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AMMONIUM-CHLORIDE POISONING
1274 later in others ? And why should it occur more readily after injury of some regions of the brain than of others ? PSEUDOTUMOR CEREBRI
THE term " pseudotumor cerebri " is commonly applied in the United States to the clinical syndrome which in this country is more often referred to as otitic hydrocephalus, benign intracranial hypertension, toxic hydrocephalus, or serous meningitis. This disorder is marked by protracted increase in the intracranial pressure, but focal neurological symptoms and signs are lacking and the cerebrospinal fluid is normal.1 The most prominent symptoms are headache and blurred vision, while diplopia due to unilateral or bilateral sixth-nerve palsies is common; tinnitus, nausea, and vomiting are less usual. Bilateral papilloedema is invariably present, and its severity may be unexpected in view of the patient’s apparent well-being. Consciousness is never disturbed, but in a small proportion of cases the papillcedema may be so severe as to threaten vision. This condition can never be safely diagnosed on clinical evidence alone: ventriculography is an essential step in differential diagnosis as some patients with intracranial neoplasms present with an identical clinical picture. The syndrome was first described by Quincke2 in 1893, and in 1936 Davidoff and Dyke 3 found that in such cases ventriculography revealed a normal outline. It later became clear that meningeal inflammation was not a feature, there being no pleocytosis or increase of protein in the cerebrospinal fluid. Many of the earliest cases on record were associated with otitis media; and Symonds4 coined the term " otitic hydrocephalus ", suggesting that the condition probably resulted from thrombosis of intracranial venous sinuses, and that, if the sagittal sinus were involved, venous obstruction and impaired absorption of the cerebrospinal fluid might contribute to the rise in pressure. In recent years, because of chemotherapy and antibiotics, fewer and fewer cases have been described in association with otitis media: Foley5 in 1955 reported 13 otitic " and 47 " non-otitic " cases. While the syndrome occasionally follows head injury or complicates cachexia or malignant disease (when it usually results from sagittal-sinus thrombosis), the majority of cases nowadays are in women of childbearing age, in whom it is commonly related to pregnancy or to menstruation.5 Foley pointed out that often the cerebral ventricles are reduced in volume. Hence he agreed with Dandy6 that the condition must be due to (a) obstruction to the venous outflow from the cranium, or (b) dilatation of the arterioles, or (c) swelling of the brain itself. While in some cases the unquestionable cause is intracranial venous-sinus thrombosis, which can be demonstrated by venography, cerebral oedema of undetermined aetiology is, it now seems, a more usual cause. Thomas7 in 1933 described the case of a woman in whom generalised "
oedema, headache, and bilateral papilloedema developed with each menstrual period; and recent studies of the papilloedema which may occur in the Guillain-Barre 1. Paterson, R., De Pasquale, N., Mann, S. Medicine, Baltimore, 1961, 40, 85. 2. Quincke, H. Samml. klin. Vortr. 1893, no. 67 (Inn. Med. 23, 655). 3. Davidoff, L. M., Dyke, C. G. J. nerv. ment. Dis. 1936, 83, 700. 4. Symonds, C. P. Brain, 1931, 54, 55. 5. Foley, J. ibid. 1955, 78, 1. 6. Dandy, W. E. Ann. Surg. 1937, 106, 492. 7. Thomas, W. A. J. Amer. med. Ass. 1933, 101, 1126
after poliomyelitis lo 11 have suggested that cerebral oedema is responsible. A similar explanation has been advanced for the symptoms and signs of increased intracranial pressure which sometimes develop in Addison’s disease.12-14 These observations suggested to Paterson et al. that the syndrome of " pseudotumor cerebri " might often be due to an endocrine disturbance. They report a series of 17 cases of the condition, all in women of reproductive age; there was often associated obesity or menstrual irregularity, or the condition developed during or shortly after pregnancy, and in 4 cases there was galactorrhaea. The urinary levels of 17-ketosteroids and of 17-hydroxycorticosteroids were usually normal, but Paterson et al. give cogent reasons for suggesting that physiological hyperpituitarism is often at least partly responsible for the cerebral oedema-though " they add that pseudotumor cerebri " is a syndrome of
syndrome
8 9
or
multiple aetiology. The illness is, as a rule, benign and self-limiting, though it may persist for many months; but when, occasionally, papilloedema endangers vision, operative decompression is required. Paterson et al.1 found that in 5 out of 6 cases of pseudotumor cerebri administration of prednisone or methyl-prednisolone led to rapid improvement, and it seems justifiable to undertake steroid therapy in proven "
"
of this disorder where demonstrated.
cases
no
definite
cause can
be
AMMONIUM-CHLORIDE POISONING
AMMONIUM chloride is widely used in small doses as an expectorant and diaphoretic and in larger doses as a diuretic and in order to make the urine persistingly acid. In the U.S.A. it is also used for weight reduction and is incorporated in preparations sold directly to the public for this purpose. The B.P. dosage of ammonium chloride as a diuretic is 3-6 g. daily in divided amounts; but it may be administered in a dosage of up to 8 g. daily without producing more than mild asymptomatic acidosis.15 The acidosis arises because a hydrogen ion (H+) is released from the ammonium ion (NH4) when ammonia (NH3) from it is converted to urea by the liver. Ammonium chloride is therefore potentially toxic because of this release of hydrogen ions and because ammonia is itself toxic. The prevention of toxicity depends on good renal function, for the elimination of the hydrogen ions, and on good hepatic function, for speedy conversion of the ammonia to urea. Two instances of ammonium-chloride poisoning in apparently healthy subjects are reported by Relman et al.1’ Both were in women, one of whom was attempting to slim; she took 82 g. of the compound in forty-eight hours. The symptoms were headache, nausea, vomiting, and hyperpnoea, with progressive drowsiness and confusion. The urine of both patients contained protein and was acid (pH 4-8 and 5-0) and of low specific gravity (1-010 and 1-001). Biochemical investigations revealed profound hyperchloraemic acidosis. Treatment with large amounts of intravenous sodium bicarbonate and lactate (691 mEq. 8. Ford, F. R., Walsh, F. B. Bull. Johns Hopk. Hosp. 1943, 73, 391. 9. Joynt, R. J. Neurology, 1958, 8, 8. 10. Weiman, C. G., McDowell, F. H., Plum, F. Arch. Neurol. Psychiat.
1951, 66, 122. Gass, H. H. J. Dis. Child. 1957, 93, 640. Boudin, G., Funck-Brentano, J. L., Gayno, M. Bull. Soc. Méd. Hôp. Paris, 1950, 66, 1736. 13. Walsh, F. B. Arch. Ophthal., N.Y. 1952, 47, 86. 14. Jefferson, A. J. Neurol. Psychiat. 1956, 19, 21. 15. The Extra Pharmacopoeia: Martindale; vol. 1, p. 1222. London, 1958. 16. Relman, A. S., Shelburne, P. F., Talman, A. New Engl. J. Med. 1961, 264, 848. 11. 12.
1275
in twenty hours in one patient and 643 mEq. in fortyeight hours in the other) produced rapid clinical recovery; but
hyperventilation tended
to
persist rather longer than
would have been expected from the biochemical data, and during treatment severe hypokalaemia developed after six hours. After recovery the proteinuria disappeared and the ability to concentrate urine reverted to normal. In these two cases the dosage far exceeded that recommended; but there is evidence that with impaired renal, hepatic, or cardiac function less excessive doses may cause toxic manifestations. Symptoms of ammonium-chloride intoxication have been reported in patients with18renal dysfunction who have taken as little as It is known, too, that in severe liver disease 5 g. daily.l’ the blood-ammonia level is raised,l9 and that, when this is so, hepatic coma may be precipitated by giving ionexchange resins which act by releasing the ammonium ion and taking up sodium.20 In chronic cardiac disease, ammonium chloride in dosages of 4 to 6 g. daily by mouth has been found to cause anorexia, hyperpnoea, lethargy, and drowsiness. 21 Accordingly ammonium chloride is . contraindicated when there is renal or hepatic disease, and its use in the management of cardiac oedema should be undertaken with care. Courses of treatment involving more than 4 g. daily should always be intermittent; and if the patient becomes anorexic, dyspnoeic, or lethargic the possibility of ammonium-chloride intoxication must be considered. HOSPITAL PLANNING "
By the time a modern hospital is built it is already twenty years behind the times." Expressing this view at a London meeting arranged last week by King Edward’s Hospital Fund, Mr. Gordon Friesen, a consultant in hospital planning from Washington, D.C., attributed the time-lag to a failure of basic policy in the planning of hospitals. The practice, he said, is to start with a somewhat sketchy idea of the function of the new hospital and its various departments, to put up a building of what is thought to be about the right size, and then, Procrusteslike, to adapt the organisation to fit the building. In other words, function is made to depend on structure, whereas in Mr. Friesen’s opinion the organisation of the hospital should be planned in very considerable detail-including detail of fixed and movable equipment-before pencil is put to paper, beyond a scribble. Or, as he expresses it, " develop the organisation and put a roof over it In the United States 70% of the maintenance cost of a hospital is for salaries and wages (the figure in Great Britain is about 60%) and in both countries under present conditions the figure is likely to rise. If a good hospital service, therefore, is not to price itself out of existence, it must conserve labour, especially skilled labour, by applying to the utmost the method of automation borrowed from industry. Time-and-motion studies have shown that a high proportion of work at present done in hospital is non-productive, and that less of a nurse’s time should, for instance, be spent in fetching and carrying. A bricklayer for generations has had a hod-carrier to mix his mortar and carry his bricks, enabling him to devote his whole energies to the skilled work of bricklaying. Is not a nurse as
important
as a
bricklayer ?
17. Keith, N. M., Barrier, C. W., Whelman, M. J. Amer. med. Ass. 1925,
85, 799.
18. Sleisenger, M. H., Freedberg, A. S. Circulation, 1951, 3, 837. 19. Kirk, E. Acta. med. scand. 1936, suppl. 77. 20. Gabuzda, G. J., Phillips, G. B., Davidson, C. S. New Engl. J. Med.
1952, 246, 124.
21. Sievers, M. L., Vander, J. B. J. Amer. med. Ass. 1956, 161, 410.
Mr. Friesen would adopt a conveyor-belt system for everything possible in a hospital except the patient: indeed he has done this in a number of hospitals on which he has been engaged in the U.S.A. By this means he claims that the savings in running costs will pay for the capital cost of the hospital in twenty years. (He estimates the annual maintenance cost at 40% of the capital cost.) His conception of the structure of a modern hospital is that the inpatient accommodation should be piled vertically, with 60 beds to a floor; the total bed-capacity is thus fixed at the outset. But the supporting services-outpatient
accommodation, laboratories, X-ray department, theatres, and so on-are planned horizontally so as to give flexibility and scope for expansion as investigations multiply and special procedures are devised. On the bottom floor of the vertically planned inpatient block is a central area for the mechanical washing and autoclaving of all soiled articles from the wards-instruments, bedpans, crockery, and linen (the laundry is adjoining). After being autoclaved, the articles are prepacked (linen packs, instrument packs, &c.) ready to be sent back to the wards by hoists fitted with automatic ejectors to eject packs at any required floor. Soiled articles and garbage for disposal (" trash ") come down from the wards in appropriate hoists or chutes. All supplies, linen, drugs, crockery, hardware, and food are centralised. Pneumatic conveyor tubes are freely used for the circulation of mail and sending of reports, records, pathological specimens (in standard containers), and drugs from one part of the hospital to another. Whenever possible, equipment-laboratory benches, desks, refrigerators, and even shelves-is mounted on castors, for flexibility and ease of cleaning. Inpatients are in rooms with 2 beds or sometimes 4. Each room has its own w.c. and shower (it is contended that by vertical planning this is not expensive) and communicates by microphone with the centrally placed nurses’ station. Each patient has his own urinal and bedpan, which after use are placed in a small compartment off the patient’s room by a nurse who then calls on the microphone for an attendant to take it away and send it to be emptied, cleaned, sterilised, and replaced. With soiled linen the procedure is similar. Patients’ meals, selected from a menu, are prepared by the dietitian staff in the central kitchen and sent up ready served on a tray for each patient. In commenting on these very interesting developments we have to admit that in Britain our thoughts on hospitals tend to be rather old-fashioned. But it does seem that some of Mr. Friesen’s generally admirable precepts need to be treated with a dash of circumspection. A certain amount-not overdone-of repetitive work, to-ing and fro-ing, fetching and carrying, making-do and mending, is not without value in the training of the young studentnurse, who after qualification may find herself called on to nurse the sick under conditions where push-button automation and fingertip control are not within reach. Moreover the conveyor-belt philosophy, if carried too far, could produce a state of mind where mechanical efficiency replaced humanity. A Frankenstein monster would then have been created; and, despite our earnest intentions, the patient himself would be on the conveyor belt. But, whether or not one agrees entirely with Mr. Friesen, one cannot but be carried along by his infectious enthusiasm; and the King’s Fund is to be thanked for making his voice heard last week by so many hospital planners in this country.
THE term " pseudotumor cerebri " is commonly applied in the United States to the clinical syndrome which in this country is more often referred to as otitic hydrocephalus, benign intracranial hypertension, toxic hydrocephalus, or serous meningitis. This disorder is marked by protracted increase in the intracranial pressure, but focal neurological symptoms and signs are lacking and the cerebrospinal fluid is normal.1 The most prominent symptoms are headache and blurred vision, while diplopia due to unilateral or bilateral sixth-nerve palsies is common; tinnitus, nausea, and vomiting are less usual. Bilateral papilloedema is invariably present, and its severity may be unexpected in view of the patient’s apparent well-being. Consciousness is never disturbed, but in a small proportion of cases the papillcedema may be so severe as to threaten vision. This condition can never be safely diagnosed on clinical evidence alone: ventriculography is an essential step in differential diagnosis as some patients with intracranial neoplasms present with an identical clinical picture. The syndrome was first described by Quincke2 in 1893, and in 1936 Davidoff and Dyke 3 found that in such cases ventriculography revealed a normal outline. It later became clear that meningeal inflammation was not a feature, there being no pleocytosis or increase of protein in the cerebrospinal fluid. Many of the earliest cases on record were associated with otitis media; and Symonds4 coined the term " otitic hydrocephalus ", suggesting that the condition probably resulted from thrombosis of intracranial venous sinuses, and that, if the sagittal sinus were involved, venous obstruction and impaired absorption of the cerebrospinal fluid might contribute to the rise in pressure. In recent years, because of chemotherapy and antibiotics, fewer and fewer cases have been described in association with otitis media: Foley5 in 1955 reported 13 otitic " and 47 " non-otitic " cases. While the syndrome occasionally follows head injury or complicates cachexia or malignant disease (when it usually results from sagittal-sinus thrombosis), the majority of cases nowadays are in women of childbearing age, in whom it is commonly related to pregnancy or to menstruation.5 Foley pointed out that often the cerebral ventricles are reduced in volume. Hence he agreed with Dandy6 that the condition must be due to (a) obstruction to the venous outflow from the cranium, or (b) dilatation of the arterioles, or (c) swelling of the brain itself. While in some cases the unquestionable cause is intracranial venous-sinus thrombosis, which can be demonstrated by venography, cerebral oedema of undetermined aetiology is, it now seems, a more usual cause. Thomas7 in 1933 described the case of a woman in whom generalised "
oedema, headache, and bilateral papilloedema developed with each menstrual period; and recent studies of the papilloedema which may occur in the Guillain-Barre 1. Paterson, R., De Pasquale, N., Mann, S. Medicine, Baltimore, 1961, 40, 85. 2. Quincke, H. Samml. klin. Vortr. 1893, no. 67 (Inn. Med. 23, 655). 3. Davidoff, L. M., Dyke, C. G. J. nerv. ment. Dis. 1936, 83, 700. 4. Symonds, C. P. Brain, 1931, 54, 55. 5. Foley, J. ibid. 1955, 78, 1. 6. Dandy, W. E. Ann. Surg. 1937, 106, 492. 7. Thomas, W. A. J. Amer. med. Ass. 1933, 101, 1126
after poliomyelitis lo 11 have suggested that cerebral oedema is responsible. A similar explanation has been advanced for the symptoms and signs of increased intracranial pressure which sometimes develop in Addison’s disease.12-14 These observations suggested to Paterson et al. that the syndrome of " pseudotumor cerebri " might often be due to an endocrine disturbance. They report a series of 17 cases of the condition, all in women of reproductive age; there was often associated obesity or menstrual irregularity, or the condition developed during or shortly after pregnancy, and in 4 cases there was galactorrhaea. The urinary levels of 17-ketosteroids and of 17-hydroxycorticosteroids were usually normal, but Paterson et al. give cogent reasons for suggesting that physiological hyperpituitarism is often at least partly responsible for the cerebral oedema-though " they add that pseudotumor cerebri " is a syndrome of
syndrome
8 9
or
multiple aetiology. The illness is, as a rule, benign and self-limiting, though it may persist for many months; but when, occasionally, papilloedema endangers vision, operative decompression is required. Paterson et al.1 found that in 5 out of 6 cases of pseudotumor cerebri administration of prednisone or methyl-prednisolone led to rapid improvement, and it seems justifiable to undertake steroid therapy in proven "
"
of this disorder where demonstrated.
cases
no
definite
cause can
be
AMMONIUM-CHLORIDE POISONING
AMMONIUM chloride is widely used in small doses as an expectorant and diaphoretic and in larger doses as a diuretic and in order to make the urine persistingly acid. In the U.S.A. it is also used for weight reduction and is incorporated in preparations sold directly to the public for this purpose. The B.P. dosage of ammonium chloride as a diuretic is 3-6 g. daily in divided amounts; but it may be administered in a dosage of up to 8 g. daily without producing more than mild asymptomatic acidosis.15 The acidosis arises because a hydrogen ion (H+) is released from the ammonium ion (NH4) when ammonia (NH3) from it is converted to urea by the liver. Ammonium chloride is therefore potentially toxic because of this release of hydrogen ions and because ammonia is itself toxic. The prevention of toxicity depends on good renal function, for the elimination of the hydrogen ions, and on good hepatic function, for speedy conversion of the ammonia to urea. Two instances of ammonium-chloride poisoning in apparently healthy subjects are reported by Relman et al.1’ Both were in women, one of whom was attempting to slim; she took 82 g. of the compound in forty-eight hours. The symptoms were headache, nausea, vomiting, and hyperpnoea, with progressive drowsiness and confusion. The urine of both patients contained protein and was acid (pH 4-8 and 5-0) and of low specific gravity (1-010 and 1-001). Biochemical investigations revealed profound hyperchloraemic acidosis. Treatment with large amounts of intravenous sodium bicarbonate and lactate (691 mEq. 8. Ford, F. R., Walsh, F. B. Bull. Johns Hopk. Hosp. 1943, 73, 391. 9. Joynt, R. J. Neurology, 1958, 8, 8. 10. Weiman, C. G., McDowell, F. H., Plum, F. Arch. Neurol. Psychiat.
1951, 66, 122. Gass, H. H. J. Dis. Child. 1957, 93, 640. Boudin, G., Funck-Brentano, J. L., Gayno, M. Bull. Soc. Méd. Hôp. Paris, 1950, 66, 1736. 13. Walsh, F. B. Arch. Ophthal., N.Y. 1952, 47, 86. 14. Jefferson, A. J. Neurol. Psychiat. 1956, 19, 21. 15. The Extra Pharmacopoeia: Martindale; vol. 1, p. 1222. London, 1958. 16. Relman, A. S., Shelburne, P. F., Talman, A. New Engl. J. Med. 1961, 264, 848. 11. 12.
1275
in twenty hours in one patient and 643 mEq. in fortyeight hours in the other) produced rapid clinical recovery; but
hyperventilation tended
to
persist rather longer than
would have been expected from the biochemical data, and during treatment severe hypokalaemia developed after six hours. After recovery the proteinuria disappeared and the ability to concentrate urine reverted to normal. In these two cases the dosage far exceeded that recommended; but there is evidence that with impaired renal, hepatic, or cardiac function less excessive doses may cause toxic manifestations. Symptoms of ammonium-chloride intoxication have been reported in patients with18renal dysfunction who have taken as little as It is known, too, that in severe liver disease 5 g. daily.l’ the blood-ammonia level is raised,l9 and that, when this is so, hepatic coma may be precipitated by giving ionexchange resins which act by releasing the ammonium ion and taking up sodium.20 In chronic cardiac disease, ammonium chloride in dosages of 4 to 6 g. daily by mouth has been found to cause anorexia, hyperpnoea, lethargy, and drowsiness. 21 Accordingly ammonium chloride is . contraindicated when there is renal or hepatic disease, and its use in the management of cardiac oedema should be undertaken with care. Courses of treatment involving more than 4 g. daily should always be intermittent; and if the patient becomes anorexic, dyspnoeic, or lethargic the possibility of ammonium-chloride intoxication must be considered. HOSPITAL PLANNING "
By the time a modern hospital is built it is already twenty years behind the times." Expressing this view at a London meeting arranged last week by King Edward’s Hospital Fund, Mr. Gordon Friesen, a consultant in hospital planning from Washington, D.C., attributed the time-lag to a failure of basic policy in the planning of hospitals. The practice, he said, is to start with a somewhat sketchy idea of the function of the new hospital and its various departments, to put up a building of what is thought to be about the right size, and then, Procrusteslike, to adapt the organisation to fit the building. In other words, function is made to depend on structure, whereas in Mr. Friesen’s opinion the organisation of the hospital should be planned in very considerable detail-including detail of fixed and movable equipment-before pencil is put to paper, beyond a scribble. Or, as he expresses it, " develop the organisation and put a roof over it In the United States 70% of the maintenance cost of a hospital is for salaries and wages (the figure in Great Britain is about 60%) and in both countries under present conditions the figure is likely to rise. If a good hospital service, therefore, is not to price itself out of existence, it must conserve labour, especially skilled labour, by applying to the utmost the method of automation borrowed from industry. Time-and-motion studies have shown that a high proportion of work at present done in hospital is non-productive, and that less of a nurse’s time should, for instance, be spent in fetching and carrying. A bricklayer for generations has had a hod-carrier to mix his mortar and carry his bricks, enabling him to devote his whole energies to the skilled work of bricklaying. Is not a nurse as
important
as a
bricklayer ?
17. Keith, N. M., Barrier, C. W., Whelman, M. J. Amer. med. Ass. 1925,
85, 799.
18. Sleisenger, M. H., Freedberg, A. S. Circulation, 1951, 3, 837. 19. Kirk, E. Acta. med. scand. 1936, suppl. 77. 20. Gabuzda, G. J., Phillips, G. B., Davidson, C. S. New Engl. J. Med.
1952, 246, 124.
21. Sievers, M. L., Vander, J. B. J. Amer. med. Ass. 1956, 161, 410.
Mr. Friesen would adopt a conveyor-belt system for everything possible in a hospital except the patient: indeed he has done this in a number of hospitals on which he has been engaged in the U.S.A. By this means he claims that the savings in running costs will pay for the capital cost of the hospital in twenty years. (He estimates the annual maintenance cost at 40% of the capital cost.) His conception of the structure of a modern hospital is that the inpatient accommodation should be piled vertically, with 60 beds to a floor; the total bed-capacity is thus fixed at the outset. But the supporting services-outpatient
accommodation, laboratories, X-ray department, theatres, and so on-are planned horizontally so as to give flexibility and scope for expansion as investigations multiply and special procedures are devised. On the bottom floor of the vertically planned inpatient block is a central area for the mechanical washing and autoclaving of all soiled articles from the wards-instruments, bedpans, crockery, and linen (the laundry is adjoining). After being autoclaved, the articles are prepacked (linen packs, instrument packs, &c.) ready to be sent back to the wards by hoists fitted with automatic ejectors to eject packs at any required floor. Soiled articles and garbage for disposal (" trash ") come down from the wards in appropriate hoists or chutes. All supplies, linen, drugs, crockery, hardware, and food are centralised. Pneumatic conveyor tubes are freely used for the circulation of mail and sending of reports, records, pathological specimens (in standard containers), and drugs from one part of the hospital to another. Whenever possible, equipment-laboratory benches, desks, refrigerators, and even shelves-is mounted on castors, for flexibility and ease of cleaning. Inpatients are in rooms with 2 beds or sometimes 4. Each room has its own w.c. and shower (it is contended that by vertical planning this is not expensive) and communicates by microphone with the centrally placed nurses’ station. Each patient has his own urinal and bedpan, which after use are placed in a small compartment off the patient’s room by a nurse who then calls on the microphone for an attendant to take it away and send it to be emptied, cleaned, sterilised, and replaced. With soiled linen the procedure is similar. Patients’ meals, selected from a menu, are prepared by the dietitian staff in the central kitchen and sent up ready served on a tray for each patient. In commenting on these very interesting developments we have to admit that in Britain our thoughts on hospitals tend to be rather old-fashioned. But it does seem that some of Mr. Friesen’s generally admirable precepts need to be treated with a dash of circumspection. A certain amount-not overdone-of repetitive work, to-ing and fro-ing, fetching and carrying, making-do and mending, is not without value in the training of the young studentnurse, who after qualification may find herself called on to nurse the sick under conditions where push-button automation and fingertip control are not within reach. Moreover the conveyor-belt philosophy, if carried too far, could produce a state of mind where mechanical efficiency replaced humanity. A Frankenstein monster would then have been created; and, despite our earnest intentions, the patient himself would be on the conveyor belt. But, whether or not one agrees entirely with Mr. Friesen, one cannot but be carried along by his infectious enthusiasm; and the King’s Fund is to be thanked for making his voice heard last week by so many hospital planners in this country.