Influence of nutritional status on child mortality in rural Zaire

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8. Stablein DM, Miller JD, Choi SC, Becker DP. Statistical methods for determining prognosis in severe head injury. Neurosurgery 1980; 6: 243-48. 9. Knaus WA, Rauss A, Alperovitch A, et al. Do objective estimates of chances for survival influence decisions to withhold or withdraw treatment? Med Decis Making 1990; 10: 163-71. 10. Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet 1975; i: 480-84. 11. Jennett B, Teasdale G, Braakman R, Minderhoud J, Knill-Jones R. Predicting outcome in individual patients after severe head injury. Lancet 1976; i: 1031-34. 12. Titterington DM, Murray GD, Murray LS, et al. Comparison of discrimination techniques applied to a complex data set of head injured patients. JR Statist Soc A 1981; 144: 145-75. 13. Spiegelhalter DJ. Evaluation of clinical decision aids with an application to dyspepsia. Statist Med 1983; 2: 207-16. 14. Murray GD, Murray LS, Barlow P, et al. Assessing the performance and clinical impact of a computerised prognostic system in severe head injury. Statist Med 1986; 5: 403-10. 15. Jennett B, Teasdale G, Fry J, et al. Treatment for severe head injury. J Neurol Neurosurg Psychiatry 1980; 43: 289-95. 16. Harari RJ, Narayan RK, Iacono L, Ishman R, Ghajar J. Marked

variability in the management of severe head injury at trauma centres in the United States. J Neurosurg 1992; 76: 397A. 17. Adams ID, Chan M, Clifford PC, et al. Computer aided diagnosis of acute abdominal pain: a multicentre study. BMJ 1986; 293: 800-04. 18. Wellwood J, Spiegelhalter DJ, Johannessen S. How does computer aided diagnosis improve the management of acute abdominal pain? Ann R Coll Surg Engl 1992; 74: 140-46. 19. Wyatt J. Lessons learned from the field trial of ACORN, an expert system to advise on chest pain. In: Barber B, Cao D, Qin D, eds. Proceedings of the sixth world conference on medical informatics, Singapore. Amsterdam: North Holland, 1989: 111-15. 20. Imbus SH, Zawacki BC. Autonomy for burned patients when survival is unprecedented. N Engl J Med 1977; 297: 308-10. 21. Cohen H. Response to automony for severely burned patients. N Engl J Med 1977; 297: 1182. 22. Gibson RM, Stephenson GC. Aggressive management of severe closed head trauma: time for reappraisal. Lancet 1989; ii: 369-71. 23. Feldman Z, Contant CF, Robertson CS, Narayan RK, Grossman RG. Evaluation of the Leeds prognostic score for severe head injury. Lancet 1991; 337: 1451-53. 24. de Dombal FT. Ethical considerations concerning computers in medicine in the 1980s. J Med Ethics 1987; 13: 179-84.

Influence of nutritional status on child rural Zaire

the association between nutritional is obvious for extreme malnutrition, the issue is not so clear for mild to moderate undernutrition. We have investigated this association in children of 0-5 years in the rural area of Bwamanda, Zaire, where an integrated development project, with good medical facilities, has operated for 20 years. A random cluster sample of 5167 children was taken; newborn infants and immigrants were included at six quarterly survey rounds from October, 1989, until February, 1991. All surveys included clinical and anthropometric assessment of nutritional status. Deaths were recorded up to April, 1992; there were 246 deaths. Marasmus, kwashiorkor, and other causes of death were defined by the verbal autopsy method and checked against medical records kept at the central hospital and the peripheral dispensaries. As expected, we found an increased risk of death in severe malnutrition. When deaths directly attributed to marasmus or kwashiorkor were excluded, mild to moderate stunting or wasting were not associated with higher mortality in the short term (within 3 months of the previous study round) or in the long term (from 3-30 months after study entry). The commonest causes of death were malaria and anaemia. Extreme marasmus and kwashiorkor caused 16% of deaths, and are important causes of death even in this favoured area with an integrated

Although

status and

mortality risk

development project. Nutritional interventions should be targeted more selectively so that children with moderate malnutrition can be protected from progression to marasmus or kwashiorkor.

mortality in

Introduction Our project is a semilongitudinal study among children aged 0-5 years of the relation between nutritional status and mortality. The existence of such a relation is obvious in extreme situations, such as disaster areas and refugee camps, where children clearly die from hunger. In most developing countries, a more appropriate question is whether mortality risk is also increased in mildly to moderately undernourished children who are not in hospital. If so, is it only because there is progression towards more severe malnutrition, or does mild to moderate malnutrition in itself increase the risk of death from non-nutritional (ie, mostly infectious) causes? The issue is still unresolved. Reports on the mortality risk associated with mild to moderate malnutrition are conflicting. There have been studies that did not show an increased mortality risk in moderate

malnutrition from Asia1 and from African Other studies have shown a gradual increase in risk of death with worsening nutrition.5-10 Our study was done in a relatively favoured area of Zaire, where an integrated development and health programme has been in operation for more than 20 years; the prevalence of diarrhoea and measles is low compared with many other parts of Africa. Our main aim was to assess, in a representative sample of young children, short-term and long-term mortality risks associated with different degrees of undernutrition, defined clinically as well as anthropometrically. The design differs from that of previous studies in that nutritional status at death was also taken into account. We decided to include this feature so that we could fmd out whether any increase in risk of death for mild malnutrition was due to worsening nutritional status. The study is part of a research project on maternal determinants of child health and care in a rural tropical area. ADDRESSES: Centre for Human Genetics (J. Van den Broeck, MD) and Department of Paediatrics (Prof R. Eeckels, MD), University of Leuven; and Institute of Tropical Medicine, Antwerp (Prof J. Vuylsteke, MD), Belgium. Correspondence to Dr J. Van den Broeck, Centre for Human Genetics, Herestraat 49, 3000 Leuven, Belgium.

1492

TABLE I-NUMBERS OF CHILDREN PER SURVEY ROUND

Subjects and methods The Bwamanda health zone is a rural area of 10 000 km2 with about 130 000 inhabitants. Subsistence economy prevails, and maize and cassava are the staple foods. 98-5% of the population is of the Ngbaka ethnic group. There is virtually no socioeconomic stratification, and the female literacy rate is almost zero. Medical facilities in the zone are unusually good for Zaire. The integrated development project of Bwamanda runs a well-equipped central hospital staffed, at the time of the study, by both foreign and local doctors. There are also ten peripheral dispensaries run by male nurses. The average distance from a village to the nearest dispensary is about 5 km. Chloroquine is available at low cost. Oral rehydration salts and penicillin are the standard treatments for diarrhoea and acute respiratory infections, respectively. Vaccination according to the Expanded Programme on Immunisation scheme is applied routinely. The five diseases vaccinated against are rare; measles and pertussis occur only sporadically in the very young. Ground water pumps provide good-quality water in every village. Between 1980 and 1984, infant and child mortality rates in the zone were 98-0 and 38-2 per thousand, which compares favourably with other parts of northern Zaire." The main health problem is hyperendemic malaria. The splenic index in our cohort ranged from 30% in the fourth to 63% in the sixth survey round. 1989 statistics from Bwamanda hospital list malaria and anaemia as the most frequently diagnosed disorders in paediatric inpatients. Acquired immunodeficiency syndrome is limited to a minority of occupational categories, such as soldiers and lorry drivers, and has been seen only very exceptionally in children. Children aged 0-5 years were our target population. A random cluster sample of 16 villages was taken from the total of 52 villages. All children of 0-5 years and their mothers were enrolled after a census based on home visits. The cohort was followed up every 3 months between October, 1989, and March, 1991. The evolution of the cohort size is summarised in tablei. For each survey round the number of newly entered children (newborn children and immigrants) is given, together with the numbers lost by death or emigration. In the sixth survey round (1991) children bom in 1984, who were by that time older than 5 years, were excluded and no longer examined. We did ascertain, however, whether or not they were alive, and they were included in the long-term mortality study. At each round pretested questionnaires were completed by fifteen trained nutritional interviewers with the help of a reference manual. Data collection was done at special under-5 clinics, followed by house-to-house visits to children who were not presented at the under-5 clinics. Information recorded at each round included a standard clinical examination, anthropometric measures (weight, height or length, and arm circumferences) and data on interval-morbidity, feeding practices, socioeconomic conditions, and mortality. Anthropometric measurements were done by two experienced observers in accordance with standard procedures.ll,12 The coverage of the medical examination and the anthropometric measurements ranged between 81% and 89%. Absence from any of the survey rounds was due to emigration, short stay in another village, or temporary absence of the mother. In the latter two cases, children were seen at one or more of the following rounds. Data collection was supervised continuously in the villages by one of us. Individual anthropometric measures were transformed into standard deviation scores (SDS) with the National Center for Health Statistics standards.l3 The birth date, which must be known for SDS calculations, was noted on the "road to health" chart or the identity papers of the parents for about 90% of children. For the others birth dates were determined by a careful interview of the mother with a local events calendar. Variables studied were weight for age, height for age, weight for height (WFH), and mid-upperarm circumference for age (ACFA). National Center for Health Statistics data for ACFA were available only for children older than 1 year. Interviewers were trained to make a clinical diagnosis of malnutrition. We defined kwashiorkor by the presence of pitting oedema of the ankles. Signs of marasmus were old man’s face, loose skin over the glutei, signs of loss of subcutaneous fat, and abnormal

visibility of skeletal structures. Mild to moderate malnutrition was diagnosed in the presence of isolated muscle wasting (ie, a

disproportion between the volumes of limbs and abdomen at inspection or reduced muscle volume and consistency at palpation both). During each round, deaths of children during the time since the last round were noted. Parents were asked about the date of death, and a diagnosis was made by the verbal autopsy method.14,15 This method has been shown to provide reliable diagnoses of malnutrition and measles outside hospital.14 Furthermore, kwashiorkor ("z16 mbulu koyo" or "disease of the drowned fish"), extreme marasmus ("zèlè uma"), and measles ("gbanganza") are disorders well known by the Ngbaka population. Verbal autopsy is less sensitive and specific for other diseases, but tentative diagnoses were made for diarrhoea (WHO criteria), malaria (high fever without coughing or respiratory distress), and acute respiratory infection (tachypnoea with or without fever and coughing). To ensure completeness and enhance reliability, reported deaths were checked against two other sources of information-funeral registers kept by catechists and death registers kept by the nurses at the peripheral dispensaries. Of the children who died, 76% had been treated at the local dispensary or the central hospital during the final illness and the diagnosis made by verbal autopsy was checked with their medical records. In April, 1992, a special mortality survey was done to register deaths from April 15,1991,to April 15,1992, by the same methods. Possible deaths among emigrated (5%) or temporarily absent children were investigated by interview of the remaining family members in the village. The analysis of the relation between nutritional status and mortality could not include children who were never examined before they died; most of these were bom and died within a 3-month or

interval between survey rounds. Thus, 20 neonatal deaths and some postnatal deaths are not included (8-1% of deaths). Children were stratified into risk groups according to clinical and anthropometric (SDS classes) nutritional categories at baseline. 6 Short-term mortality was defined as death within 3 months of last assessment, long-term mortality as death 3-30 months after first assessment. For the assessment of short-term mortality risk, all surviving children were included in every successive 3-month period;6,16 rates are presented as, the number of deaths per number of periods. For the assessment of long-term mortality the method of childtrimesters at risk was used; rates are given as the number of deaths TABLE II-CAUSES OF DEATH

1493

TABLE III-PRIMARY CAUSE OF DEATH IN RELATION TO AGE AT DEATH

*Percentages = % of total deaths in that age group. tTotal deaths in that age group

as a

percentage of all deaths.

per number of observed child-trimesters between 3 and 30 months

after entry to the study. were done for deaths directly attributed to malnutrition and deaths due to other causes. Owing to small numbers, age stratification could be done only for the analysis of deaths from non-nutritional causes. Relative risks were used to compare death rates associated with different degrees of nutritional statuS.17 All analyses were done with the SAS statistical package.18

Separate analyses

extreme

Results 246 deaths (table 11). Kwashiorkor was reported in 9% and marasmus in 8%. Extreme malnutrition was the direct cause of death in about 1 in 6. The contributions of kwashiorkor and marasmus are almost equal. The median prevalence over all survey rounds was 0-2% for kwashiorkor and 3-2% for marasmus. Malaria was the most frequent primary cause of death. In 57 cases (23 %) a second cause of death was recorded, most commonly severe anaemia. For all diagnoses combined, anaemia was the second most common cause of death after acute malaria, followed by acute respiratory infection and diarrhoea. The exact age at death was known in 240 cases. Table III shows age at death in relation to cause (first diagnosis). For all causes combined, 26% of deaths were in children of 0-5 months; the proportion decreased with increasing age. 2 There

were

(10%) of 21 deaths among children aged 18-23 months were from marasmus or kwashiorkor compared with 13 (39%) of 33 among those aged 36-72 months. No child died from kwashiorkor before age 18 months. Mortality at 30 months was 34% (128/3786) among children seen at the first round and 3-2% (16/506) among those not examined because of temporary absence (X2=0-07, p>0-1). Thus, coverage rates did not affect estimates of mortality. Table IV shows mortality rates from extreme malnutrition (ie, marasmus or kwashiorkor); the two causes of death were pooled because separate analyses showed similar results. Short-term mortality (within a 3-month period) was significantly associated with the presence, at the beginning of the period, of low SDS scores (WFA below - 3, HFA below - 4, WFH below -1, or ACFA below - 3 SDS) or of clinically defined kwashiorkor and severe marasmus. The relative risks were extremely high, though with very wide confidence intervals, for WFA below -4 SDS, ACFA below -4 SDS, and kwashiorkor. Long-term mortality from extreme malnutrition was increased even when the baseline WFA was below - 2 SDS. Muscle wasting without signs of extreme marasmus or kwashiorkor (mild malnutrition-assessed clinically) did carry an increased

TABLE IV-MORTALITY FROM EXTREME MALNUTRITION

I.

*Deaths from extreme malnutrition per 3-month period, according to anthropometric or clinical status at start of period. tDeaths from extreme malnutrition per child-tnmesters at risk between 3 and 30 months after study entry, according to anthropometric RR = relative risk. #=significantly (p<0 05) greater than 1

I

or

clnical status at first assessment

1494

TABLE V-MORTALITY FROM NON-NUTRITIONAL CAUSES BY AGE

*RR

significantly (p<0 05)

greater than

1.

mortality risk, but only in the risks

were

short term. Overall, relative much smaller in the long than in the short

term.

shows mortality rates from non-nutritional causes, excluding deaths directly attributed to kwashiorkor or extreme marasmus. Severe marasmus, kwashiorkor, and extremely low anthropometric measures at baseline were all associated with significantly increased risks of death from non-nutritional causes within 3 months in infants younger than 18 months. In the older children there was no relation between nutritional status and short-term mortality. By contrast, long-term non-nutritional mortality in infants was not significantly associated with baseline anthropometric or clinical nutritional status. In older children, there was no significant relation between baseline nutritional status and long-term mortality except for WFA below -2 SDS and extreme marasmus at baseline. Further analyses of deaths from non-nutritional causes showed that diarrhoea and severe anaemia, but not acute malaria, accounted for the increased death rates in the lowest SDS classes. Table

v

Discussion This is the largest published study on the relation between nutritional status and mortality in a representative sample of children under 5 years old in the tropics. Despite the low prevalence of malnutrition and the good medical facilities in the study area, kwashiorkor and marasmus contributed to 16% of deaths and were the commonest causes of death among children older than 3 years. Not surprisingly, severe malnutrition at baseline had a poor prognosis, especially in the short term. It is interesting that in infants with the lowest anthropometric scores short-term mortality from non-nutritional causes was also increased. We suggest two explanations for the fact that extreme malnutrition was not recognised at the deaths of these children. First, some children with extreme malnutrition

could have died after, and despite, substantial recuperation. Second, some very stunted children (eg, those born prematurely) may not seem clinically malnourished despite extremely low anthropometric measures. It is important to emphasise that, when deaths directly due to extreme malnutrition were excluded, we did not find increased death rates in the moderately or mildly malnourished, either in the short term or in the long term (table v). Anthropometric indicators of nutritional status did not distinguish children who would die or survive. At any cutoff level, the sum of specificity and sensitivity was low; death was a rare event even in the undernourished. Studies from Kasongo3 and Guinea-Bissau4 also failed to find an association between nutritional status and mortality but their results have been disputed because measles epidemics during these studies could have masked a possible association. In the area of our study, because of widespread immunisation, measles occurred only sporadically. Our findings accord with those of Chen and coUeagues1 who found in Matlab, Bangladesh, no difference in death risks among normal children and those with mild or moderate malnutrition. Most other Asian studies,6-10 however, including one16 in the same area as that of Chen et al’s study, have found a clear association between nutritional status and mortality. It is likely that the high incidence of diarrhoea caused the association between malnutrition and mortality in these studies. Other factors possibly leading to malnutrition, and at the same time enhancing death rates, include extreme poverty, poor availability of medical care, preferential care of boys, and poor water quality. In our study area, these factors were present to a lesser degree. The prevailing pattern of diseases was different in our area. As Waterlow has pointed out,19 one cannot expect much influence of nutrition on mortality in areas where malaria is hyperendemic. In our study nutritional status was related to deaths from diarrhoea and anaemia but not to deaths from

1495

malaria, acute respiratory infections, or other causes which, together, accounted for the majority of deaths. Whatever factors were most important in reducing the

acute

undernutrition-mortality association in our area, we conclude that mild wasting and stunting do not have a bad prognosis as long as they do not deteriorate to extreme marasmus or kwashiorkor. A possibly rewarding policy could be to target nutritional interventions more selectively to protect children with mild muscle wasting or stunting from progression to marasmus or kwashiorkor. This study also shows that well-trained paramedical staff are capable of making a clinical diagnosis of severe malnutrition and identifying children with greatly increased risks of death. The findings of 26% of deaths from acute malaria and 24% from anaemia were obtained from a combination of verbal autopsies and medical records; however, they are similar to Bwamanda hospital statistics obtained after completion of this study. In the Kasongo study3 (Zaire, 1977), malaria and anaemia were classified among the rarer miscellaneous causes. Anaemia is now recognised as an important cause of morbidity and mortality in African children admitted to hospital2O but is rarely cited as a cause of death outside hospital, possibly because the diagnosis by verbal autopsy is less reliable14 and the relative contributions of sickle-cell anaemia, ankylostomiasis, recurrent malaria, and other causes are unclear. Malaria and anaemia should be made priorities for interventions to improve child survival. Diarrhoea as a cause of death was not common in our area (11%) as in Kasongo (12%)3 and in the Bwamanda inpatients (9%). These rates contrast with the predominant role of diarrhoeal mortality in the Asian studies .6 7,9,10 Acute respiratory infections were the commonest cause of death in children younger than 1 year, despite the availability of standard antibiotic treatment at the dispensaries.21 We thank the Nutricia Research Foundation for support; Prof H.

Devlieger, ProfR. Vleitinck, Prof H. Van den Berge, Dr H. Van Loon, Dr S. Hurigo, Dr G. Coppens, and Prof G. Carrin for help and support; Mr G. Van den Broeck, Ms D. Celen, and Mr W. Meulemans for technical support; Mr N. Ndadua, Mr L. Kessedanya, Ms Y. Akembi, and Dr B. Bolingo for help in supervision of the survey activities; Mr S. Sido for valuable anthropometric work; and all other nutritional interviewers without whom this research would not have been possible.

REFERENCES

LC, Chowdhury A, Huffman SL. Anthropometric assessment of energy-protein malnutrition and subsequent risk of mortality among preschool aged children. Am J Clin Nutr 1980; 33: 1836-45. 2. Kasongo Project Team. Growth decelerations among under-5-year-old children in Kasongo (Zaire): II relationship with subsequent risk of dying and operational consequences. Bull WHO 1986; 64: 707-09. 3. Van Lerberghe W. Kasongo: child mortality and growth in a small African town: a longitudinal study of 6228 children from Kasongo (Zaire). London: Smith-Gordon, 1989. 4. Smedman L, Sterky G, Mellander L, Wall S. Anthropometry and subsequent mortality in groups of children aged 6-59 months in Guinea-Bissau. Am J Clin Nutr 1987; 46: 369-73. 5. Lindskog U, Lindskog P, Cartensten P, Larsson J, Gebre-Medhin M. Childhood mortality in relation to nutritional status and water supply—a prospective study from rural Malawi. Acta Pediatr Scand 1988; 77: 260-68. 6. Kielmann AA, McCord C. Weight-for-age as an index of risk of death in 1. Chen

children. Lancet 1978; i: 1247-50. 7. Sommer A, Lowenstein MS. Nutritional

and mortality: a Clin Nutr 1975; 28:

status

prospective validation of the Quack-stick. Am J

287-92. 8. Katz J, West KP, Tarwotjo I, Sommer A. The importance of age in evaluating anthropometric indices for predicting mortality. Am J Epidemiol 1989; 130: 1219-26. 9. Alam N, Wojtiniak B, Mujibur Rahaman M. Anthropometric indicators and risk of death. Am J Clin Nutr 1989; 49: 884-88.

10.

Heywood

P. The functional

significance of malnutrition-growth

and

prospective risk of death in the highlands of Papua New Guinea. J Food Nutr 1982; 39: 13-19. 11. Van Loon H, Vlietinck R, Vuylsteke J, Engelen G, Van den Broeck J. Comparison of elementary epidemiologic data, mortality and anthropometry of nine different regions in Zaire. Leuven: University of Leuven, 1989. 12. Van Loon H.

Epidemiology of

malnutrition in

developing countries

Thesis, University of Leuven, Belgium, 1987. 13. National Centre for Health Statistics. NCHS Growth charts. Monthly Vital Stat Rep 1976; 25 (suppl). 14. Snow RW, Armstrong JRM, Forster D, et al. Childhood deaths in Africa: uses and limitations of verbal autopsies. Lancet 1992; 340: 351-55. 15. Kalter HD, Gray RH, Black RE, Gultiano SA. Validation of the diagnosis of childhood morbidity using maternal health interviews. Int J Epidemiol 1991; 20: 192-98. 16. Briend A, Bari A. Critical assessment of the use of growth monitoring for identifying high risk children in primary health care programmes. BMJ 1989; 298: 1607-11. 17. Morris JA, Gardner MJ. Calculating confidence intervals for relative risks, odds ratios, and standardised ratios and rates. In: Gardner J, Altman D, eds. Statistics with confidence. London: BMJ 1989: 50-52. 18. SAS Institute 1988. SAS user’s guide: statistics, release 6.03. North Carolina: SAS Institute. 19. Waterlow JC. Protein energy malnutrition. London: Edward Arnold, 1992. 20. Lackritz EM, Campbell CC, Ruebush TK, et al. Effect of blood transfusion on survival among children in a Kenyan hospital. Lancet 1992; 340: 524-28. 21. Suzawal S, Black RE. Meta-analysis of intervention trials on casemanagement of pneumonia in community settings. Lancet 1992; 340: 528-33.

From The Lancet Jerusalem Jerusalem lies some 2400 feet above the level of the Mediterranean and 3700 feet above the Dead Sea.... The older parts of the city are built upon a vast accumulation of rubbish, the debris of previous cities, in places over 100 feet deep. Modern Jerusalem has in normal times about 80,000 inhabitants, over two-thirds being Jews, most of whom depend largely upon charity. As Jerusalem is inhabited by representatives of all the nations of Christendom, is visited annually by thousands of tourists and pilgrims from all parts, and is a "Sacred" City in the eyes of Christians, Jews, and Moslems, its sanitary condition cannot continue a matter of indifference, as it has been to a large extent under the Turkish Government. Almost all efforts made to improve the condition of the city have come from outside sources, and many radical improvements ... as to water-supply, drainage, &c, have been persistently thwarted by the Turkish authorities.... The water-supply of Jerusalem has ever been a problem. The ancient spring known as the "Virgin’s Spring" or to the Arabs "Ain Umm ed Deraj" (lit, the Spring of the Mother of the Steps), and known in the Old Testament as Gihon, originally, no doubt, gave a fresh and plentiful supply. But though it is now at times fairly plentiful-but intennittent-the quality is bad. The other source, Bir Eyyub, is a deep well with a perennial supply at the bottom of equally sewage-tainted water. In Roman times-possibly originally a little earlier-great aqueducts were made to bring water to the city, but the most that reaches the city now is a 4-inch iron pipe.... This is the only really fresh water available, but the whole site of the city is riddled with cisterns of many kinds.... The only disease which seems to have been taken seriously in the Turkish Empire is cholera, and most elaborate, but fantastic and ridiculous, precautions are taken from time to time to exclude this disease.... It must not be thought that all this want of health organisation was taken lightly by the medical men of the city. The difficulty has been the supineness of the Turks, the jealousy of all the various nationalities and their unwillingness to work together, and the want of close union and cooperation on the part of the medical men. (Feb 23,1918)