POSTGRAD. MED. J. (1964), 40, 414

THE DIAGNOSIS AND MANAGEMENT OFPULMONARY EMBOLISM

D. W. BARRITr, M.D., M.R.C.P.Consultant Physician, United Bristol Hospitals.

EMBOLISM of the pulmonary arteries presentsin one of three main ways. Most dramatic isacute failure of the circulation. A large clotobstructs more than half of the cross-sectionof the pulmonary tree at the bifurcation ofthe main stem or the hila of both lungs. Morecommonly it is the development of an infarctat the base of one or both ilungs that givesevidence of an embolism which has lodgedsome hours before. Rarely, repeated smallemboli, which do not separately give rise tosymptoms or signs, may lead to mountingpulmonary hypertension and chronic rightheart failure.The Attendant Circumstances

Pulmonary embolism is distincly uncommonin patients who have previously been healthyand fully mobile but attention was drawn tothis possibility by Homan's (1943) report of11 such cases. Of the 120 cases of pulmonaryembolism reported by Short (1952), three werewell and fully mobile at the time of theirfirst symptom.Any patient confined to bed for a few days

may develop the disease. Especially at riskare those ill with heart disease (Carlotti, Hardy,Linton and White, 1947; Short, 1952; Byrne,1955), neoplasms (Trousseau, 1877; Sproul1938), injuries to the bones of the legs (Sevittand Gallagher, 1959), recent operations(Barker Nygaard, Walters and Priestley, 1940)or thrombophlebitis (Byrne, 1955). Althoughalmost every patient with pulmonary embolismor pulmonary infarction has a source of throm-bus formation in the venous system of theabdomen or legs, the condition will be diag-nosed on the evidence in the heart or lungs.In two necropsy studies, McLachlin and Pater-son (1951) found venous thrombosis in all of19 cases of pulmonary embolism and in theseries of Sevitt and Gallagher (1959) 32 of 38patients with venous thrombosis had pulmonaryembolism. Clinical methods of detecting venousthrombosis are, however, imperfect and in theabsence of signs in the legs the absence ofextensive thrombosis cannot be assumed. Thus,in Sevitt's patients, 9 of 17 who died of pul-monary embolism were without clinical evi-dence of thrombosis.

In a clinical study of 72 patients with pul-monary embolism reported by Barritt andJordan (1961), 32 were found to have tender-ness of the calf on squeezing, 20 cedema ofthe leg, 10 superficial thrombophlebitis, 17varicose veins and 16 no abnormal signs. Clini-cal evidence of a possible source in the leg may,therefore, be taken as a confirmatory sign ofpulmonary embolism but in its absence noconclusions can be drawn.Evidence of Obstruction to the Pulmonary Tree

Massive embolism of the pulmonary arterymay be followed by immediate loss of con-sciousness and death within minutes. Thepatient is usually cyanosed and the pulse rapidand of very low volume. If the patient sur-vives, evidence of severe circulatory obstructionwill persist and the following are the principalclinical features:

Breathlessness and Restlessness. Anxietyaccompanies breathlessness which may showitself with the least movement about the bed.This immediate breathlessness is not due topleural pain but indicates a profound disturb-ance of ventilation. Orthopncea is unusual.

Faintness. With low levels of blood pressurethere may be feelings of faintness or loss ofconsciousness on sitting up. Faintness in theearly period of getting out of bed after oper-ations should be viewed with particularsuspicion.

Central Chest Pain. Discomfort in the centreof the chest is indistinguishable from the painof myocardial infarction. Radiation to thearms or jaw is uncommon but the pain may besevere and occasionally may last for hours.

Tachycardia. A rise in heart rate is a veryfrequent accompaniment of pulmonary embo-lism. In cases where the first symptoms arethose of the development of an infarct, pulsecharts frequently show a sharp rise in heartrate some hours before the onset of pleuralpain, and this serves to date the arrival of theembolus. Paroxysmal arrhythmias also occur.Short (1952) considered that five of his 120patients developed atrial fibrillation as a resultof embolism and one other had ventriculartachycardia. Barritt and Jordan (1961) con-firmed the onset of atrial fibrillation in four

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FIG. 1.-SuccessiveElectrocardiograms takenbefore operation, afterthe occurrence of mas-sive embolism (Post-op.19th day) and after 16days' anticoagulant

treatment.

of their 72 patients and paroxysmal supra-ventricular tachycardia in a fifth. The onsetof atrial fibrililation during the course of heartdisease should, therefore, lead to thought beinggiven to the possibility that pulmonary embo-lism has occurred.

Hypotension. An abrupt fall in blood pres-sure can be taken to indicate a reduced cardiacoutput. Occasionally, the diagnosis is first sug-gested when routine records of blood pressureshow a fall in systolic pressure to less than100 mm. Hg. As in other low output statesan obvious fall in systolic pressure duringinspiration may be a feature but pulsus para-

doxus on palpation is rare. With the low bloodpressure and poor volume pulse the skin iscold and clammy.

Cyanosis. Arterial oxygen desaturation isvery difficult to detect in the patient with acold skin, but cyanosis of the tongue andmucous membranes is occasionally obvious andarterial puncture will then confirm the desatur-ation. An increase in the dead space withinthe lung and disturbance of ventilation per-fusion ratio, together with diminished compli-ance are likely to be the causative mechanisms.

Raised right atrial pressure. Obstruction tothe outflow from the right ventricle leads to

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a rise in right atrial pressure that may be obvi-ous in the neck. In others, breathlessness isaccompanied by such large variations in intra-thoracic pressure, that the mean right atrialpressure cannot be estimated clinically.

Auscultation of the Heart. Auscultation ofthe heart gives little informaation. In thepresence of tachycardia gallop rhythm may beheard. In a small number of patients, frictionsounds are present for short periods at the baseof the heart. Abrupt distension of the pul-monary artery or of the right ventricle areprobably responsible.The Electrocardiogram

Characteristic changes can be expected in theelectrocardiogram of patients with massiveembolism of the pulmonary arteries. Theseconsist of a shift to the right of the electricalaxis of the heart with clockwise rotation andT-wave changes in right ventricular leads. Cut-forth and Oram (1958) analysed records from50 cases of pulmonary embolism, of which 28showed evidence of a fall in blood pressureor a rise in venous pressure (severe cases) and22 neither feature (mild cases). These authorsconsidered the following three electrocardio-graphic patterns to be diagnostic of pulmonaryembolism:

1. S1, Q3, T3 plus right ventricular T-waveinversion.

2. Si, T3 or T3 plus right ventricular T-waveinversion.

3. Si, Q3, T3 plus right bundle branch block.Of their 28 severe cases, 18 showed these

patterns and nine of the remaining ten showedchanges considered to be suggestive of pul-monary embolism. Of their 22 mild cases,there was diagnostic evidence of pulmonaryembolism in the electrocardiogram in half.Barritt and Jordan (1961) noted T-wave inver-sion in V1 and V2 in 14 of their patients, ofwhom 11 also showed T-wave inversion inleads II or III or aVf. Transient right bundlebranch block was present in a further fourpatients. Of these 18, there was a fall inblood pressure and other evidence of massiveembolism in 16. Changes in the electricalposition of the heart were present in 13others whilst of 12 patients with normal ECGsnone had a fall in blood pressure. Obviouschanges in the electrocardiogram, therefore, arelikely in severe cases and suggestive evidencemay strengthen the diagnosis in those with lesscirculatory disturbance.

In a small number of acutely ill patients withlow blood pressure and high venous pressure,the electrocardiogram may be less helpful.Medd and McBrien (1962) cite patients withmassive pulmonary embolism with S-T depres-sion or T-wave changes in left precordial leads

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which suggest the presence of coronary arterydisease. Figure 2 shows the electrocardiogramin a woman of 40 years whose first symptomwas a brief attack of effort syncope whilst onholiday. Very high venous pressure with tachy-cardia, small volume pulse and pulsusparadoxussuggested the diagnosis of cardiac tamponade.Shortly after attempted aspiration of the peri-cardium she died and at necropsy massive,repeated embolism of the pulmonary arterieswas found.Evidence of Pulmonary InfarctionWhen thrombus becomes tightly packed in

a branch of the pulmonary artery, symptomsand signs of pulmonary infarction usually fol-low. This is more likely to occur when theembolus passes beyond the bifurcation intoone or both branches towards the periphery ofthe lung. Only the lower lobes are usuallyaffected and one may assume that this isbecause blood flow to the upper lobe isextremely small at rest in the upright position(Dollery, Hugh-Jones, Matthews, 1962).Pleural Pain-Friction and Effusion

Pleural pain is the commonest symptom todraw attention to pulmonary embolism. It maybe slight or severe and on one or both sides.A friction rub may or may not accompanyit. In patients whose embolism is dated by theonset of faintness, breathlessnes or tachycardia,pleural pain may follow some hours later. Apleural effusion may develop. The fluid isusually bloodstained.Cough and Ha?moptysis

Cough, with the production of a small quan-tity of sputum, is frequently present. Hemop-tysis, which varied in amount from a speckof blood on one occasion only, to heavy stain-ing of the sputum for many days, was presentin 31 of 72 of Barritt and Jordan's patients.Breathlessness and Cyanosis

In the presence of pulmonary infarction,dypncea is most commonly the result of pleuralpain. The pain is avoided by taking shallow,rapid breaths. More severe breathlessnesspoints to a high degree of circulatory obstruc-tion. Cyanosis is usually inconspicuous exceptin the presence of extensive bilateral infarction.Physical Signs in the Chest

Breathing is usually quiet but increasedrespiratory variation in venous pressureobserved at the root of the neck may pointto diminished lung compliance.

Percussion of the chest usually confirms thepresence of a lung lesion because resonance isimpaired at the affected base. The loss of

resonance rarely amounts to stony dullness.In contrast to the findings with consolidationof lobar pneumonia, breath sounds and voicesounds are diminished over an infarct. Bron-chial breathing is a rare finding. The most fre-quent auscultatory sign is the presence of rales.Rales are rarely absent in pulmonary infarction,and are present at both bases in about half thecases, thus pointing to the presence of clotsin both lungs.Fever and Jaundice

Fever is an almost invariable accompanimentof pulmonary infarction. Characteristically,fever is present at the time of onset of pleuralpain or hemoptysis. With effective anti-coagulant therapy and without the addition ofantibiotic agents, fever soon disappears. Jaun-dice is much less frequent, especially in theabsence of congestive heart failure.The Chest RadiographAlthough the patient cannot be taken to the

X-ray Department, and despite breathlessnessand pain at the time of the examination,changes in the chest radiograph will usually befound at the first examination in the ward.Short (1951) described such changes in 85 of94 patients examined. The abnormalities wereinfarct shadows in 88 per cent, pleurisy in 56per cent, elevation of the diaphragm in 39 percent, and multiple infarcts in 43 per cent. Thesepositive radiological changes were usuallypresent within 12 hours of infarction. A nega-tive chest X-ray should not weigh heavilyagainst the diagnosis of pulmonary embolism,particularly if the film is of poor quality.Embolism without infarction may be presentand here the radiological changes may be muchless conspicuous. Shapiro and Rigler (1948)considered the characteristic abnormalities inembolism without infarction to be increasedradio-translucency and ischmmia of the involvedpulmonary segment, with abrupt terminationof the embolised pulmonary artery.Pulimonary Function Tests

Obstruction of a major branch of the pul-monary artery must necess-arily cause an impor-tant disturbance of pullmonary function. Per-fusion of the affected lung segment will cease,ventilation of the unperfused lung will continueand when infarction occurs the inflammatoryprocess will disturb the lung further. Robin,Forkner, Bromberg, Croteau and Travis (1960)discussed the alveolar gas exchange in pul-monary embolism. They list three major com-ponents of disturbance: arterial oxygendesaturation, hyper-ventilation, and the

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FIG. 3.-Successive tracings with aninterval of three hours in anelderly patient with extremely highvenous pressure but no orthopncea.Pulmonary embolism was suspectedand consideration was given tosurgical exploration. Progressivechanges of left bundle branch blocksuggested myocardial infarction andnecropsy confirmed the diagnosis.

development of differences between the CO2tension of arterial blood and the end-tidalair as a result of dilution of alveolar air bynewly-formed dead space. Measurement ofthe arterial-end tidal difference is clearly notan easy technique in an ill and breathlesspatient, and others have found difficulty inusing this as a diagnostic test.Angiocardiography

Possible use of angiocardiographic techniquesin the acutely ill patient are considered subse-quently when differential diagnosis isdiscussed.

Differential Diagnosis of Massive PulmonaryInfarctionWhen the physician is faced with a cardio-

vascular emergency in a patient with very lowcardiac output, high venous pressure andcentral chest discomfort, the usual differen-tial diagnosis is between massive pulmonaryembolism and myocardial infarction. The dis-tinction is usually not difficult for evidenceof incipient pulmonary cedema together withthe onset of an injury current in the electro-cardiogram make the di.agnosis of myocardialinfarction. In the absence of these two features

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in the early hours of the emergency the cir-cumstances of the attack may weight tihe scalesin one direction or another. Clear evidence ofvenous disease of the legs suggests pulmonaryembolism, and a fleck of blood stained sputumin the absence of wet lungs is confirmatory.Again, electrocardiography will usually bringconfidence to the diagnosis of embolism. If thepatient's condition is not deteriorating, relianceshould be placed on serial electrocardiogramsat frequent intervals (Fig. 3). An early rise inserum glutamic oxalacetic transaminase favoursmuscle necrosis from myocardial infarction.

It may be felt that the differential diagnosisis barely of practical importance as treatmentof these two conditions is so similar. Therewill, however, be occasions when considera-tion is given to the idea of surgical removalof an embolus and, under these circumstances,diagnosis must be certain. There may be aplace here for more adequate X-ray visuali-sation of the disturbance in the pulmonaryvascular tree. High quality plain films of thehila of the lungs will repay close study. Thepossibility of the bedside use of contrast radio-graphy needs to be further explored. Robband Steinberg (1939) claimed that accuratestudies could be made of arterial and venouspatterns of the lung by injection of contrastmedium into an arm vein with the patientsitting before a casette. Williams and Wilcox(1963) have recently made a study using thistechnique in 50 patients with pulmonary embo-lism. All the patients tolerated the procedurewell but few details are given of the severityof their illness or the type of apparatus used.Mention is made of the possibility of thisapproach to the problem of the patient inwhom surgical exploration is considered. Proofof major obstruction to vessels and localisationof the main areas of embolism might then beconsidered a necessary preliminary to opera-tion.When the emergency presents with paroxy-

smal arrhythmia differential diagnosis is likelyto be more difficult. Treatment of the arrhyth-mia will take priority. The possibility ofpulmonary embolism should always be con-sidered when arrhythmia occurs in the courseof heart disease of all types. The distinctionfrom cardiac tamponade will not arise fre-quently. Where doubt exists a diagnosticaspiration is essential but one hopes thatexploration of the pr=cordium with ultrasoundrecording may display or exclude a pericar-dial effusion without the use of a needle.

Pulmonary infarction must usually bedistinguished from pneumonia especially inthe post-operative period. No single feature isin itself decisive with the exception of thediagnostic electrocardiographic change whichwill be present in the minority of cases whena lung lesion is prominent. Physical signsof venous thrombosis will be present in themajority, and it is the combination of venousthrombosis and an appropriate pulmonaryiesion that points to the diagnosis mostfrequently. Difficulties arise when there are noabnormal signs in the legs. Pneumonia willthen often be diagnosed and antibiotics pres-cribed. The majority of patients will recoverwith these measures, but there will often besurprises as the late development of leg signsor recurrence of chest troubles, or even fatalembolism correct the diagnosis.Where doubt exists response to ianticoagu-

lant therapy will sometimes give diagnostichelp. With the infusion of heparin, fever mayvanish within hours and not recur.

Repeated Minor Emboli leading to Progres-sive Pulmonary HypertensionWith the widespread recognition of the

value of anticoagulant therapy in curingvenous thrombo-embolism, repeated majorembolisation leading to progressive right heartfailure is a rare condition. A small groupof patients exist, however, who exhibitprogressive pulmonary artery obstruction whohave minimal clinical evidence or no clinicalevidence at all of pulmonary embolism orinfarction. This condition appears in previous-ly healthy people who have not been confinedto bed. Goodwin, Harrison and Wilcken(1963) described 11 such patients and Wilhelm-sen, Selander, Soderholm, Paulin, Varnauskasand Werko (1963) and a further 10. There islittle except evidence of major filling defectsin the pulmonary arteriogram, to distinguishthis condition from so called primary pulmo-nary hypertension. Thus, the patients presentwith breathlessness of effort, effort syncope,chest pain and hemoptysis. The electrocar-diogram shows right ventricular dominanceand catheterisation confirms the pulmonaryhypertension. Goodwin lays great stress onthe necessity for early recognition of thiscondition as successful arrest of the conditionwith anticoagulant treatment can be hopedfor only before pulmonary hypertensionbecomes established. Slight effort dyspnceawith hyperventilation at rest is the clue. Underthese circumstances arterial-end tidal CO2

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gradients may well be demonstrated andarterial oxygen desaturation on effort is likely.Management of Venous Thrombo-Embolism

It would be inappropriate to discuss thetreatment of pulmonary embolism withoutconsidering prophylaxis first. Attempts todiminish the incidence of pulmonary embolismin hospital by systematically allowing patientsto get out of bed at an earlier stage of theirillness have met with little success. This isprobably because at an early stage of recoveryfrom illness or operations the level of activityis of necessity very low and nothing is gainedby exchanging bed rest for chair rest.

This has led to a study of the use ofanticoagulant drugs given prophylactically topatients who are especially at risk. Sevitt andGallagher (1959) in their classical studycompared 150 elderly patients with fracturedhips (control series) with a similar numberwho were given Phenindione routinely soonafter admission to hospital. This prophylacticuse of Phenindione resulted in complete free-dom from pulmonary embolism in the periodof treatment, whereas in the control series18 per cent of patients developed pulmonaryembolism and 10 per cent died of it. There wasalso a great saving in venous thrombosis in thelegs. In a somewhat similar study, Chalmers,Marks, Bottomley and Lloyd (1960) tested theuse of prophylactic anticoagulant therapy inselected groups of gynecological and obstetricpatients. In all they tested 1877 patients in afive year period and made a comparison witha preceding five year period when prophylacticanticoagulants had not been used. They toofound an impressive reduction in venousthrombosis and pulmonary embolism intreated patients. A strong case can, therefore.be made for the use of anticoagulants givenprophylactically to patients who are at specialrisk.A different approach to the problem has

been suggested by Sharnoff, Kass and Mistica(1962) on the basis of a state of increasedblood coagulability as demonstrated by Lee-White clotting time values. They administeredHeparin subcutaneously before operation andbefore mobilising the patient in the post-operative period. Their recommendations werenot supported by a sufficiently extensive clinicaltrial to prove the value of this type of therapy.Treatment of Massive Embolism with Circula-tory FailureAs in other circulatory or respiratory emer-

gencies, reassurance of the patient is of prime

importance. The relief of anxiety by theconfidence of the physician, aided wherenecessary by pain relieving drugs, will domuch to economise respiratory effort anddiminish heart rate.When the pulmonary artery becomes nearly

completely obstructed by a large clot, immedi-ate therapy can only be directed to sustainin-the contractile force of the right ventricle. Solong as sufficient blood can be forced pastthe obstruction to maintain an impoverishedcirculation it can be expected that the emboliwill tend to be packed into smaliler branches,thus allowing fulil perfusion of some areas ofthe lung. In the critical period, maintenanceof arterial oxygen saturation and perfusionpressure in the coronary circulation, and controlof the heart rate are likely to assist theventricle.

Arterial oxygen saturation will certainlyfall under these circumstances and high con-centrations of oxygen should be given by facemask.With low central aortic pressure, coronary

blood flow will fall. Mephentermine sulphate,metaraminol or infusions of angiotension ornoradrenaline should be used if the systolicblood pressure falls below 90 mmHg. In thepresence of signs of tachycardia or paroxysmalarrhythmia rapid digitalisation is indicated.

Heparin should be given at once to dis-courage the formation of fresh thrombus atsites where blood flow is obstructed by theembolism.

If the patient survives long enough for thesemeasures to be put into operation then he canexpect to recover with continued medicaltherapy. Of the 53 patients in Barritt andJordan's (1960) treated series, none died ofpulmonary embolism who survived longenough to receive the first injection of Heparin.

This favourable outcome cannot, however,be expected in every case and some patientsmay survive for a number of hours with afaling blood pressure before they die. Inthese exceptional circumstances the questionof surgical removal of the emboli may nowbe rationally considered. Reports of success-ful removal of clot have been givenby Hampson, Milne and Small (1961) whooperated at normal temperature without per-fusion, by Alison, Dunnill and Marshall (1960)operating after surface cooling of their patientto 290 C and by Cooley, Beall and Alexander(1961) using cardiopulmonary bypass.A planned operation of this type should

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certainly only be carried out if deteriorationcontinues in spite of intensive medical treat-ment.

In patients who die within minutes of theirembolism, attempts to restore the circulationby continued external cardiac compressionand artificial ventilation may succeed fromtime to time. Such methods are well directedto the younger patient stricken unexpectedlyby a fatal circulatory disturbance.Management of Pulmonary InfarctionThe question of more prolonged therapy

of pulmonary embolism can be consideredunder this heading. Additiona'l features whichcall for further mention are pleural pain andfever. Pethidine is a suitable drug for therelief of the pain of pulmonary infarction and50-100 mg. by intramuscular injection can begiven at once and repeated if need be.

Unless there are strong contraindications,anticoagulant treatment will always be given.Recent operations are rarely a great hazard.In patients with a history suggesting activepeptic ulceration it may be preferable to useHeparin as the only anticoagulant drugthroughout the course of treatment. Heparinmay be given by intermittent intravenous injec-tion or by continuous infusion for many days.The latter method has the advantage that thenormal clotting mechanism is restored veryrapidly if the infusion is terminated. Usually,an oral anticoagulant will be administered atthe same time as Heparin is started so thatHeparin is discontinued after 36-48 hours asthe oral anticoagulant takes over. Phenindionehas been used most extensively in Britain inthe last decade but occasional reports of serioustoxic reactions affecting kidney, liver and bonemarrow have led some authors to question itssuitability (Holman). High levels of dosageare called for and one stage Quick times shouldbe prolonged to 21-3 times control times.

Antibiotic therapy is usually unnecessary forfever will fall soon after the infarct begins toheal, in the same way as in myocardial infarc-tion. Pulmonary infarcts can, however, becomeinfected with organisms from the upper respir-atory tract and this possibility should be bornein mind. Anticoagulant therapy should be con-tinued until clinical evidence of infarction has

been cleared and evidence of active disease inthe leg has subsided. By this time, clearing ofthe changes on X-ray of the chest will usuallybe evident and in most cases a three weeks'course of treatment is adequate. If there arestill signs of infarction, either on olinical orradiological grounds at the end of three weeks,then therapy should be prolonged. Occa-sionally, there will be recurrence of signs inthe chest or leg and then a second course oftreatment will be called for and it shouldbe prolonged for four to six weeks. Occasion-alsly, continued treatment for 6-12 months maybe necessitated by recurring evidence ofthrombo-embo'ism. Ligation of veins will veryrarely be indicated.Thrombolytic Therapy

Fibrinolytic enzymes may find a place in thetreatment of pulmonary embolism. It is clearfrom the natural history of the condition thatlarge clots are spontaneously lysed in the pul-monary artery and it is logical, therefore, toattempt to assist this process. To this end,activators of the Plasminogen-Plasmin reaction,particularly Streptokinase, have been used.Preparations of Streptokinase carry a risk offebrile reactions and in the critical state of thecirculation after massive embolism this hazardcontra-indicates the use of this type of therapyat the present time. Results with Heparin areso good that new remedies should not be useduntil more evidence is available of their superi-ority. Caution concerning the use of strepto-kinase has been expressed by McNicol, Douglasand Bayley (1962) who made a detailed studyof Streptokinase infusions in patients with vas-cular occlusions.

Repeated Embolism with Pulmonary Hyper-tension

This uncommon condition calls for the insti-tution of anticoagulant treatment at the earliestpossible moment and the treatment should bepressed for months, or years, until all clinicaland laboratory evidence of the disease hasdisapeared.

In the presence of heart failure, digitalisshould be added but if this becomes necessary,arrest of the changes in the pulmonary arterycannot be expected.

REFERENCESALLISON, P. R., DUNILL, M. S. T., MARSHALL, R. (1960): Pulmonary Embolism. Thorax, 15, 273.BMKER, N. W., NYGAARD, K. K., WALTERS, W., PRIESTLEY, J. T. (1940): A Statistical Study of Post-Operative

Venous Thrombosis and Pulmonary Embolism. Proc. Mayo. Clin., 15, 769.BARRirr, D. W., JoRDAN, S. C. (1960): Anticoagulant Drugs in the Treatment of Pulmonary Embolism. A

Controlled Trial. Lancet i, 1309.

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BARRITT, D. W., JORDAN, S. C. (1961): Clinical Features of Pulmonary Embolism. Lancet, i, 729.BYRNE, J. J. (1955): Phlebitis. New Engl. J. Med., 253, 579.CARLOTTI, J., HARDY, B. I., LINTON, R. R., WHITE, P. D. (1947): Pulmonary Embolism in Medical Patients.

J. Amer. med. Ass., 134, 1447.CHALMERS, D. G., MARKS, J., BOTTOMLEY, J. E., LLOYD, 0. (1960). Post-Operative Prophylactic Anti-

coagulants. A 5-year Study in an Obstetric and Gynmcological Unit. Lancet, ii, 220.COOLEY, A. D., BEALL, A. C., ALEXANDER, J. K. (1961): Acute Massive Pulmonary Embolism. Successful

Surgical Treatment Using Temporary Cardio-pulmonary Bypass. J. Amer. med. Ass., 177, 283.CUTFORTH, R. H., ORAM, S. (1958): The Electrocardiogram in Pulmonary Embolism. Brit. Heart J., 20, 41.DOLLERY, C. T., HUGH-JONES, P., MATHEWS, C. M. E. (1962): Use of Radio-Active Xenon for Studies

of Regional Lung Function. Brit. med. J., 2, 1006.GOODWIN, J. F., HARRISON, C. V., WILCKEN, D. E. L. (1963): Obliterative Pulmonary Hypertension and

Thrombo-Embolism. Brit. med. J., 1, 701 and 707.HAMPSON, J., MILNE, A. C., SMALL, W. P. (1961): The Surgical Treatment of Pulmonary Embolism. Lancet,

ii, 402.HOLMAN, V. Personal Conmmunication, and in Press.HOMAN, J. (1943): Pulmonary Embolism due to Quiet Venous Thrombosis and Simulating Cardiac and

Pulmonary Disease. New Engl. J. Med., 229, 309.MCLACHLIN, J., PATERSON, J. C. (1951): Some Basic Observations on Venous Thrombosis and Pulmonary

Embolism. Surg. Gynec. Obstet., 93, 1.McNICOL, G. P., DOUGLAS, A. S., BAYLEY, C. (1962): Experience with Streptokinase Infusions. Lancet ii,

1297.MEDD, W. E., MCBRIEN, D.J. (1962): Acute Pulmonary Embolism with Electrocardiographic Changes

Mimicking Coronary Artery Disease. Lancet, ii, 944tROBB, G. P., STEINBERG, E. (1939): Visualisation of the Chambers of the Heart. Amer. J. Roentgenol, 41,

1.ROBIN, E. D., FORKNER, E. C., BROMBERG, P. A., CROTEAU, J. R., and TRAVIS, D. M. (1960): Alveolar

Gas Exchange in Clinical Pulmonary Embolism. New Engl. J. Med., 262, 283.SEVITT, S., GALLAGHER, N. G. (1959)): Prevention of Venous Thrombosis and Pulmonary Embolism in

Injured Patients. Lancet, iJ, 981.SHAPIRO, R., RIGLER, L. G. (1948): Pulmonary Embolism without Infarction. Amer. J. Roentgenol, 60,

460.SHARNOFF, J. G., KASS, H. H., MISTICA, B. A. (1962): A Plan of Heparinisation of the Surgical Patient to

prevent Postoperative Thromboembolism. Surg. Gynec. Obstet, 115, 75.SHORT, D. S. (1951): A Radiological Study of Pulmonary Infarction. Amer. J. Med., 44, 233.SHORT, D. S. (1952): A Survey of Pulmonary Embolism in a General Hospital. Brit. Med. J., 1, 790.SPROUL, E. E. (1938): Carcinoma and Venous Thrombosis: The Frequency of Association of Carcinoma

in the Body or Tail of the Pancreas with Multiple Venous Thrombosis. Amer. J. Cancer, 34, 566.TROUSSEAU, A. (1877): Clin. Med. Hotel-Dieu. Paris: Bailliere.WILHELMSEN, L., SELANDER, S., SODERHOLM, B., PAULIN, S., VARNAUSKAS, E., WERKO, L. (1963): Recurrent

Pulmonary Embolism. Medicine (Baltimore), 42, 335.WILLIAMS, J. R., WILcOX, W. C. (1963): Pulmonary Embolism. Roentgenographic and Angiographic Con-

siderations. Amer. J. Roentgenol, 89, 333.

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