases of establishedileus. But of far greater importance are the acutedeficits of water and electrolytes so commonly seenin patients with ileus, their importance lying notso much in their being primary aetiologicalfactors, but in their tendency to predispose to andexacerbate the condition. Most of the currentinterest centres around the effects of potassiumdepletion, but it must not be forgotten that altera-tions in water and salt balance can influence gutmotility. As long as 20 years ago several workers(Perazzo, I937) showed that alterations in theplasma concentration of sodium altered gutmotility, and more recently Marriott (I947) hascommented on the greatly delayed gastric emptyingtime seen in patients with salt depletion.The possible connection between paralytic ileus

and potassium deficiency was first suggested byRandall et al. (I949), who described three typicalcases of post-operative potassium deficiency, all ofwhom, amongst other signs, showed markedchronic ileus. The association between the twoconditions is now well recognized. On the onehand, it is a common clinical experience to findthat patients with established ileus are hypo-kalaemic and improve when they receive potassium;and, on the other hand, ileus is a characteristicmanifestation of potassium depletion (Lans et al.,1952). Some workers have gone so far as to suggestthat potassium deficiency is indeed the cause ofparalytic ileus. Streeten and Ward McQuaid(1952), in a study of 13 cases, found that duringthe period of ileus there was an excess urinary lossof potassium, with a lowering of the plasma con-centration, and that during recovery there was aretention of potassium. They suggested that para-lytic ileus is due to potassium deficiency, in itsturn due to prolonged adrenocortical activity inthe face of an inadequate potassium intake.Streeten and Vaughan Williams (I952) investigatedthe same point experimentally in dogs and foundthat the production of a severe intracellularpotassium depletion caused a marked depressionof gut motility, but the conditions produced inthese experiments varied in important respectsfrom those seen clinically.There is no doubt that potapsium depletion

depresses gut motility, that in some cases of severeileus the administration of this ion is essential to

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recovery, and that in any case of prolonged ileus theexistence of potassium depletion should always beconsidered. There is no real evidence, however,that potassium depletion in itself can cause trueileus, though it is without doubt an important sub-sidiary factor in that by depression of gut motilityit may convert a case of severe ' wind ' into one oftrue ileus and seriously prolong and aggravate theestablished condition.To summarize, the underlying factor in the

aetiology of paralytic ileus is a period of reflexinhibition of gut motility occurring after manyoperations. Usually this passes off uneventfully,but may not do so if the patient is an air swallower.If only moderate quantities of air are swallowed,nothing worse will ensue beyond so-called post-operative' wind '; but if excessive air is swallowedor the impairment of gut motility is unduly pro-longed, distension will become marked and avicious circle set up, leading to frank ileus. Potas-sium depletion, by virtue of its depression of gutmotility, is an important subsidiary factor whichmay precipitate and prolong ileus. In that ileusleads to severe losses of water and electrolytes, theeffect of potassium depletion is both progressiveand cumulative.

Clinical FeaturesThe clinical picture of paralytic ileus is too well

known to require detailed description. In the earlystages distension is the prominent sign, but as thecondition progresses vomiting becomes increasinglymarked and with it the well-known stigmata ofwater and electrolyte depletion, until in the enddeath ensues as a result of peripheral circulatoryfailure and toxic absorption from the distended,devitalized intestine. Apart from distension, themost significant abdominal sign is the completesilence on auscultation of the abdomen, brokenonly by an occasional tinkling, high-pitched noteresulting from passive movement of the intestines.If necessary, the diagnosis may be confirmed byX-ray, plain films of the abdomen showing acharacteristic picture with fluid levels in both smalland large intestine. It may be very difficult todecide whether or not the ileus is accompaniedby an actual peritonitis, and in the presence ofgreatly distended intestine careful judgment isneeded to determine the significance of tendernessand rebound tenderness, but if these are marked,and particularly if localized, they probably indi-cate the presence of peritonitis.On occasion it may be difficult to differentiate

between paralytic ileus and plastic peritonitisgiving rise to complete or partial organic obstruc-tion of the intestines at multiple sites from fibrinousadhesions. Both conditions tend to develop afteran incident of general peritonitis and their clinical

picture may be similar. However, ileus usually-comes on two to four days afterwards, whilstobstruction due to plastic adhesions develops later,often eight to io days after the peritonitis. Pain,as opposed to discomfort, is unusual in ileus, butif the obstruction is essentially organic there willgenerally be some intestinal colic, at least in theearly stages, with increased bowel sounds. Further,in organic obstruction radiology will generallyshow no gas in the large gut, as opposed to itsgeneralized distribution in ileus.

TreatmentPreventionAs previously emphasized, the critical aetiological

factor in paralytic ileus is the. development ofdistension. This is much more easily preventedthan it is controlled and relieved when once it has-developed. Accordingly, in clinical practice theemphasis must be, not on treatment, but onprophylaxis, and particularly the prevention ofdistension.

Considering first pre-operative measures, ex-cessive purgation during the days immediatelyprior to operation should be avoided and if the-bowel requires emptying a simple enema is prefer-able. Secondly, ileus is particularly likely todevelop in nervous, highly-strung patients, and itis important that such people receive adequate-sedation before operation; despite their mild de-pressant effect on the bowel, barbiturates in suit-able doses are invaluable for this purpose. Thirdly,.and of greater importance than these simple points,if the intestines are distended they should, when--ever possible, be deflated before operation is under-taken. In many cases the nature of the disease willnot allow of delay in surgery, but when this ispossible great benefit can come from deferring-operation whilst the intestine is deflated by suctiondown a Miller-Abbott or Ryle's tube. It is im-possible to lay down rules for how long such treat-ment should be persevered with, but, providedcare is taken to see that there is no progressive,intra-peritoneal inflammatory process and that the-patient's fluid and electrolyte equilibrium ismaintained, there is usually little or no harm incontinuing intestinal suction for several days.There is no doubt that if complete deflation of theintestine can be achieved the operation itself willbe much simpler and the patient's recoverysmoother.The anaesthetist also has an important part to

play in preventing ileus, as he can, unless careful,allow considerable quantities of air to enter thestomach. Maddock et al. (I949) showed that during-the smooth induction of an inhalational anaesthetic-only a negligible quantity of air enters the stomach,but in a patient who became obstructed during-

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induction 720 ml. of air were aspirated from thestomach. This consequence of an obstructed air-way is not generally recognized and is an additionalreason for maintaining a clear airway duringanaesthesia. Modern anaesthetic techniques alsohave their special danger, in that under certaincircumstances positive pressure anaesthesia canforce air down the gullet into the stomach, par-ticularly if positive pressure is applied via a face-piece to a patient receiving muscle-relaxant drugs.Accordingly, every effort should be made to avoidusing positive pressure, except down an endo-tracheal tube. Both these points are well-acceptedanaesthetic teaching, but their neglect may lead toserious consequences after operation.

During the course of the operation, to diminishirritation of the peritoneum the intestines shouldbe handled as little and as gently as possible, andcare should be taken to minimize soiling of theperitoneum with bowel contents, pus, etc. If it isessential to open the abdomen with distendedintestines, whenever possible these should be de-flated before the abdomen is closed. This can bedone quite safely by inserting a sucker into the gutthrough a small opening and then evacuating thefluid and gaseous contents by threading the in-testine over the sucker. In addition to facilitatingclosure of the abdomen, there is good clinicalevidence that this procedure is of great value inpreventing ileus in this type of case, and it is awise rule never to close the abdomen over distendedintestines unless there is some urgent contra-indication to this simple manoeuvre.

It is, however, the management after surgerythat is of supreme importance in preventing ileus,particularly in cases undergoing major abdominalsurgery or with definite peritonitis. The stomachmust be kept empty, or at the very least preventedfrom distension, until such a time as normalmotility has returned to the intestines. This canonly be done by restricting the fluid intake bymouth, and possibly in addition by carrying outgastric suction, until such time as normal bowelsounds return and the patient passes flatus eitherspontaneously or with the aid of glycerine sup-positories. The restriction of fluids by mouth aftermajor abdominal surgery is so well known as toneed no further comment. The place of suction is,however, more controversial. Some authoritiesrecommend gastric suction routinely after allmajor abdominal operations, whilst others onlyuse it when ileus is impending or established. Acompromise between these two views is probablythe best. It is wise to start suction immediatelyafter operation in all cases where there is extensivehandling of the intestines or where there is definiteperitonitis, but in other cases it seems justifiableto watch the patient's progress and then pass a

tube if there is any significant distension, if thepatient is nauseated or vomits, or shows pronouncedaerophagy. Once started, suction should continueuntil bowel sounds have returned and the oralbalance shows that fluids are passing on normallyinto the intestine. If at this stage flatus has notbeen passed, a glycerine enema or suppositorieswill usually produce the desired result. Laxativesare contraindicated, as they may retard the returnof normal bowel motility.

This compromise policy mnay on occasion allowdefinite distension, even mild ileus, to develop, butit saves many patients from the discomforts of anaso-gastric tube and, provided such a tube ispassed promptly if there are any signs of ileusdeveloping, little harm is likely to occur. It seemsto make little difference whether the tube isaspirated continuously or intermittently, providedthe intervals between aspiration do not exceed onehour. If 30 to 6o ml. of water are given by mouthdirectly after aspiration the intermittent methodshows at once when the stomach starts to emptyitself, and continuous suction is only requiredwhen large quantities of air or fluid must beremoved. Some authorities advise that a Miller-Abbott tube should be passed into the intestinebefore operation and used post-operatively for pro-phylactic aspiration. Save for the purpose ofrelieving pre-operative distension, this seemsillogical, as it is obviously preferable to remove theair from the stomach before it has got into theintestines, and it is not unknown for it to benecessary, with a tube well down in the intestines,to pass a Ryle's tube as well to control distension.

Generally it will only be necessary to restrictoral fluids and use gastric suction for two to threedays after operation, but during this time the fluidand electrolyte balance must be maintained, usuallyby giving intravenous fluids in appropriate quanti-ties (Le Quesne, 1957). Of great interest in respectto the prevention of ileus is the question as towhether this intake should contain potassium. Ifnone is given, a potassium deficit must necessarilydevelop, this being accentuated by the potassiumdiuresis, which occurs in the first 24 to 48 hoursafter operation. As mentioned, a potassium deficitundoubtedly predisposes to ileus, and it seemsillogical to allow such a deficit to develop and thenperhaps later have to treat its results. It is un-necessary and possibly unwise to give potassiumfor the first 24 to 48 hours after operation, but ifintravenous fluids must be continued thereafter itis quite safe if the usual precautions are taken. Areasonable intake is 6 g. KCI (8o m. Eq K) per 24hours, and this is conveniently given together withthe daily ration of salt (4.5 g.; 8o m.Eq Na) in2 1. of 2.5 per cent. dextrose. It is wise to take atleast two hours running in each 0.5 1. of this

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solution. During the last four years we have giventhis solution to a very large number of patients.No complications have been found to arise fromthis treatment and balance studies show that thisintake prevents the development of any significantdeficit without the risk of a dangerous retention ofpotassium. It is difficult to prove that by thismeans many cases of ileus have been prevented,but it is our clear clinical impression that this isso and it certainly prevents the development ofsevere potassium depletion.

The Established CaseBy application of the measures outlined it should

be possible to prevent most patients developingflorid ileus with severe distension and fluid losses.Cases will be met with in which the motility of theintestines is unduly slow in returning, who developsome degree of distension and who lose consider-able quantities of fluid by suction, but it is usuallypossible to prevent the development of classicalileus provided suction is persevered with and thefluid intake maintained, with adequate replace-ment of abnormal losses. Patience is essential inhandling these cases. It is preferable to continue' drip and suction' for 24 hours too long than 24hours too little, as if too much is given orally tooearly or the bowels stimulated by purgatives ordrugs before peristalsis is re-established the returnof normal bowel function can be distinctly re-tarded. In some cases the long delay of return ofbowel function raises the possibility that there maybe an organic obstruction, due probably toadhesions. It is probably wise only to operate onsuch cases when there is strong evidence of organicobstruction and a laparotomy in the hope of findingsome situation capable of correction is rarely ofbenefit. It is in cases of this sort that the possibilityof a potassium deficit must be carefully considered,particularly if none has been given. Whilst clinicalevidence can suggest most strongly this diagnosis,it should always be confirmed by estimation of theserum potassium concentration, and an E.C.G.may be helpful. If confirmed, the deficit should bereplaced in the usual way (see Le Quesne, 1957, fordetails of diagnosis and treatment of K depletion).The treatment of established ileus is essentially

similar to its prophylaxis. In the past manysurgeons have advocated the use of active measuresdesigned to stimulate the gut by the use of tur-pentine or ox-bile enemata, the administration of aspinal anaesthetic, or the use of drugs, such aspitocin or carbachol. In some cases these methodsmay achieve success, presumably by breaking thevicious circle caused by increasing distension. Butsuch treatment is illogical, usually ineffective, andoften positively harmful. The intestines cannot be

made to resume"normal peristalsis and attempts todo so are more likely to delay than expedite thenatural return of function. But recovery can beencouraged by preventing the entry of further airinto the intestines, by relieving distension, and bycorrecting any disturbances in fluid and electrolytebalance.These objects are achieved by gastro-intestinal

suction and by the intravenous administration offluids. Again there is the question as to whetherto use a gastric or Miller-Abbott tube. Theprotagonists of this latter tube argue that if itpasses the pylorus it will deflate the upper coil ofthe bowel, which will then regain its peristalticactivity and push the tube into the next loop andso on down the bowel. The difficulty lies in gettingthe tube to pass the pylorus when the alimentarytract is immotile, and even when this has beenachieved the tube will not prevent the furtherswallowing of air. Most surgeons find that astomach tube passed into the intestine is simplerand just as effective. By this means further entryof air into the intestines can be prevented and,owing to regurgitation, sufficient deflation can beachieved to allow of recovery of peristalsis.

Aside from suction, the most important part ofthe treatment of established ileus lies in the restora-tion and maintenance of fluid and electrolytebalance. This involves all the problems connectedwith the assessment and replacement of pre-existing deficits of salt and water, the replacementof observed losses, and the diagnosis and treatmentof potassium depletion. These problems lie outsidethe scope of this paper, but it must be emphasizedthat, despite the great importance of potassiumdepletion in ileus, the correct handling of thepatient's water and sodium balance remains ofparamount importance and demands first con-sideration.A further problem arises with respect to the

use of sedatives, especially morphia, in the treat-ment of paralytic ileus. There is still controversyregarding the effect of morphia on the motility ofthe gut, but it is probable that, in man, it diminishesperistalsis whilst increasing the tone of the in-testine. In view of this it is sometimes argued thatthe drug is contraindicated in patients with ileus,but this is to overlook its powerful central effects,which are essentially beneficial in that they allayapprehension, relieve pain and ensure rest topatients badly in need of all these. The weight ofclinical evidence undoubtedly supports the viewthat morphia is a drug of the utmost value in thesepatients and that only benefit can come from givingit in adequate dosage, both in the prevention andtreatment of paralytic ileus.Bibliography continued on page 6a6

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abnormal losses, the making good of her estab-lished deficit, blood transfusion and ultimately thegiving of her post-operative fluid requirements.At her second operation recurrence of the

disease was found in the terminal ileum and thesigmoid colon was also severely affected. A ter-minal ileostomy was therefore established, whichfurther increased the need for intravenous fluidreplacement.

This infusion was maintained for a total of 17days and transmitted a total of 50 1. of fluid,including blood. There were no complicationsand the patient was intensely grateful for her vena

caval infusion, having had the experience of aconventional superficial vein infusion at the timeof her first operation.

SummaryI. The technique of introducing intrav'enous

fluids direct into the venae cavae by means of apolythene cannula is described.

2. The indications for using this technique andits advantages are discussed.

3. The results are given of a series of cases inwhich this method has been used.

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Continued from page 6i i-Paralytic Ileus: L. P. Le Quesne. D.M.. F.R.C.S.BIBLIOGRAPHY

BISGARD, J. D., and JOHNSON, E. K. (1939), Ann. Surg.,II0, 8o2.

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