1034 S.A. MEDICAL JOURNAL 8 December 1962

POSTOPERATIVE DISTURBANCES IN PULMONARY VENTILATION*J. C. NICHOLSON, F.F.A.R.C.S., Johannesburg

RESPIRATORY OBSTRUCTION

OR DEPRESSION

Fig. 1. Simplified diagram illustrating the vicious circlesof hypoxia and hypercapnia with the possible escapemechanisms.

* Based on a paper presented at the 43rd South AfricanMedical Congress (M.A.S.A.), Cape Town, 24 - 30 September1961.

THE IMMEDIATE POSTOPERATIVE PERIOD

Briefly summarized, the two main dangers at this stageare obstruction to the respiratory passages, which is pre­disposed to by the loss of reflex tone in the musclesguarding the upper respiratory tract, and depression ofpulmonary ventilation, which may have a complex andvariable aetiology, but in which drugs used in connectionwith the anaesthetic often play an important part. Thetwo, conditions are often present together and, when thisis the case, each necessarily aggravates the effects of theother. Both obstruction and depression interfere with the

two main functions of breathing, thus leading to hypoxiaand hypercapnia, either of which, if not relieved, becomesa vicious circle with further deterioration of pulmonaryventilation (Fig. 1).

There are natural defence mechanisms by which escapefrom these vicious circles is possible in favourable cir­cumstances (Fig. 1). Hypoxia causes reflex stimulation ofpulmonary ventilation through receptors in the aortic andcarotid bodies before the respiratory centre succumbs tothe effects of oxygen lack; and a raised carbon-dioxidetension in' the blood is a powerful respiratory stimulantbefore depressant concentrations are reached. Unfor­tunately, if pulmonary ventilation is already seriouslydepressed by drugs or other agencies, these compensatorymechanisms may not be much in evidence and, withprogressive hypoxia and hypercapnia, death from respi­ratory failure is inevitable in the absence of effectiveintervention.

The prevention and management of postoperative respi­ratory obstruction is largely a matter of competent super­vision, but depressed pulmonary ventilation is a morecomplex and insidious factor from which, broadly speaking,serious complications may arise in two ways:

(a) From an error in the assessment of the adequacyand permanence of the re-establishment of normalbreathing after anaesthesia.

Cb) From the development of postoperative apnoea orgrave respiratory depression requiring prolonged specializedtreatment with artificial pulmonary ventilation.

Both these problems will be discussed.

POSTOPERATIVE PULMONARY VENTILATION

The transition from pulmonary ventilation under anaes­thesia to normal breathing, after the discontinuation ofthe operation and anaesthetic, often involves considerableadjustment between the patient and his respiratory en­vironment during which conditions may favour the develop­ment of hypoxia and hypercapnia and may contribute toa faulty assessment of his pulmonary function. Maximumreadjustment is called for when the change is from passivepulmonary ventilation by intermittent positive pressure tonormal breathing in the atmosphere but, even whenspontaneous breathing has been allowed to continuethrougbout the operation, significant changes in the com­position of the respiratory medium, the physiologicaldead space, and the tidal and minute volumes have tobe considered.

Where rich oxygen mixtures have been used, it isobviously important to make sure that the patient does notbecome cyanosed when their administration is stopped.Further, the termination of the operation is frequentlyassociated with a temporary functional decline in pul­monary ventilation, often accompanied by a fall in bloodpressure. This is due mainly to cessation of surgical .stimu­lation while some reduction in the carbon-dioxide contentof the respiratory medium may be an additional factor.In a normal semi-closed anaesthetic, especially if an endo-

\~reSSlOnof

IHypercapniOl Pulmonary

~oti1at~o

Escape I::tY initialstimulation ofpulmonary venHationt¥ carbon dioxide. 1

/DepreSSiC\Pulmonary IHypoxia Iventlat~~

Escape t¥ reflexstim.Jation ofplimonary ventUationvia aortic & carotidbodies.

Complications affecting pulmonary ventilation constituteone of the most important causes of morbidity andmortality associated with surgery and anaesthesia. Themost dangerous time for the development of serious dis­turbances in pulmonary ventilation is the immediate post­operative period, especially before the return of conscious­ness.

While he is in the operating theatre, the patient'srespiratory requirements are a first priority to the anaes­thetist, but after his return to the ward there is oftena deterioration in the standard of treatment and supervisionthat is available at the very time when it may be mostneeded. So well-recognized is this danger that the provisionof special recovery wards for the postoperative manage­ment of surgical patients has come to be an acceptedessential in all modem hospital planning. Unfortunatelyit is likely to be many years before the ideals embodiedin this concept become a practical reality on a wide scaleand, in the meantime, the hazards concerned must con­stantly be borne in mind.

S.A. TYDSKRIF VIR GENEESKUNDE8 Desember 1962

tracheal tube is used, the flow of gases has an insufflationeffect which assists pulmonary ventilation and considerablyreduces the physiological de.ad space. In these circum­stances a very small tidal volume may be sufficient foradequate pulmonary ventilation, but may be insufficientwhen the patient is left to breathe in the surroundingair. The necessary adjustment to an increased tidal volumeusually takes place within a few minutes, but if pulmonaryventilation ha~ been unduly depressed, the change maybe delayed or prevented leading to the rapid developmentof hypoxia.

The use of muscle relaxants has emphasized the necessityof ensuring the normal return of both diaphragmatic andintercostal action at the end of the operation and, whenneostigmine is used for decurarization, sufficient time mustbe allowed to be certain that its effect is permanent. Thisprecaution is particularly important where the overalldose of relaxant has been considerable, or when the lastfraction has been given within half-an-hour of thetermination of the anaesthetic.

Premature and excessive sedation, after return to theward, may also be dangerous. Not only is pulmonaryventilation likely to be further depressed, but sometimesfull anaesthesia may be re-established. This may easilylead to disaster if the patient is not carefully watched.

Briefly, the end of the operation and anaesthetic marksan important period of readjustment during which care andpatience are essential to make sure that this readjustmenthas takeD place effectively.

CAUSES OF POSTOPERATIVE AP OEA

In the foregoing section the complications discussed havebeen relatively minor degrees of respiratory depressionwhich may become dangerous if not properly handled;but total apnoea (or something approaching it) may beapparent at the end of the operation and may requireprolonged special treatment with artificial ventilation.Many factors may cause or contribute to a 'postoperativeapnoea' but, in the majority of cases, the use of neuro­muscular block plays an important part, and the term wascertainly not widely used before the advent of the musclerelaxants. Since there is already an abundant literature onthe subject,l a brief summary of currently accepted viewswill suffice. It is convenient to divide the main aetiologicalfactors into the three groups:

1. DrugsDrugs are usually the precipitating cause of a post­

<operative apnoea. They may be centrally acting agents,used either with premedication or as part of the anaes­thetic, or peripherally acting muscle relaxants. A combined-effect is sometimes seen where neuromuscular block is.accompanied by injudiciously deep narcosis.

2. Errors in VentilationThe two possible errors in the artificial ventilation of

.a patient during anaesthesia are overventilation leading to:acapnia, and underventilation leading to hypercapnia.

Overventilation, by washing out CO2 from the blood,may cause temporary depression of breathing, but isunlikely to be an important cause of a prolonged andintractable apnoea, since subnormal pulmonary ventilationwill allow CO2 to build up again so that the condition

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will tend to right itself. Acapnia, therefore, doe not leaddirectly to a vicious circle, and its main significance ithat the patient must be carefully watched 0 that hypoxiais not allowed to develop.

Underventilation is much more erious because highconcentrations of CO2 are depressant It follows that, evenif hypoxia is avoided, inadequate pulmonary ventilationfrom this cause will mean that the patient has alreadyentered the vicious circle of hypercapnia.

It has been suggested that the stretch receptors in thelungs may be fatigued by the prolonged use of intermittentpositive-pressure ventilation, especially if overventilationhas been practised. Reflexes set up by rhythmically in­flating the lungs certainly play an important part inhelping to maintain respiratory quiescence during con­trolled breathing and it is possible that some sluggishnesson the part of the patient to resume active breathing mayresult To what extent this could be a major cause ofserious apnoea is, however, problematical.

3. Conditions in the PatientThis, in some respects, is the most important group,

since it comprises factors which may upset calculationsrelating to anaesthetic technique, especially in respect ofthe use of muscle relaxants. The condition from whichthe patient suffers which may contribute to postoperativerespiratory failure may arise from acute or chronicpathological changes or may be an inherent constitutionalfactor. Further, such factors may either pre-exist or developduring the course of the operation, and therefore cannotalways be anticipated. Without attempting to give a com­plete list of these factors, a few of the more importantones will be mentioned:

(a) Intestinal obstruction. Severe cases of intestinalobstruction are notorious for their liability to be followedby postoperative apnoea after the use of muscle relaxants.The features believed to be responsible are toxaemia,dehydration and electrolyte imbalance, especially potassiumdeficiency.2

(b) Emphysema. Although this condition has no directinfluence on the duration or intensity of neuromuscularblock, the increased dead space, the high threshold forC02, and the frequent dependence of these patients onsome degree of hypoxia as a normal respiratory stimulus,may present problems during the period of changeoverfrom intermittent positive-pressure ventilation to normalbreathing.

(c) Myopathies and neuropathies. The presence ofmyasthenia gravis greatly exaggerates and prolongs theeffect of d-tubocurarine or gallamine, which should neverbe used in these cases. Carcinomatous neuropathyS mayalso be associated with abnormal response to musclerelaxants, while the rare dystrophia myotonica,~ on tbeother hand, seems to react normally with relaxants, butprolonged apnoea may follow the use of small doses ofthiopentone in patients with this condition.

(d) Deficiencies in the serum pseudocholinesterase. Thismay be responsible for protracted apnoea following theuse of depolarizing relaxants. Patients with p eudo­cholinesterase deficiency often suffer from cacbexia,anaemia and impaired liver function, but may be, to allappearances, perfectly normal. It has been bown that

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1036 S.A. MEDICAL JOUR "AL 8 December 1962

there are two different forms of pseudocholinesterase,typical and atypical, and that the atypical form lacks thenormal ability to hydrolyse suxamethonium.5 The twoforms may be present in different proportions in differentindividuals, and investigation of a Canadian communityshowed 96'4% to have an adequate proportion of theactive form; 3·6% had a slight to moderate deficiency,and about 1 in 3,000 were grossly deficient. Sensitivityto suxamethonium appears to have a familial basis.s.7

(e) Circulatory failure. Patients suffering from shock,haemorrhage and toxaemia, may go into respiratoryfailure from the effects of medullary hypoxia, and circu­latory failure thus adds a central effect to the peripheralparalysis of the respiratory muscles by relaxants. Thereduced blood supply to the muscles also intensifies theeffect of the block itself.s In clinical practice circulatoryfailure, on account of the frequency with which it isencountered, is a very important factor in postoperativerespiratory complications.

THE SIGNIFICANCE OF POSTOPERATIVE APNOEA THE

GRAVELY ILL PATIENT

The wide general use of neuromuscular block with inter­mittent positive-pressure ventilation in anaesthesia, andeven more the successful long-term employment of thistechnique in the treatment of tetanus and poliomyelitis,tend to encourage the outlook that postoperative apnoeais an inconvenient, rather than a dangerous, complication.This view seems justified when one is dealing with reason­ably fit subjects and, in particular, the surprise apnoeaswhich sometimes follow the use of comparatively smalldoses of suxamethonium can be confidently expected torespond to patience and correct management, in thesepatients.

In gravely ill patients, on the other hand, apnoea maybe a dangerous complication and, in this class, there aremany postoperative deaths in which failure of pulmonaryventilation is a factor. Where muscle relaxants have beenadministered to such gravely ill patients, it is temptingto accept that respiratory failure is purely incidental andthis is doubtless often correct. In other instances, however,it seems to have more significance and the extent to whichthe supervention of this complication may swing thebalance is of considerable importance.

On theoretical grounds alone, it would be unwise tounderestimate the effect of a protracted postoperativeapnoea. Natural breathing is an important stimulus to thecirculation which the most elaborate methods of artificialventilation cannot entirely replace; the patient can illafford to dispense with this stimulus at the end of a longand severe operation. Although ventilation by intermittentpositive pressure is highly satisfactory in the presence ofa well-maintained circulation, this is not the case wherethere is a tendency to circulatory failure, since such venti­lation raises the intrapulmonary pressure, thereby obstruct­ing the return of blood to the left heart and furtherdecreasing the output. While its use during the operationis justified by the great advantages gained from theemployment of neuromuscular block, any protraction ofthe period of enforced artificial ventilation is veryundesirable.

In an attempt to throw further light on this problem,

cases from the records of deaths in association withanaesthesia at the Johannesburg General Hospital, cover­ing the past 12 years, have been studied. The criteriagoverning their selection were:

1. Muscle relaxants and intermittent positive-pressureventilation were employed in accordance with generallyaccepted techniques.

2. Death was in the immediate postoperative period(up to 36 hours) without the return of consciousness.

3. Apnoea (or grossly inadequate pulmonary ventilation)was apparent at the end of the operation.

While not a condition of selection, all the subjects werein the poor-risk category, often to a marked extent relativeto the operative procedures undertaken. In all, 15 caseswere studied and were found to fall naturally into one orother of 3 groups: (a) cases where exposure to hypoxiawas a possible factor, (b) cases showing primary respiratoryfailure, and (c) cases where progressive circulatory failurewas the dominant feature.

(a) Hypoxia a Possible Fact'or (4 Cases)In each case in this group, following the administration

of prostigmine, the patient's pulmonary ventilation wasjudged to have been sufficiently restored for him to bereturned to the ward but, thereafter, cardio-respiratorydeterioration manifested itself, from which recovery didnot take place.

The hiatus between the time of leaving the theatre andthe summoning of assistance leaves an unfortunate elementof doubt about the sequence of events, and the possibilitythat the patient was exposed to hypoxia cannot be dis­missed. Whether he would have survived, even withfull recovery-room facilities, is also a matter of purespeculation.

(b) Primary Respiratory Failure (3 Cases)These cases presented a clear picture of primary respi­

ratory failure, since apnoea was present from the begin­ning, but a fair circulation had been maintained for aconsiderable time by artificial ventilation. In view of thefact that failure of pulmonary ventilation undoubtedlypreceded circulatory collapse, the anaesthetic techniquemust at least be regarded as a precipitating factor.

(c) Circulatory Failure (8 Cases)This formed the largest group, and the subjects were

obviously in very poor condition relative to the operationsto which they were submitted; the dominant feature beingprogressive circulatory failure as the operation proceeded.If a patient to whom muscle relaxants have been adminis­tered becomes moribund during the course of the opera­tion, it will naturally be impossible to restore normalbreathing in the terminal stages and it is reasonable toaccept the failure of pulmonary ventilation as a purelyincidental factor. This view was further supported byseveral similar cases (not included in the series reviewed)in which secondary cardiac arrest occurred while theoperation was still in progress.Conclusions

The conclusions to be drawn from these observations arethat, although respiratory failure in the gravely ill patientis often nothing more than part of the general pictureof dissolution, postoperative apnoea, in this type of case.

Desember 1962 S.A. TYDSKRIF VIR GENEESKUNDE 1037

is an extremely dangerous complication which can meanthe difference between death and survival and which issomething the anaesthetist must be at great pains to avoid.In this respect, the cases in group (b) are particularlysignificant.

PREVENTION OF POSTOPERATIVE AP 'OEA

While much is now known about the causation and treat­ment of postoperative apnoea, the subject of its preventionappears to have received little attention. This is not sur­prising, for prevention belongs more to the art, as opposedto the science, of anaesthesia, where each case has to beassessed and handled on its own merits and the individualjudgement and experience of the anaesthetist are the vitalfactors. It is certain that different experts would havewidely different approaches to the problem, with muchthe same degree of success. No hard-and-fast rules canbe laid down and it is only possible to mention a fewgeneral principles:

1. Careful pre-operative observ~tion is necessary toavoid missing any signs or symptoms which might havea bearing on the patients' response to muscle relaxants orother drugs.

2. Where factors such as dehydration or electrolyteimbalance are present, every effort should be made tocorrect them 'before operation is undertaken.

3. Great caution in the use of muscle relaxants isrequired when dealing with certain types of case. Whilethis seldom amounts to an absolute contraindication, itmay be desirable to utilize every available means to limitthe total dose, and restraint is especially necessary in longand severe operations, particularly in the later stages. Tothis end, other methods of securing satisfactory relaxation

may be used and intercostal block, spinal or extraduralanaesthesia, may sometimes merit consideration.

4. With regard to general anaesthe ia it is well toremember that, of the methods available, inhalationanaesthesia has the greatest measure of flexibility and free­dom from cumulative depressant effects.

5. Finally, it is impossible to overemphasize the impor­tance of carefully as e sing the patient's respiratory con­dition at the end of the operation and keeping him underobservation, with appropriate treatment, if there is anysign of inadequate pulmonary ventilation.

SUMMARY

Serious disturbances of pulmonary ventilation usuallymanifest themselves in the immediate postoperative period.Danger to the patient may arise from: (a) failure torecognize a slight or moderate degree of respiratorydepression at the end of the operation, and the subsequentestablishment of a vicious circle of hypoxia and hyper­capnia; or (b) the presence of apnoea (or grossly inade­quate pulmonary ventilation) which fails to respond totreatment. .

In patients who are gravely ill, postoperative failure ofpulmonary ventilation is, in itself, a dangerous com­plication which is likely to hasten the onset of circulatoryfailure.

REFERENCES

1. Churchill-Davidson, H. C. (1959): Anesthesiology, 20. 535.2. Foldes, F. F. (1959): Ibid., 20. 464.3. Croft. P. B. (1958): Brit. Med. J., 1. 181.4. Dundee, J. W. (1952): Curr. Res. Anesth., 31, 257.5. Kalow, W. and Genest, K. (1957): Canad. J. Biochem .• 35. 339.6. Kalow, W. and Staron, N. (1957): Ibid.• 35. 339.7. Bush, G. H. (1961): Brit. J. Anaesth., 33. 454.8. Wylie, W. D. and Churchill-Davidsnn, H. C. (1961): A Practice of

Anaesthesia, p. 115. London: L1oyd-Luke.

INTRAMURAL HAEMATOMA OF THE DUODENUM

F. A. K. VAN WYK, M.B., CH.B., M.MED. (CHIR.) (PRET.), and A. M. GLEN, M.B., CH.B., F.R.C.S. (EDlN.), Pretoria

Intramural haematoma is a rare cause of duodenalobstruction. Other causes are congenital defects of theduodenum, annular pancreas, anomalies of rotation, neo­plasms of the duodenum and the ampulla of Vater, gall­stones and foreign bodies, the superior mesenteric arterysyndrome, and invasive tumours surrounding theduodenum.

The first report of a case of duodenal obstruction causedby intramural haematoma was that of MclaugWan in1838.1 The first patient to survive operation for anintestinal intramural haematoma was reported in 1914by VogeI,2 who evacuated a subserosaI haematoma of thesigmoid colon.

Up to 1959u 41 cases of intramural haematoma ofvarious parts of the intestine had been reported. Twenty­one of these occurred in the duodenum. Two further casesare added in this paper.

CASE 1

On 15 October 1961 Mr. G.H.A., a thin wiry young man, wasthrown to the ground while dismounting from his horse. Helanded on his belly with his right arm beneath him. The fall

was not unduly severe, and he rose at once complaining onlyof pain in the right elbow. X-rays taken the same day showeda crack-fracture. of the head of the radius. A plaster wasapplied and he ;'vas allowed to return home.

At about 4 p.m. the next day he complained of upperabdominal discomfort slightly to the left of the midline. Thissoon became a severe pecsistent pain accompanied by increasingnausea, and followed shortly thereafter by vomiting. Some ofthe vomitus contained blood which appeared to be reasonablyfresh, and he was therefore admitted to hospital.

On admission the patient was in great pain and obviouslyshocked. The upper abdomen was rigid and the clinical picturewas highly suggestive of rupture of a hollow viscus. StraightX-ray plates of the abdomen showed no free gas, and noevidence of intestinal obstruction or ileus.

The usual supportive therapy was instituted and the patientwas prepared for operation.

OperationThe abdomen was opened through a right upper paramedian

incision. A small amount of pink- tained, clear fluid waspresent in the peritoneal cavity. 0 perforation was found.The entire third part of the duodenum presented as a tense,distended, dark-blue sausage-shaped mass extending distallyto the duodenojejunal junction, and sh~ly defined at bothlimits. This appearance was thought to be due to haemorrhagewithin the lumen and an incision was planned to evacuate the