- Email: [email protected]
FIBRILLATION, FAILURE, AND THE FOXGLOVE
891
THE LANCET, APRIL 17,1982
did slightly less well: in the first year only a quarter had X-ray clearing; 2907o showed improvement and 10% had disease progression. Of 11 patients with pulmonary disease without associated hilar
adenopathy (stage III), only 1 improved spontaneously. Erythema nodosum was much more often seen in females than in males, as were uveitis and articular complaints. Hypercalcaemia was detected in 6.6% of patients, most of whom were male. Factors which pointed to a poorer prognosis were: age at diagnosis more than 40; stage II and stage III disease; unchanged chest X-ray at 1 year; extrathoracic lymph node involvement; cutaneous lesions; and hypercalcaemia. The Danish review provides useful confirmation
that, in stage I sarcoidosis, specific treatment is seldom needed. In stage II disease therapy may be required, but there is a case for postponing decisions about treatment for a year after diagnosis, unless there is rapid progression of pulmonary disease. In stage III sarcoidosis, treatment is nearly always indicated if the disease is still active. It is in these patients with stage III, and also in those with "stable" stage II sarcoidosis, that assessment of disease activity would be of greatest value. Time will tell whether bronchoalveolar lavage, and perhaps gallium-67 scanning, together with serum ACE measurement, will fulfil their promise-for assessment and management.
A HEADLINE to an editorial in Nature1 a few weeks ago proclaimed: "Doves in false garb: the claim by the antinuclear movement of professional support is mostly a sham". Not all Nature’s readers agreed2-4 and the editor5 was provoked into renewing his strictures on those professional groups who are calling attention to the dangers of nuclear war. There was no sham about the Second Congress of International Physicians for the Prevention of Nuclear War held in Cambridge, England, on April 3-6, to which we referred in a leader last week (p. 835). The First Congress of I.P.P.N.W. was held a year earlier in Fairlie, Virginia, and 11 countries were represented. In Cambridge the number of countries had nearly trebled and the movement is gaining force, despite the reluctance of some doctors to enter into what they regard as a strictly political argument. Unfortunately, the doctors of China, France, and India, three of the nuclear powers, did not send delegates to Cambridge to join in the protest against the continuation of the arms race and against the acceptance of nuclear war as a survivable event-when, in fact, medicine and its practitioners have virtually no help to offer if the worst should happen. We reproduce on p. 900 some of the messages and conclusions from the I.P.P.N.W. Congress.
386. 4 Britten S. Doves in false garb Nature 1982; 296: 386. 5 Editorial. Professional propaganda. Nature 1982; 296: 380.
SINCE William Withering observed that extracts of foxglove helped his patients with dropsy, controversy has , surrounded the use of digitalis in clinical practice. The therapeutic role of digitalis after myocardial infarction is perhaps the most contentious. Does digitalis help postinfarction arrhythmias or does it increase that risk? Does digitalis have any effect in cardiogenic shock? How much does digitalis improve the haemodynamic performance of the failing heart? These questions continue to be asked 70 years after Herrickl recommended that digitalis should be given to all patients after a myocardial infarction. On both experimental and clinical evidence, digitalis is clearly the drug of choice in atrial arrhythmias such as fibrillation, flutter, and supraventricular tachycardias.2 It seems to work partly by a direct effect on the function of the contracting, myocardium3 and partly by an increase in ,
atrioventricular block which slows the ventricular rate.4 Despite the arrhythmogenic properties detectable in the laboratory, digitalis does not seem to increase the incidence of arrhythmias when given to patients with myocardial
infarction.2,5 Should digitalis be given in cardiogenic shock? In those few patients who have been studied, little or no improvement in left ventricular performance has been achieved; and, in animals, cardiac output sometimes falls after digitalis. There seems therefore no place for digitalis in the management of cardiogenic shock except when there is an atrial arrhythmia. In clinically apparent acute left ventricular failure complicating myocardial infarction, some small benefits have been seen. Digitalis increases the blood flow to the ischaemic area6 and decreases the amount of ST elevation’ in dogs, increases myocardial contractility (both in laboratory
animals8 and in human beings 9), and increases left ventricular ejection fraction. Most work in man has shown a modest
THE RESPONSIBILITY TO PROTEST
1 Editorial Doves in false garb Nature 1982; 295: 542. 2 Meredith C. Doves in false garb. Nature 1982; 296: 386. 3 Hartog M, Baumer JH, Fleming PJ, Hall MJ. Doves in false
FIBRILLATION, FAILURE, AND THE FOXGLOVE
garb. Nature 1982, 296:
increase in cardiac output and a small decrease in left ventricular filling pressure; 11 so digitalis may be of some benefit in acute failure. The evidence for benefit of digitalis in chronic heart failure remains uncertain. There are risks with digitalis toxicity, especially in the elderly,12 and some of the initial benefits’of digitalis may be lost with time.’3 In patients
JB. Clinical features of sudden obstruction of the coronary arteries. JAMA 1912; 59: 2015-20. 2. Rahimtoola SH, Gunnar RM. Digitalis in acute myocardial infarction: help or hazard? Ann Intern Med 1975; 82: 234-40. 3. Smith TW, Haber E. Digitalis (second of four parts). N Engl J Med 1973; 289: 1. Herrick
1010-15.
MacKenzie J. Digitalis. Heart 1911; 2: 273-386. Reicansky I, Conradson T-B, Holmberg S, Ryden L, Waldenstrom A, Wennerblom B. The effect of intravenous digoxin on the occurrence of ventricular tachyarrhythmias in acute myocardial infarction in man. Am Heart J 1976, 91: 705-11. 6. Watanabe T, Covell JW, Maroko PR, Braunwald E, Ross J. Effects of increased arterial pressure and positive inotropic agents on the severity of myocardial ischaemia in the acutely depressed heart. Am J Cardiol 1972; 30: 371-77. 7. Vatner SF, Baig H, Manders WT, Murray PA. Effects of a cardiac glycoside on regional function, blood flow and electrograms in conscious dogs with myocardial ischaemia.
4. 5.
Circ Res 1978; 43: 413-23. 8. Kumar R, Hood WB, Joison J, Gilmour DP, Norman JC, Abelmann WH. Experimental myocardial infarction. VI Efficacy and toxicity of digitalis in acute and healing phase in intact conscious dogs. J Clin Invest 1970, 49: 358-64. 9. Rahimtoola SH, Sinno MZ, Chuquimia R, Loeb HS, Rosen KM, Gunnar RM. Effects of ouabain on impaired left ventricular function in acute myocardial infarction N Engl J Med 1972; 287: 527-31 10. Morrison J, Coromilas J, Robbins M, Ong L, Eisenberg S, Stechel R, Zema M, Reiser P, Scherr L. Digitalis and myocardial infarction in man. Circulation 1980; 60: 8-16. 11 Marcus FI. Use of digitalis in acute myocardial infarction. Circulation 1980; 62: 17-19 12. Smith TW. Digoxin toxicity: epidemiology and clinical use of serum concentration measurements. Am J Med 1975; 58: 470-76. 13. Guz A, McHaffie D The use of digitalis glycosides in sinus rhythm. Clin Sci Mol Med
1978; 55: 417-21.
892
who have been on digitalis for a long time withdrawal of the drug does not lead to deterioration, provided that diuretic therapy is adjusted at the same time. 14
By far the most worrying evidence against the use of digitalis in cardiac failure after myocardial infarction is a retrospective study by Moss and colleagueslsof just under 1000 patients with myocardial infarction. They recorded several deaths within the first four months after infarction among those patients who had been treated for congestive cardiac failure with digitalis during their hospital stay and in whom ventricular ectopic beats had been recorded during continuous electrocardiography. Even after allowing for other factors that might have influenced mortality, they had to conclude that digitalis increased the early post-hospital mortality of myocardial infarction patients in whom there had been combined electrical and mechanical dysfunction. They were unable to assess the relevance of the interaction of digitalis and antiarrhythmic agents such as quinidine, or the role of hypokalaemia. A prospective study is needed to confirm or refute this evidence.
QUALITY ASSURANCE IN THE BLOOD BANK MOST of the serious errors in blood transfusion are committed outside the laboratory. Nonetheless, every clinician who transfuses blood will want to be reassured that compatibility tests are competently done. Although methods vary widely, a compatibility test consists of mixing the patient’s serum and the donor’s red cells, incubating them, and determining whether a specific antigen-antibody reaction has occurred. The best way to ensure correct results is to select a set (usually four) of sensitive but robust techniques and apply them with care. In Britain proficiency tests organised by the regional transfusion centres and latterly by the Blood Group Reference Laboratory. are designed to provide reassurance for the best laboratories and early warning for those whose standards may be declining. Holburn and England2 have now reported the results of the first seven U.K. national proficiency tests. The method used was to send simulated patient sera and donor cells to each regional transfusion centre for distribution among its own client laboratories. Each laboratory was to do compatibility tests by the methods in routine use and report them anonymously (under code) to the Blood Group Reference Laboratory. The marking system was based on results of the saline, albumin, and anti-human globulin techniques advocated by Tovey and Jenkins3 as the minimum acceptable compatibility test. False-positive and false-negative results were penalised. If an incompatibility was completely missed a further penalty was imposed.
Since the study set out to explore a number of questions, it is not possible to consider all the results together. In five of the tests only clinically significant antibodies were issued and 14. Hull SM, MacKintosh A. Discontinuation of maintenance digoxin therapy in general practice Lancet 1977; ii: 1054-55 15 Moss AJ, Davis HT, Conrad DL, Decamilla JJ, Odoroff CL. Digitalis-associated cardiac mortality after myocardial infarction. Circulation 1981; 64: 1150-56. 1. Editorial. Transfusion disasters. Lancet 1981; ii: 618-19. 2. Holburn AM, England JM. The UK national external quality assessment scheme in blood group serology. Compatibility testing 1979-80 Clin Lab Haemat 1982; 4: 1-2. 3 Tovey GH, Jenkins WJ Compatibility tests for blood transfusion. London: Association of Clinical Pathologists, 1980 (Broadsheet 57: Revised 1980).
all were detectable by the anti-human globulin test which is the serplogist’s most valued and flexible technique. An incompatibility was totally missed by 35% at best and 22% at worst of participants. It may be argued that the exclusion of enzyme methods from the study led some participants to report results from techniques not routinely used in their laboratories and that if the results of enzyme tests had been accepted fewer laboratories would have missed a weak reaction in the rhesus system. On the other hand, Holburn and England were satisfied that this reaction was a two plus (+ +) positive by the anti-human globulin test. Even if this result is ignored the frequency of false compatibility reports ranged from 3.5% to 12.4%. In an attempt to explore the exact sensitivity of the antihuman globulin tests in routine use several examples of diluted anti-D were distributed. Strong examples of anti-D were detected by 99.5% or more of laboratories while 9 - 5% of laboratories missed a reaction between anti-D diluted to 01IU/ml and a strongly D positive cell. With a weakly D positive cell the reaction was missed by 17-6% of laboratories. This concentration of anti-D is close to the limit of detection by the slide anti-human-globuliji test but should be readily detectable by albumin or enzyme methods. These methods are used largely because of their ability to detect weak rhesus antibodies.
What do these results tell us about overall proficiency? Only thirteen laboratories out of a total of between three and four hundred detected every incompatibility while thirty-two missed an average of two or more incompatibilities in each proficiency test. In addition, thirty-one laboratories submitted results for fewer than half of the exercises. Where do we go from here? It would be reasonable to hope that proficiency testing alone would tend to improve standardsafter all, laboratory staff are highly motivated and responsible people. Even with a large number of laboratories participating in a programme of serological proficiency testing it is difficult to identify trends. The main problem is that some exercises are easier than others. If we set aside the results with the weak anti-D and another antibody which was probably not biologically significant, the results for 1980 were marginally better than those for 1979. Inclusion of the results of enzyme tests in the assessment may improve scores with rhesus antibodies. Recent changes in the system have therefore been beneficial. Jenkins,commenting on Holburn and England’s report, describes earlier experience of regional proficiency testing. Repeated testing did not secure overall improvement although isolated causes of error were occasionally found and corrected.
Any laboratory which is dissatisfied with its performance should seek, in confidence, constructive advice from the regional transfusion director. Techniques should be scrutinised and extra controls should be used. In addition, matching staff should be given time and materials to work with sera known to contain antibodies. If these efforts are fruitless or if a laboratory will not take advice, a national working party has been set up to support regional directors in their messages to consultants in charge of under-achieving laboratories. As a last resort a regional director may be forced to the conclusion that it is no longer safe to supply blood to a particular hospital blood bank. 4.
Jenkins WJ. What is the quality of blood transfusion serology? Clin Lab Haemat 1982; 4: 3-12.
THE LANCET, APRIL 17,1982
did slightly less well: in the first year only a quarter had X-ray clearing; 2907o showed improvement and 10% had disease progression. Of 11 patients with pulmonary disease without associated hilar
adenopathy (stage III), only 1 improved spontaneously. Erythema nodosum was much more often seen in females than in males, as were uveitis and articular complaints. Hypercalcaemia was detected in 6.6% of patients, most of whom were male. Factors which pointed to a poorer prognosis were: age at diagnosis more than 40; stage II and stage III disease; unchanged chest X-ray at 1 year; extrathoracic lymph node involvement; cutaneous lesions; and hypercalcaemia. The Danish review provides useful confirmation
that, in stage I sarcoidosis, specific treatment is seldom needed. In stage II disease therapy may be required, but there is a case for postponing decisions about treatment for a year after diagnosis, unless there is rapid progression of pulmonary disease. In stage III sarcoidosis, treatment is nearly always indicated if the disease is still active. It is in these patients with stage III, and also in those with "stable" stage II sarcoidosis, that assessment of disease activity would be of greatest value. Time will tell whether bronchoalveolar lavage, and perhaps gallium-67 scanning, together with serum ACE measurement, will fulfil their promise-for assessment and management.
A HEADLINE to an editorial in Nature1 a few weeks ago proclaimed: "Doves in false garb: the claim by the antinuclear movement of professional support is mostly a sham". Not all Nature’s readers agreed2-4 and the editor5 was provoked into renewing his strictures on those professional groups who are calling attention to the dangers of nuclear war. There was no sham about the Second Congress of International Physicians for the Prevention of Nuclear War held in Cambridge, England, on April 3-6, to which we referred in a leader last week (p. 835). The First Congress of I.P.P.N.W. was held a year earlier in Fairlie, Virginia, and 11 countries were represented. In Cambridge the number of countries had nearly trebled and the movement is gaining force, despite the reluctance of some doctors to enter into what they regard as a strictly political argument. Unfortunately, the doctors of China, France, and India, three of the nuclear powers, did not send delegates to Cambridge to join in the protest against the continuation of the arms race and against the acceptance of nuclear war as a survivable event-when, in fact, medicine and its practitioners have virtually no help to offer if the worst should happen. We reproduce on p. 900 some of the messages and conclusions from the I.P.P.N.W. Congress.
386. 4 Britten S. Doves in false garb Nature 1982; 296: 386. 5 Editorial. Professional propaganda. Nature 1982; 296: 380.
SINCE William Withering observed that extracts of foxglove helped his patients with dropsy, controversy has , surrounded the use of digitalis in clinical practice. The therapeutic role of digitalis after myocardial infarction is perhaps the most contentious. Does digitalis help postinfarction arrhythmias or does it increase that risk? Does digitalis have any effect in cardiogenic shock? How much does digitalis improve the haemodynamic performance of the failing heart? These questions continue to be asked 70 years after Herrickl recommended that digitalis should be given to all patients after a myocardial infarction. On both experimental and clinical evidence, digitalis is clearly the drug of choice in atrial arrhythmias such as fibrillation, flutter, and supraventricular tachycardias.2 It seems to work partly by a direct effect on the function of the contracting, myocardium3 and partly by an increase in ,
atrioventricular block which slows the ventricular rate.4 Despite the arrhythmogenic properties detectable in the laboratory, digitalis does not seem to increase the incidence of arrhythmias when given to patients with myocardial
infarction.2,5 Should digitalis be given in cardiogenic shock? In those few patients who have been studied, little or no improvement in left ventricular performance has been achieved; and, in animals, cardiac output sometimes falls after digitalis. There seems therefore no place for digitalis in the management of cardiogenic shock except when there is an atrial arrhythmia. In clinically apparent acute left ventricular failure complicating myocardial infarction, some small benefits have been seen. Digitalis increases the blood flow to the ischaemic area6 and decreases the amount of ST elevation’ in dogs, increases myocardial contractility (both in laboratory
animals8 and in human beings 9), and increases left ventricular ejection fraction. Most work in man has shown a modest
THE RESPONSIBILITY TO PROTEST
1 Editorial Doves in false garb Nature 1982; 295: 542. 2 Meredith C. Doves in false garb. Nature 1982; 296: 386. 3 Hartog M, Baumer JH, Fleming PJ, Hall MJ. Doves in false
FIBRILLATION, FAILURE, AND THE FOXGLOVE
garb. Nature 1982, 296:
increase in cardiac output and a small decrease in left ventricular filling pressure; 11 so digitalis may be of some benefit in acute failure. The evidence for benefit of digitalis in chronic heart failure remains uncertain. There are risks with digitalis toxicity, especially in the elderly,12 and some of the initial benefits’of digitalis may be lost with time.’3 In patients
JB. Clinical features of sudden obstruction of the coronary arteries. JAMA 1912; 59: 2015-20. 2. Rahimtoola SH, Gunnar RM. Digitalis in acute myocardial infarction: help or hazard? Ann Intern Med 1975; 82: 234-40. 3. Smith TW, Haber E. Digitalis (second of four parts). N Engl J Med 1973; 289: 1. Herrick
1010-15.
MacKenzie J. Digitalis. Heart 1911; 2: 273-386. Reicansky I, Conradson T-B, Holmberg S, Ryden L, Waldenstrom A, Wennerblom B. The effect of intravenous digoxin on the occurrence of ventricular tachyarrhythmias in acute myocardial infarction in man. Am Heart J 1976, 91: 705-11. 6. Watanabe T, Covell JW, Maroko PR, Braunwald E, Ross J. Effects of increased arterial pressure and positive inotropic agents on the severity of myocardial ischaemia in the acutely depressed heart. Am J Cardiol 1972; 30: 371-77. 7. Vatner SF, Baig H, Manders WT, Murray PA. Effects of a cardiac glycoside on regional function, blood flow and electrograms in conscious dogs with myocardial ischaemia.
4. 5.
Circ Res 1978; 43: 413-23. 8. Kumar R, Hood WB, Joison J, Gilmour DP, Norman JC, Abelmann WH. Experimental myocardial infarction. VI Efficacy and toxicity of digitalis in acute and healing phase in intact conscious dogs. J Clin Invest 1970, 49: 358-64. 9. Rahimtoola SH, Sinno MZ, Chuquimia R, Loeb HS, Rosen KM, Gunnar RM. Effects of ouabain on impaired left ventricular function in acute myocardial infarction N Engl J Med 1972; 287: 527-31 10. Morrison J, Coromilas J, Robbins M, Ong L, Eisenberg S, Stechel R, Zema M, Reiser P, Scherr L. Digitalis and myocardial infarction in man. Circulation 1980; 60: 8-16. 11 Marcus FI. Use of digitalis in acute myocardial infarction. Circulation 1980; 62: 17-19 12. Smith TW. Digoxin toxicity: epidemiology and clinical use of serum concentration measurements. Am J Med 1975; 58: 470-76. 13. Guz A, McHaffie D The use of digitalis glycosides in sinus rhythm. Clin Sci Mol Med
1978; 55: 417-21.
892
who have been on digitalis for a long time withdrawal of the drug does not lead to deterioration, provided that diuretic therapy is adjusted at the same time. 14
By far the most worrying evidence against the use of digitalis in cardiac failure after myocardial infarction is a retrospective study by Moss and colleagueslsof just under 1000 patients with myocardial infarction. They recorded several deaths within the first four months after infarction among those patients who had been treated for congestive cardiac failure with digitalis during their hospital stay and in whom ventricular ectopic beats had been recorded during continuous electrocardiography. Even after allowing for other factors that might have influenced mortality, they had to conclude that digitalis increased the early post-hospital mortality of myocardial infarction patients in whom there had been combined electrical and mechanical dysfunction. They were unable to assess the relevance of the interaction of digitalis and antiarrhythmic agents such as quinidine, or the role of hypokalaemia. A prospective study is needed to confirm or refute this evidence.
QUALITY ASSURANCE IN THE BLOOD BANK MOST of the serious errors in blood transfusion are committed outside the laboratory. Nonetheless, every clinician who transfuses blood will want to be reassured that compatibility tests are competently done. Although methods vary widely, a compatibility test consists of mixing the patient’s serum and the donor’s red cells, incubating them, and determining whether a specific antigen-antibody reaction has occurred. The best way to ensure correct results is to select a set (usually four) of sensitive but robust techniques and apply them with care. In Britain proficiency tests organised by the regional transfusion centres and latterly by the Blood Group Reference Laboratory. are designed to provide reassurance for the best laboratories and early warning for those whose standards may be declining. Holburn and England2 have now reported the results of the first seven U.K. national proficiency tests. The method used was to send simulated patient sera and donor cells to each regional transfusion centre for distribution among its own client laboratories. Each laboratory was to do compatibility tests by the methods in routine use and report them anonymously (under code) to the Blood Group Reference Laboratory. The marking system was based on results of the saline, albumin, and anti-human globulin techniques advocated by Tovey and Jenkins3 as the minimum acceptable compatibility test. False-positive and false-negative results were penalised. If an incompatibility was completely missed a further penalty was imposed.
Since the study set out to explore a number of questions, it is not possible to consider all the results together. In five of the tests only clinically significant antibodies were issued and 14. Hull SM, MacKintosh A. Discontinuation of maintenance digoxin therapy in general practice Lancet 1977; ii: 1054-55 15 Moss AJ, Davis HT, Conrad DL, Decamilla JJ, Odoroff CL. Digitalis-associated cardiac mortality after myocardial infarction. Circulation 1981; 64: 1150-56. 1. Editorial. Transfusion disasters. Lancet 1981; ii: 618-19. 2. Holburn AM, England JM. The UK national external quality assessment scheme in blood group serology. Compatibility testing 1979-80 Clin Lab Haemat 1982; 4: 1-2. 3 Tovey GH, Jenkins WJ Compatibility tests for blood transfusion. London: Association of Clinical Pathologists, 1980 (Broadsheet 57: Revised 1980).
all were detectable by the anti-human globulin test which is the serplogist’s most valued and flexible technique. An incompatibility was totally missed by 35% at best and 22% at worst of participants. It may be argued that the exclusion of enzyme methods from the study led some participants to report results from techniques not routinely used in their laboratories and that if the results of enzyme tests had been accepted fewer laboratories would have missed a weak reaction in the rhesus system. On the other hand, Holburn and England were satisfied that this reaction was a two plus (+ +) positive by the anti-human globulin test. Even if this result is ignored the frequency of false compatibility reports ranged from 3.5% to 12.4%. In an attempt to explore the exact sensitivity of the antihuman globulin tests in routine use several examples of diluted anti-D were distributed. Strong examples of anti-D were detected by 99.5% or more of laboratories while 9 - 5% of laboratories missed a reaction between anti-D diluted to 01IU/ml and a strongly D positive cell. With a weakly D positive cell the reaction was missed by 17-6% of laboratories. This concentration of anti-D is close to the limit of detection by the slide anti-human-globuliji test but should be readily detectable by albumin or enzyme methods. These methods are used largely because of their ability to detect weak rhesus antibodies.
What do these results tell us about overall proficiency? Only thirteen laboratories out of a total of between three and four hundred detected every incompatibility while thirty-two missed an average of two or more incompatibilities in each proficiency test. In addition, thirty-one laboratories submitted results for fewer than half of the exercises. Where do we go from here? It would be reasonable to hope that proficiency testing alone would tend to improve standardsafter all, laboratory staff are highly motivated and responsible people. Even with a large number of laboratories participating in a programme of serological proficiency testing it is difficult to identify trends. The main problem is that some exercises are easier than others. If we set aside the results with the weak anti-D and another antibody which was probably not biologically significant, the results for 1980 were marginally better than those for 1979. Inclusion of the results of enzyme tests in the assessment may improve scores with rhesus antibodies. Recent changes in the system have therefore been beneficial. Jenkins,commenting on Holburn and England’s report, describes earlier experience of regional proficiency testing. Repeated testing did not secure overall improvement although isolated causes of error were occasionally found and corrected.
Any laboratory which is dissatisfied with its performance should seek, in confidence, constructive advice from the regional transfusion director. Techniques should be scrutinised and extra controls should be used. In addition, matching staff should be given time and materials to work with sera known to contain antibodies. If these efforts are fruitless or if a laboratory will not take advice, a national working party has been set up to support regional directors in their messages to consultants in charge of under-achieving laboratories. As a last resort a regional director may be forced to the conclusion that it is no longer safe to supply blood to a particular hospital blood bank. 4.
Jenkins WJ. What is the quality of blood transfusion serology? Clin Lab Haemat 1982; 4: 3-12.