- Email: [email protected]
ARMCHAIR AND ANTICOAGULANTS FOR CARDIAC INFARCTION
401
red cells. The usual explanation of this discrepancy is that the thyroid antibodies are directed againstcolloid in the acini which normally does not come in contact with antibody-forming cells. This may well be true, but another explanation might be derived from the fact that WITEBSKY used Freund adjuvants in his experiments, whereas EHRLICH did not. Possibly these adjuvants modify either the antigen or the body’s response to it in such a way as to obliterate the effect of the self-marker. Although this speculation is quite unsupported it might lead to some interesting experiments. At present no useful generalisations can be made; and there is nothing to tell us whether antibodies arise because of failure to acquire tolerance, because of subtle alterations in the chemical constitution of the antigens, or because some derangement of the antibody-forming mechanism renders it incapable of recognising self-markers. Professor DACIE suggested that in some cases the antibody might be made by neoplastic tissue rather than by normal antibody-forming tissues. These alternative explanations all seem at present about equally plausible. The pathogenesis of the various conditions discussed may well be heterogeneous. What is more important than the correctness of any detailed hypothesis is that a new idea has appeared in medical thought, and is going to give rise to a great deal of original work.
their
own
Annotations ARMCHAIR AND ANTICOAGULANTS FOR CARDIAC INFARCTION
IN 1952 Levine and Lown1 suggested that strict bed the best way of treating patients with cardiac infarction; and they proposed that, as soon as the initial shock had passed, patients could sit up in a comfortable armchair for some hours every day; they cited records of 81 patients so treated with a mortality of only 10%. One reason for adopting this sort of regime was to reduce the incidence of secondary embolism. It is agreed that anticoagulant treatment prevents this secondary embolism, and much of the reduction of mortality brought about by anticoagulant treatment is apparently related to this action. Helanderin Stockholm has been testing the effect of combining armchair treatment and anticoagulants, to see whether mortality from cardiac infarction can be further reduced. The patients who were having the " armchair treatment were allowed up within the first six to seven days; they sat up in their armchairs as long as they liked, they fed and washed themselves, and they were allowed to read. Usually symptoms of shock were allowed to subside before the patient was got into his chair, but if pulmonary oedema appeared the patients were got up earlier. In the third week patients were allowed to walk in the ward, and in the fourth week they could go into the corridor; after four weeks they usually went home. Helander divided his patients into three groups: (1) armchair cases treated with anticoagulant (dicoumarol); (2) armchair cases not treated with anticoagulant; and (3) cases treated with strict bed rest in the usual way and given anticoagulant. There were 112 patients in the first group, 100 in the second, and rest was not
"
1. Levine, S., Lown, B. 2.
Helander, S.
J. Amer. med. Ass. 1952, Acta med. scand. 1958, 162, 351.
148, 1365.
80 in the third. Patients who died within twenty-four hours of admission were not included, and the others were classified into three groups according to severity: group t comprised patients with all the clinical symptoms and signs of cardiac infarction, with shock and a fall in bloodpressure; group-ll patients had the usual signs of cardiac infarction, with fever, increased erythrocyte-sedimentation rate, and leucocytosis; group ill comprised the mildest " cases, which could be distinguished from angina pectoris only with the help of an E.C.G. tracing". These three groups were more or less evenly distributed among the treatment groups, except for some preponderance of rather more severe cases in the bed-rest group. The figures show that for group i, the most severe cases, the mortality for the two armchair groups was about the same (23% with anticoagulants and 20% without); but the mortality in those treated by bed rest was 44%. For group 11, the moderately severe cases, the mortality figures were: armchair plus anticoagulant 6%, armchair without anticoagulant 16%, bed rest with anticoagulant 22%. In group III there were no deaths in any of the treatment groups.
These mortality figures, taken at their face value, suggest that there is a decided advantage in getting patients out of bed as soon as possible; but such a straightforward interpretation is hardly justified. Many deaths in the severe group occurred during the second or third day after onset, but only 1 of these patients was sitting up when he died; the others " belonged to a group which was meant to sit up, if surviving ". Furthermore, embolism played a relatively small part as an immediate cause of death in all treatment groups; progressive cardiac failure, presumed extension of the infarction, or sudden death with or without preceding arrhythmia were the causes of most deaths. More patients died from progressive cardiac failure in the bed-rest group than in the armchair group, and possibly this was due to the greater incidence of pulmonary oedema in the bed-rest patients; spread of infarction was also somewhat commoner in the bed-rest group. Accordingly the part armchair treatment plays in the avoidance of late embolism cannot be assessed. Nevertheless Helander’s results do suggest that we may have gone too far in treating patients with cardiac infarcts with strict bed rest and no activity of any sort. Some textbooks mention no alternative to such a regime. On the other hand, some cardiologists, such as Morgan Jones,3 recommend a programme of progressive relaxation of rest after the first week; " the days of test flat in bed-rigidly immobile, being fed, and being uncomfortably balanced
bedpans-are, if not gone, at least, I hope, numbered," There is growing support for much earlier activity, and perhaps earlier discharge from hospital, especially if outpatient anticoagulant control can be arranged. on
he says.
CLINICAL FEATURES OF PORENCEPHALY
THE term porencephaly was used by Herschl4in 1859 describe circumscribed cystic defects of the cerebral hemispheres, arising during foetal development. The word has passed through some semantic vicissitudes, at times being used loosely to cover any condition in which large cerebral cysts formed; but it has generally retained the connotation of a congenital condition, or one that develops very early in infancy. Three possible causes have been suggested—a true developmental defect (an abiotrophy), occlusion of a major cerebral vessel with to
3. 4.
Jones, A. M. Brit. med. J. 1955, ii, 1613. Herschl, R. Vrtljschr. prakt. Heilk. 1859, 61, 59.
red cells. The usual explanation of this discrepancy is that the thyroid antibodies are directed againstcolloid in the acini which normally does not come in contact with antibody-forming cells. This may well be true, but another explanation might be derived from the fact that WITEBSKY used Freund adjuvants in his experiments, whereas EHRLICH did not. Possibly these adjuvants modify either the antigen or the body’s response to it in such a way as to obliterate the effect of the self-marker. Although this speculation is quite unsupported it might lead to some interesting experiments. At present no useful generalisations can be made; and there is nothing to tell us whether antibodies arise because of failure to acquire tolerance, because of subtle alterations in the chemical constitution of the antigens, or because some derangement of the antibody-forming mechanism renders it incapable of recognising self-markers. Professor DACIE suggested that in some cases the antibody might be made by neoplastic tissue rather than by normal antibody-forming tissues. These alternative explanations all seem at present about equally plausible. The pathogenesis of the various conditions discussed may well be heterogeneous. What is more important than the correctness of any detailed hypothesis is that a new idea has appeared in medical thought, and is going to give rise to a great deal of original work.
their
own
Annotations ARMCHAIR AND ANTICOAGULANTS FOR CARDIAC INFARCTION
IN 1952 Levine and Lown1 suggested that strict bed the best way of treating patients with cardiac infarction; and they proposed that, as soon as the initial shock had passed, patients could sit up in a comfortable armchair for some hours every day; they cited records of 81 patients so treated with a mortality of only 10%. One reason for adopting this sort of regime was to reduce the incidence of secondary embolism. It is agreed that anticoagulant treatment prevents this secondary embolism, and much of the reduction of mortality brought about by anticoagulant treatment is apparently related to this action. Helanderin Stockholm has been testing the effect of combining armchair treatment and anticoagulants, to see whether mortality from cardiac infarction can be further reduced. The patients who were having the " armchair treatment were allowed up within the first six to seven days; they sat up in their armchairs as long as they liked, they fed and washed themselves, and they were allowed to read. Usually symptoms of shock were allowed to subside before the patient was got into his chair, but if pulmonary oedema appeared the patients were got up earlier. In the third week patients were allowed to walk in the ward, and in the fourth week they could go into the corridor; after four weeks they usually went home. Helander divided his patients into three groups: (1) armchair cases treated with anticoagulant (dicoumarol); (2) armchair cases not treated with anticoagulant; and (3) cases treated with strict bed rest in the usual way and given anticoagulant. There were 112 patients in the first group, 100 in the second, and rest was not
"
1. Levine, S., Lown, B. 2.
Helander, S.
J. Amer. med. Ass. 1952, Acta med. scand. 1958, 162, 351.
148, 1365.
80 in the third. Patients who died within twenty-four hours of admission were not included, and the others were classified into three groups according to severity: group t comprised patients with all the clinical symptoms and signs of cardiac infarction, with shock and a fall in bloodpressure; group-ll patients had the usual signs of cardiac infarction, with fever, increased erythrocyte-sedimentation rate, and leucocytosis; group ill comprised the mildest " cases, which could be distinguished from angina pectoris only with the help of an E.C.G. tracing". These three groups were more or less evenly distributed among the treatment groups, except for some preponderance of rather more severe cases in the bed-rest group. The figures show that for group i, the most severe cases, the mortality for the two armchair groups was about the same (23% with anticoagulants and 20% without); but the mortality in those treated by bed rest was 44%. For group 11, the moderately severe cases, the mortality figures were: armchair plus anticoagulant 6%, armchair without anticoagulant 16%, bed rest with anticoagulant 22%. In group III there were no deaths in any of the treatment groups.
These mortality figures, taken at their face value, suggest that there is a decided advantage in getting patients out of bed as soon as possible; but such a straightforward interpretation is hardly justified. Many deaths in the severe group occurred during the second or third day after onset, but only 1 of these patients was sitting up when he died; the others " belonged to a group which was meant to sit up, if surviving ". Furthermore, embolism played a relatively small part as an immediate cause of death in all treatment groups; progressive cardiac failure, presumed extension of the infarction, or sudden death with or without preceding arrhythmia were the causes of most deaths. More patients died from progressive cardiac failure in the bed-rest group than in the armchair group, and possibly this was due to the greater incidence of pulmonary oedema in the bed-rest patients; spread of infarction was also somewhat commoner in the bed-rest group. Accordingly the part armchair treatment plays in the avoidance of late embolism cannot be assessed. Nevertheless Helander’s results do suggest that we may have gone too far in treating patients with cardiac infarcts with strict bed rest and no activity of any sort. Some textbooks mention no alternative to such a regime. On the other hand, some cardiologists, such as Morgan Jones,3 recommend a programme of progressive relaxation of rest after the first week; " the days of test flat in bed-rigidly immobile, being fed, and being uncomfortably balanced
bedpans-are, if not gone, at least, I hope, numbered," There is growing support for much earlier activity, and perhaps earlier discharge from hospital, especially if outpatient anticoagulant control can be arranged. on
he says.
CLINICAL FEATURES OF PORENCEPHALY
THE term porencephaly was used by Herschl4in 1859 describe circumscribed cystic defects of the cerebral hemispheres, arising during foetal development. The word has passed through some semantic vicissitudes, at times being used loosely to cover any condition in which large cerebral cysts formed; but it has generally retained the connotation of a congenital condition, or one that develops very early in infancy. Three possible causes have been suggested—a true developmental defect (an abiotrophy), occlusion of a major cerebral vessel with to
3. 4.
Jones, A. M. Brit. med. J. 1955, ii, 1613. Herschl, R. Vrtljschr. prakt. Heilk. 1859, 61, 59.