Treatment of Parotid Tumours
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680 recommend a therapeutic range of ratios between 1.5 and 2-5 and set the danger level at a ratio of 3. In the second method a dilution curve is prepared by dilating normal plasma with saline solution in various pro- portions and recording the clotting-times of the diluted samples. This gives a hyperbolic curve from which " per- centage prothrombin activity " corresponding to the observed prothrombin-time can be read off; thus a plasma- prothrombin time of 21 seconds corresponds to a pro- thrombin activity of 25%, and a time of 18 seconds to 35%, and so on. For safe therapeutic control, levels between 10% and 20% are aimed at. This method has been widely used, but there are difficulties about it. The curves relating clotting-time to prothrombin activity need to be checked frequently. Some workers, including QUICK, dilute the plasma with saline ; others, including STEFANINI and DAMESHEK, consider that the normal plasma must be diluted with plasma from which pro- thrombin and factor VII have been absorbed with calcium phosphate leaving the other factors intact. Another disadvantage is that the shape of the curve means that reduction in prothrombin activity has relatively little effect on the clotting-time until the level falls below about 30% ; but after this point a second or so difference in the clotting-time corresponds to a large reduction of prothrombin activity, and the method of observing the end-point hardly allows accuracy of this degree. The third method is to express the result as a " pro- thrombin index." This index is the normal plasma- prothrombin time divided by the patient’s prothrombin- time, multiplied by 100 ; desirable therapeutic levels are between 40% and 50%. It is not surprising that there has been confusion between the results of the dilution-curve method and the prothrombin index, since both are expressed as " per cent " ; and the confusion may be dangerous since 20% is a proper therapeutic result with the dilution-curve method, but indicates grave liability to haemorrhage with the prothrombin-index method. BIGGs and MACFARLANE now recommend the first method of setting a ratio as the least ambiguous, and it is the simplest to work out and use. In view of possible confusion it is clear that the method used should be agreed between the laboratory and the physician and should be clearly indicated. This is particularly necessary when a technician is in day-to- day charge of a laboratory. If laboratory control is efficiently maintained, haemorrhagic complications of anticoagulant treatment will be very rare and the physician can use this treatment with confidence. 1. Janes, R. M. Canad. med. Ass. J. 1940, 43, 554 ; Surg. Clin. N. Amer. 1943, 23, 1429. 2. Bailey, H. Brit. J. Surg. 1941, 28, 337. 3. Redon, H. Proc. R. Soc. Med. 1953, 46, 1013 ; Chirurgie des glandes salivaires. Paris, 1955. Treatment of Parotid Tumours PAROTIDECTOMY is replacing enucleation as the standard treatment of parotid tumours-partly because of belated recognition of the frequency of infiltrating types which cannot be removed by enuclea- tion, and partly because of the high recurrence-rate in mixed tumours treated by enucleation. In the 1940s three surgeons were, independently, pioneers in the establishment of parotidectomy as a routine treatment for parotid tumours-JANES 1 of Toronto, HAMILTON BAILEY 2 here, and REDON 3 of Paris. JANES had preserved an almost complete silence from the time of his original contributions, and his many admirers in this country will therefore be very glad that he took advantage of a recent visit to this country, as visiting professor of surgery to the Middle. sex Hospital, to express his views in a Moynihan lecture at the Royal College of Surgeons of England.4 Professor JANES gave two examples of a feature, common in parotid tumours, which vitiates many studies of results—namely, the long interval between primary operation and recurrence. In the cases he cited, the intervals were twenty years and twenty-nine years. He disagrees with RJiJDON on the causes of recurrence. He believes that the causes are an inadequate primary operation and implantation of tumour cells; he does not believe that the cause is that any considerable propor- tion of tumours are multicentric. He noted that a high proportion of parotid tumours are malignant-110 out of 333 in a survey at the Toronto General Hospital. " Failure to realise the very high recurrence rate following simple enucleation of benign tumours and the general belief that very few of these tumours were malignant led to complacency." In view of present knowledge, " it seems extraordinary that enucleation with or without radiation continues to be done." Be described his technique of parotidectomy, which differs only slightly from that which he originally described in 1940. Identification of the main trunk of the facial nerve is an essential preliminary. Biopsy is done, if at all, only at operation-partly because it is often difficult to make a diagnosis from small bits of tissue, partly because of the danger that " multiple recur- rences are due to seeding of the wound through rupture of the tumour capsule." " If the nerve is actually going into the tumour the condition is almost certainly malignant and the fibres or if necessary a major trunk should be sacrificed.’’ Some surgeons may be a little reluctant to accept JANES’S further conclusion that ’’ in operating upon primary benign tumours, removal of the tumour with an intact capsule and a few millimetres of surrounding normal parotid tissue is adequate ’’ ; for not only is it difficult to say for certain that any given tumour is benign, but also in inexperienced hands a limited local excision of this type will only nominally be anything more than the old enucleations. This danger will not exist in Pro- fessor JANES’S hands, but that it probably does in other hands is suggested by the fact that 35 patients in the Toronto survey are said to have had "wide local excision without identification of the facial nerve." Local excisions without identification of the facial nerve do not tend to be very wide, and fti fact there were 3 recurrences in this group. Of 25 in the same survey treated by superficial lobectomy or total parotidectomy and followed up, none have had recur- rences. The French figures point in the same direction. REDON and BELCOUR report only 1 known recur- rence following 127 total parotidectomies for mixed tumour, and moreover, of 27 patients treated by conservative parotidectomy for cancer, 11 have sur- vived for five to eleven years. MOYSE 6 found no case of recurrence in 50 primary mixed tumours treated by total conservative parotidectomy (i.e., conserving the facial nerve). Thus the case for routine super- ficial lobectomy as a minimum in parotid tumours is strong. Workers in this country will agree with Professor JANES that carcinoma that has reached the stage of 4. Janes, R. M. Ann. R. Coll. Surg. Engl. 1957, 21, 1. 5. Redon, 11., Belcour, J. Mém. Acad. Chir. 1955, 81, 991. 6. Moyse. P. Ibid, p. 999.
Transcript of Treatment of Parotid Tumours
680
recommend a therapeutic range of ratios between 1.5and 2-5 and set the danger level at a ratio of 3.
In the second method a dilution curve is prepared bydilating normal plasma with saline solution in various pro-portions and recording the clotting-times of the dilutedsamples. This gives a hyperbolic curve from which " per-centage prothrombin activity " corresponding to theobserved prothrombin-time can be read off; thus a plasma-prothrombin time of 21 seconds corresponds to a pro-thrombin activity of 25%, and a time of 18 seconds to35%, and so on. For safe therapeutic control, levelsbetween 10% and 20% are aimed at. This method hasbeen widely used, but there are difficulties about it.The curves relating clotting-time to prothrombin activityneed to be checked frequently. Some workers, includingQUICK, dilute the plasma with saline ; others, includingSTEFANINI and DAMESHEK, consider that the normal
plasma must be diluted with plasma from which pro-thrombin and factor VII have been absorbed with calcium
phosphate leaving the other factors intact. Another
disadvantage is that the shape of the curve means thatreduction in prothrombin activity has relatively littleeffect on the clotting-time until the level falls belowabout 30% ; but after this point a second or so differencein the clotting-time corresponds to a large reduction ofprothrombin activity, and the method of observing theend-point hardly allows accuracy of this degree.The third method is to express the result as a " pro-
thrombin index." This index is the normal plasma-prothrombin time divided by the patient’s prothrombin-time, multiplied by 100 ; desirable therapeutic levelsare between 40% and 50%.It is not surprising that there has been confusionbetween the results of the dilution-curve methodand the prothrombin index, since both are expressedas
"
per cent " ; and the confusion may be dangeroussince 20% is a proper therapeutic result with thedilution-curve method, but indicates grave liabilityto haemorrhage with the prothrombin-index method.BIGGs and MACFARLANE now recommend the firstmethod of setting a ratio as the least ambiguous, andit is the simplest to work out and use. In view of
possible confusion it is clear that the method usedshould be agreed between the laboratory and the
physician and should be clearly indicated. This is
particularly necessary when a technician is in day-to-day charge of a laboratory. If laboratory control isefficiently maintained, haemorrhagic complications ofanticoagulant treatment will be very rare and the
physician can use this treatment with confidence.
1. Janes, R. M. Canad. med. Ass. J. 1940, 43, 554 ; Surg. Clin.N. Amer. 1943, 23, 1429.
2. Bailey, H. Brit. J. Surg. 1941, 28, 337.3. Redon, H. Proc. R. Soc. Med. 1953, 46, 1013 ; Chirurgie des
glandes salivaires. Paris, 1955.
Treatment of Parotid TumoursPAROTIDECTOMY is replacing enucleation as the
standard treatment of parotid tumours-partlybecause of belated recognition of the frequency ofinfiltrating types which cannot be removed by enuclea-tion, and partly because of the high recurrence-ratein mixed tumours treated by enucleation. In the1940s three surgeons were, independently, pioneers inthe establishment of parotidectomy as a routinetreatment for parotid tumours-JANES 1 of Toronto,HAMILTON BAILEY 2 here, and REDON 3 of Paris.JANES had preserved an almost complete silence fromthe time of his original contributions, and his manyadmirers in this country will therefore be very gladthat he took advantage of a recent visit to this
country, as visiting professor of surgery to the Middle.sex Hospital, to express his views in a Moynihanlecture at the Royal College of Surgeons of England.4
Professor JANES gave two examples of a feature,common in parotid tumours, which vitiates manystudies of results—namely, the long interval betweenprimary operation and recurrence. In the cases he cited,the intervals were twenty years and twenty-nine years.He disagrees with RJiJDON on the causes of recurrence.He believes that the causes are an inadequate primaryoperation and implantation of tumour cells; he does notbelieve that the cause is that any considerable propor-tion of tumours are multicentric. He noted that a
high proportion of parotid tumours are malignant-110out of 333 in a survey at the Toronto General Hospital." Failure to realise the very high recurrence rate
following simple enucleation of benign tumours andthe general belief that very few of these tumours weremalignant led to complacency." In view of presentknowledge, " it seems extraordinary that enucleationwith or without radiation continues to be done." Bedescribed his technique of parotidectomy, which differsonly slightly from that which he originally describedin 1940. Identification of the main trunk of the facialnerve is an essential preliminary. Biopsy is done, ifat all, only at operation-partly because it is oftendifficult to make a diagnosis from small bits of tissue,partly because of the danger that " multiple recur-rences are due to seeding of the wound through ruptureof the tumour capsule." " If the nerve is actuallygoing into the tumour the condition is almost certainlymalignant and the fibres or if necessary a major trunkshould be sacrificed.’’ Some surgeons may be a littlereluctant to accept JANES’S further conclusion that’’ in operating upon primary benign tumours, removalof the tumour with an intact capsule and a fewmillimetres of surrounding normal parotid tissue is
adequate ’’ ; for not only is it difficult to say forcertain that any given tumour is benign, but also ininexperienced hands a limited local excision of thistype will only nominally be anything more than theold enucleations. This danger will not exist in Pro-fessor JANES’S hands, but that it probably does inother hands is suggested by the fact that 35 patientsin the Toronto survey are said to have had "widelocal excision without identification of the facialnerve." Local excisions without identification of thefacial nerve do not tend to be very wide, and fti factthere were 3 recurrences in this group. Of 25 in thesame survey treated by superficial lobectomy or totalparotidectomy and followed up, none have had recur-rences. The French figures point in the same direction.REDON and BELCOUR report only 1 known recur-rence following 127 total parotidectomies for mixedtumour, and moreover, of 27 patients treated byconservative parotidectomy for cancer, 11 have sur-vived for five to eleven years. MOYSE 6 found no caseof recurrence in 50 primary mixed tumours treatedby total conservative parotidectomy (i.e., conservingthe facial nerve). Thus the case for routine super-ficial lobectomy as a minimum in parotid tumoursis strong.Workers in this country will agree with Professor
JANES that carcinoma that has reached the stage of4. Janes, R. M. Ann. R. Coll. Surg. Engl. 1957, 21, 1.5. Redon, 11., Belcour, J. Mém. Acad. Chir. 1955, 81, 991.6. Moyse. P. Ibid, p. 999.
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clinical diagnosis has a very bad prognosis. On theother hand, there is great hope in the fact that somany carcinomas supervene on tumours which havebeen inactive for many years. Operation in thisinactive phase should cure the disease. ProfessorJANES’S main message is that all tumours of the
parotid should be radically treated when first detected.
1. Bagley, C. Arch. Neurol. Psychiat., Chicago, 1932, 27, 1133.2. Hawkins, C. F., Rewell, R. E. Guy’s Hosp. Rep. 1946, 95, 88.3. Daws, R. A. Brit. J. Surg. 1957, 44, 582.4. Curtis, J. B. J. Neurol. Psychiat. 1949, 12, 167.5. Werner, A. Ibid, 1954, 17, 57.
Apoplexy of YouthYouNG adults who die after intracranial hoenior-
rhage are usually found at necropsy to have an
aneurysm of the circle of Willis or of a main cerebral
artery. Of those who survive some are not shown tohave a vascular abnormality, though presumablythis is present in most cases. But sometimes no causecan be found even at necropsy. When neoplasm,obvious trauma, blood dyscrasias, hypotension,eclampsia, and polyarteritis nodosa are excluded,there remains quite a large number arising in
apparently healthy young persons with no obviousvascular lesions. For a long time it was thought thatthe late effects of trauma were responsible ; but
angiography has yielded some evidence that spon-taneous
" intracerebral haemorrhages may be causedby a small angioma. BAGLEY 1 showed that such an
angioma may be demonstrable only by microscopicexamination ; his work has been confirmed 2 andthere has been a tendency to attribute every suchcase to a cryptic hsemangioma. To explain the factthat in some cases, even on the most careful examina-
tion, no angioma is detectable, it has been suggestedthat the tiny vascular abnormality is destroyed by thehaemorrhage itself.Whatever the ætiology of the condition, its natural
history has become clear in the light of recent studies.A previously healthy young person of either sex is
suddenly seized unaccountably with headache. Con-sciousness may be lost immediately, but usually thesymptoms progress slowly. The patient begins tovomit, and’ over a period of hours or days paralysisdevelops in part or the whole of one side of the body,with drowsiness, stupor, or even coma. Some patientsdie more or less at once in coma, but a substantial
proportion (a third to a half) survive, either presentingthe picture of a rather rapidly expanding cerebraltumour or recovering spontaneously with some
residual defect. In the subacute and chronic casesthere is usually some focal disturbance-hemi-paresis, dysphasia, sensory impairment of cerebraltype, or visual defect-and the cerebrospinal-fluid(c.s.F.) pressure in the early stages may be elevated,sometimes grossly. Focal fits, neck stiffness, a positiveKernig’s sign, or other evidence of meningeal irritation,or blood-stained C.S.F., may confirm the diagnosis,but all these signs may be absent. Angiography isoften negative ; but sometimas a dilated vein arousessuspicion of the presence of a pathological arterio-venous shunt.3 Rapid serial angiography may be morehelpful in revealing small angiomas.4 A gas ventricu-logram shows, in about half the cases, a cavity commu-nicating with the lateral ventricle. 5 Electro-encepha-lography usually reveals such widespread abnormality
that localisation is possible only to one side or the other.If the patient dies a recent clot of blood is discoveredin one or other hemisphere or in the cerebellum.’ 6
It is not yet settled whether trauma plays a partin this condition or whether there is a vascular lesionwhich gives rise to rupture. It has been suggestedthat an arteriovenous shunt can give rise to a hoemor-rhage from the venous side, because the pressure thereis so far above the ordinary venous pressure ; but it ishard to believe that such a haemorrhage could com-pletely destroy the arterial end of the angioma andeliminate all traces of its presence. About half thepatients give a history of some trauma to the head-quite often trivial. The various hypotheses connectingthe condition with trauma should not be too summarilydismissed. 7 Believing that necrotic softening ofcerebral tissue led ultimately to haemorrhage, 8SYMONDS held similarly that an original blood-
cyst caused by injury could later have a secondaryhaemorrhage into it. It has often been suggested thatangiospasm might be severe enough to damage thedistal vascular wall, with haemorrhage after the
spasm passed off.9 This all seems rather unlikely ifall otherwise-unexplained heematomas are to beaccounted for uniformly. On the other hand, it isdifficult to identify any normal structures in the closevicinity of an ante-mortem haemorrhage; so it is
perhaps not strange that only some of these tinyhaemangiomas should be identified.Treatment fortunately does not depend on a
final decision on cause. An intracerebral clot was firstevacuated by CUSHING in 1903 10; and spontaneoushaematoma in a young person was first treated
surgically by PENFIELD in 1933.11 The modern era ofsurgical treatment of the condition started withCRAiG and AnsoN’s report in 1936.12 Some patientssoon die : these often have deeply placed vascularabnormalities, usually near the midline.13 Othersrun a subacute course. If the haematoma is suitablyplaced, the quickest and most satisfactory way ofdealing with it is by full craniotomy ; the haematomais sucked out under direct vision, the walls are
examined, and any abnormality (often none is seen)is coagulated or removed. Where a high-pressurehaematoma is in a situation where operation mightcause further detriment to speech or to some otherimportant cerebral function, or where the pressure isobviously not dangerously high, rapid and completeresolution may follow tapping of the collection of blood,through a burr-hole by means of an ordinary braincannula. In the more chronic cases, the haematomasare presumably at or near normal venous pressure,and they often resolve spontaneously-presumablywith the development of a typical golden collection.There may be small repeated haemorrhages,12 buttrue recurrence of the haematoma has not been recorded.No-one is likely to see a very large number of these
cases ; so it is all the more important that the conditionbe widely known. For appropriate treatment maysave the patient’s life.6. Plicher, C. Arch. Neurol. Psychiat., Chicago, 1941, 46, 416.7. Bollinger, O. Uber traumatische Spätapoplexie. In Internat.
Beitrage zur wiss. Med. Festschrift Rud. Virchow. Berlin, 1891.8. Symonds, C. P. Brit. med. J. 1940, i, 1048.9. De Jong, R. N. Arch. Neurol. Psychiat., Chicago, 1942, 48, 257.
10. Cushing, H. Amer. J. med. Sci. 1903, 125, 1017.11. Penfield, W. Canad. med. Ass. J. 1933, 28, 369.12. Craig, W. McK., Adson, A. W. Arch. Neurol. Psychiat., Chicago,
1936, 35, 701.13. Crawford, J. V., Russell, D. S. J. Neurol. Psychiat. 1956, 19, 1.
