Postgraduate Medical Journal (1985) 61, 915-923 Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from

Marasmus- 1985

D. Barltrop and B.K. Sandhu Department ofChild Health, Charing Cross and Westminster Medical School, London, UK.

Introduction Dr Wilfred J. Pearson writing for the first volume of In 1959 Jelliffe coined the term protein-calorie this Journal in 1925 defined marasmus (Greek: maras- (PCM) of early childhood to include mos, wasting) as 'a chronic state of malnutrition of a mild, moderate and various types of severe degrees of severe grade' but pointed out that 'we must retain the malnutrition. The advent of the International System conception ofcases varying in severity from those who of Units (SI) resulted in the introduction of the term simply show an insufficient gain or stationary weight protein energy malnutrition (PEM). The World with few systemic changes, to the most extreme form Health Organisation (WHO, 1973) defined PEM as which is merely the end result of repeated nutritional follows: 'A range of pathological conditions arising or constitutional disturbances.' He described oedema from coincidental lack, in varying proportions, of in some cases as a complication of marasmus. The protein and calories, occurring most frequently in clinical picture of the syndrome, later described as infants and young children and commonly associated , was not generally recognized at this with '. This is not dissimilar from Wilfred time, although a number of authors had described it Pearson's view of marasmus. (Czerney & Keller, 1928). In order to treat and, more importantly, to prevent a

In 1933 Cicely D. Williams, a paediatrician working condition effectively, evolution and causes must be copyright. in the Gold Coast of Africa described a 'nutritional understood. It is therefore necessary to consider disease ofchildhood associated with a maize diet' and marasmus within the context ofPEM. The aim ofthis attributable to protein deficiency. She named it kwa- paper is to review the current state of knowledge shiorkor (taken from the Ga language of Ghana, the concerning the pathophysiology, aetiology, clinical disease ofthe deposed baby when the next one is born). presentation and treatment of marasmus in the con- Her classical description included oedema, chiefly of text of it being considered as one of a spectrum of hands and feet, wasting, diarrhoea, irritability and syndromes produced by severe protein energy mal- dermatosis. This paper attracted much attention in the nutrition (PEM). medical literature and clinical of similar

descriptions http://pmj.bmj.com/ disease subsequently appeared from many other coun- tries. Paradoxically the more commonly encountered Classification type of malnutrition, marasmus, was neglected and until recently did not attract detailed scientific inves- Although a methodology for the assessment ofPEM is tigation. needed, it is still not clear exactly what should be The original view that kwashiorkor resulted from assessed, and there is a lack of agreement about protein lack in the presence of adequate, even excess classification among experts in this field. Until recent- carbohydrate, in contrast to marasmus which foll- ly the method of classification used was that in- on October 3, 2021 by guest. Protected owed deficiency of energy alone, is not now accepted. troduced in 1942 by Gomez and his colleagues (1956) Thus it has been shown that the protein: energy ratio based upon weight for age, in which the weight of the of diets eaten by children developing washiorkor is child was expressed as a percentage of the expected adequate but total energy is deficient (Rutishauser & weight of a healthy child of the same age using a local Frood, 1973; Goplan, 1968). However, it has become or other appropriate standard (Table I). apparent that malnutrition produces a spectrum of A Wellcome working party (1969) considered the syndromes ranging from simple growth failure alone classification of PEM and agreed that the term to both pure and mixed syndromes of marasmus, marasmus should be applied to children who have less marasmic kwashiorkor and kwashiorkor. than 60% of the expected weight for age and no oedema i.e. Gomez's severe or 3rd degree malnutri- Correspondence: D. Barltrop, M.D., F.R.C.P., Westminster tion. However Gomez's method assumed that children Children's Hospital, Vincent Square, London SW1P 2NS, of any given age should have the same weight and this UK. assumption is incorrect. In 1972, Waterlow published © The Fellowship of Postgraduate Medicine, 1985 Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from 916 D. BARLTROP & B.K. SANDHU

Table I Classification of PEM (Gomez, 1956) In the UK 3rd degree PEM is rare and is usually secondary to some underlying organic disease but may Severity % ofstandard(Harvard) occasionally be due to child abuse. normal > 90% mild (1st degree) 89-75% moderate (2nd degree) 74-60% Clinical presentation severe (3rd degree) <60% This will vary with the degree and duration of PEM, the age of the child and the presence of associated Table H Classification of PEM according to wasting and , mineral and trace element deficiencies. In stunting (after Waterlow et al., 1972) order to prevent marasmus it is important that these early changes are understood and recognized. PEM of Stunting Wasting all degrees is most common in the post-weaning phase (heightfor age) (weightfor height) (9 to 24 months of age) but can occur at any age. Failure of breast feeding and inadequate artificial 0=>95% 0=>90% can lead to marasmus in the first 9 months of 1 = 95-90% 1 = 90-80% feeding 2 = <90-85% 2 = 80-70% life. 3=<85% 3=<70% Mild PEM 0 denotes normal, and 1, 2, and 3, mild, moderate and severe PEM. The main clinical presentation of mild PEM is that of with retarded physical growth and a classification based on both weight and height(Table development revealed by anthropometric abnor- II). He labelled present malnutrition 'wasting' malities. There is also an increased risk of infection measured by loss ofweight related to height; and past and retardation ofmental development. Anaemia may malnutrition 'stunting' seen in retarded height for age. be present; activity is diminished and the hair around

This system is now generally accepted and in 1977, the temples may be sparse. copyright. WHO published recommendations primarily based Anthropometric abnormalities include: (1) cessa- upon it (Waterlow et al., 1977). However, it needs to be tion or slowing of weight gain or ; (2) translated into simpler terms for use in the busy slowing or cessation of height gain; (3) normal or routine clinic. diminished weight/height ratio; (4) decreased mid-arm Other anthropometric measurements such as mid- circumference; (5) delayed bone maturation and (6) arm circumference, skinfold thickness, mid-arm and normal or diminished skin fold thickness. head circumference ratio have been used but re- Weight and height are the most useful indices producibility is poor for the first two and there is an providing that the age of the child is known. Patterns age limitation for the third. of growth failure, however, vary considerably and chronic disease, apart from nutritional deficiency, http://pmj.bmj.com/ may also contribute to the problem. Prevalence Children with mild PEM have a high rate of infection particularly with gastroenteritis, measles and Despite considerable research, UN resolutions and . In tropical areas the risk of contracting development programmes, there is more malnutrition , hookworm and schistosomiasis is also in- in the world now than existed 30 years ago (Latham, creased and it is therefore important to assess the There is an 1982). increasinggap between the people of nutritional status of any child presenting with an on October 3, 2021 by guest. Protected the rich and poor nations and there has been a failure infection or infestation. Both the morbidity and to reduce malnutrition and hunger due to . The mortality due to infestations are considerably in- reasons for the failure of development and for in- creased in children with PEM (Scrimshaw & Behar, creased inequality are beyond the scope of this paper. 1961; Chandra, 1983). Point prevalence figures for PEM collected by WHO (Bengoa, 1974) based on 77 surveys suggested Severe form of PEM - marasmus that about 100 million children throughout the world are suffering from moderate or severe PEM at any one The presenting features are gross failure to thrive time. The relative prevalence of marasmus and kwa- accompanied by irritable crying or apathy. The child shiorkor worldwide is not known but marasmus has a shrunken, wasted and stark appearance due to ranged up to 95% or more ofcases ofsevere malnutri- loss of subcutaneous fat. The fontanelle, if present, tion in Beirut (McLaren, 1966) and Santiago (Monck- may be sunken due to and the eyes appear eberg, 1966). large. There is marked wasting ofthe buttocks and the Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from MARASMUS- 1985 917

abdomen is usually distended. The degree ofwasting is proportion of the residual fat (up to 50%) may be in extreme and, by definition, the child is less than 60% the liver (fatty liver) although there is no relationship of expected weight for age and may be well under between liver and subcutaneous fat. In the liver the fat, 40-50% of expected weight. In chronic cases length mainly triglycerides, first appears in the periportal may also be markedly affected so that the weight/ area and then spreads to the central vein area and height ratio may be unaltered. In acute cases the child distends the liver cells. Fatty liver is thought to result is grossly for height; skinfold thickness, from a combination of increased flux of fatty acids mid-arm circumference and chest/head circumference from adipose tissue together with decreased hepatic are all markedly reduced. The child may be anorexic synthesis of beta-lipo-proteins which normally trans- but may be ravenously hungry. There is usually port triglycerides from the liver. The lipo-protein chronic, watery diarrhoea but the stools may be semi- synthesis is especially sensitive to lack of protein and solid; vomiting may be a feature in some cases. The the liver changes are more marked in kwashiorkor child is listless and physical and mental development is than marasmus. On recovery the excess fat disappears retarded. The child may be anaemic and may have from the liver over about 3 weeks and usually there is signs of . no residual damage unless infection or hepatic toxins In pure marasmus, the signs ofkwashiorkor such as are involved. oedema, dermatosis, scarcity and dyspigmentation of Absorption offat and fat soluble is usually hair, angular stomatitis, and cheilosis are not present. impaired, although steatorrhea does not usually occur Children with marasmic kwashiorkor weigh less than in PEM. The following play a role in the pathogenesis 60% of expected weight but, in addition, have one or of fat malabsorption: (a) reduced intestinal transit more signs of kwashiorkor. time; (b) impaired micellar solubilization oflipids due to abnormalities in bile acid metabolism caused by changes in the bacterial flora of the upper gut (Sch- Pathophysiology neider & Viteri, 1974); (c) impaired intraluminal digestion due to low pancreatic lipase; (d) abnormal There are marked changes in amount and distribution transport ofdigested lipids due to decreased beta-lipo-

of body water, fat, minerals and total body protein. protein. In contrast to marasmus, the body fat in copyright. kwashiorkor may be well preserved. Total body water (TBW) Body protein There is gradual increase in TBW as a percentage of body weight. There is a direct relationship between Children with PEM have a greater deficit oftotal body weight deficit and total body water content (Hansen et protein than body weight compared to normal chil- al., 1968) and hence children with most marked tissue dren of the same height. In severe cases total body wasting have the greatest TBW. Increase in TBW is proteinmay be reduced to around 50%; muscle mass is associated with a proportionate rise in extracellular particularly reduced and be as low as 30% of

may http://pmj.bmj.com/ fluid (ECF) but children with oedema have more ECF normal (Montgomery, 1962) with a relative increase in than those without. interstitial collagen and reduction in cellular protein/ DNA ratio. Minerals Protein metabolism There is a decrease in total body potassium of the order of 10-33% (Garrow et al., 1965). In addition to In severe PEM there is marked hypoalbuminaemia potassium loss with nitrogen, potassium is lost in the and total albumin mass may be reduced by 50%. This on October 3, 2021 by guest. Protected diarrhoeal stools resulting in a cellular deficit. Mann et occurs despite reduction in albumin catabolism (re- al. (1972) using a 4K counting technique have shown duced by half) and is due to the extreme sensitivity of that total body potassium is of the order of 39 mmol/ albumin synthesis to protein intake and particularly kg in marasmus, 31mmol/kg in kwashiorkor and lack of the branched chain amino acids, leucine, 45-55 mmol/kg in normal controls. There is depletion isoleucine and valine (Waterlow & Alleyne, 1971). of other minerals. Total body sodium, calcium and There is net movement of albumin from the extravas- phosphorus are depleted to 93%, 77%, and 79% of cular to the intravascular pool so that the former is expected values (Garrow et al., 1965). relatively more depleted. Gamma globulins are not affected by PEM. Protein Bodyfat digestion, although slightly reduced, is adequate des- pite depression of pancreatic exocrine secretion; pan- Normally fat constitutes around 19% ofbody weight. creatic P cell function may also be depressed although In marasmus this may fall to around 5% and a high a cell function and glucagon secretion are normal. Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from 918 D. BARLTROP & B.K. SANDHU

Absorption of nitrogen from a milk diet may be aspirates of children with PEM have been found to reduced by 10-20% compared to normal (from 90% contain unconjugated bile acids (Gracey et al., 1973). to 70%-80%). Nitrogen retention, however, is much Unconjudated bile acids are known to be small more efficient and remains high during treatment until intestinal secretagogues and may play a role in the almost normal growth rates have been restored. pathogenesis ofprotracted diarrhoea in these children. Changes in the gastrointestinal tract Immunological changes Diarrhoea is a major problem in malnutrition and the Infection, particularly with Gram negative organisms, two together have been estimated to cause over 5 is very common in severe PEM, particularly of the million deaths among children every year (Rohde & gastrointestinal, respiratory and urinary tracts and Northrup, 1976). A vicious cycle is established may lead to septicaemia. The patients may not exhibit whereby a child who is malnourished and more prone clinical signs of infection such as fever. Children with to infection gets repeated attacks ofgasteroenteritis or PEM have been found to have evidence of depressed protracted diarrhoea which result in further malnutri- cell mediated immunity (CMI) as measured by skin tion. The pathogens responsible for the diarrhoea tests and lymphocyte transformation and may also include rotavirus, enteropathogenic and enterotox- show thymic atrophy (Smythe et al., 1971; Lomnitzer igenic E.coli, salmonella, shigellae, Giardia lamblia, et al., 1976). Secretory IGA may be reduced and may Entamoeba histolytica and campylobacter. The path- play a role in of gastrointestinal and res- ogenesis ofthe protracted diarrhoea is rather complex piratory tracts (Reddy et al., 1976). and in addition to enteric infection other factors may Serum immunoglobulins are usually normal but play a part including the following. antibody response to specific viral or bacterial antigen may be impaired (Faulk et al., 1974), with obvious (a) Many studies have shown implications for immunization programmes. Live bac- that, in PEM, disaccharidase levels are reduced, terial or viral vaccines may be more immunogenic (and lactase being the most severely affected, and may be hence effective) than killed ones. It has been suggested low or absent in two thirds of the children. The that for optimum response, immunization program-copyright. pathogenesis of enzyme changes is not fully under- mes should be preceded by a supplementation stood but may represent mucosal damage or decreased programme. production due to protein deficiency. In severe cases The total white cell count is usually normal but sucrose and glucose intolerance may occur. After neutrophil function abnormalities have been des- clinical recovery lactase levels may not recover fully cribed (Rosen et al., 1974; Sbarra et al., 1974). although the child may tolerate milk feeds. All components of serum complement except C4 may be reduced. (b) Abnormalsmallbowel mucosa The mucosal chan- All these abnormalities are reversed with treatment ges may range from almost normal villi to severe and recovery. http://pmj.bmj.com/ villous atrophy with only convolutions or ridges being visible on microscopy. Shiner et al. (1973) found that Central nervous system changes in PEM there are gross epithelial cell changes with a brush border which is sparse and has markedly Apathy and irritability are well known features of shortened microvilli. The nuclei were found to be severe PEM and may be related to low brain potas- irregular, the mitochondria disrupted and cytoplasmic sium but the effect on long term intellectual develop- organelles showed a lack of organization. Biopsies ment has not been established. Animal experiments on October 3, 2021 by guest. Protected often show intense mucosal and submucosal infiltra- suggest that inadequate nutrition in early life can have tion by lymphocytes and plasma cells. On treatment, a permanent effect on brain size and cell number. In recovery of the jejunal mucosa may be slow and take humans the adult number of neurones are already months before it is complete. It is now established that present at mid-pregnancy and in order to have any in the small intestine villi are the site of absorption of effect PEM would have to be present from early solute and water and the crypts are the site of pregnancy or for a long time in order to affect glial secretion. In children with PEM who have a protrac- multiplication and myelinization (Dobbing, 1974). ted secretory diarrhoea the altered villus to crypt ratio However the brains of children dying in the first year may play a role. of life with severe PEM have shown reduction in the number of brain cells in the cerebrum (WHO, 1974). (c) Unconjugatedbile acids Infestation or contamin- Clinical studies also give conflicting results as social ation of upper gastrointestinal tract (GIT) with bac- factors cannot be completely excluded (Grantham- teria may lead to deconjugation of bile salts. Jejunal McGregor et al., 1980; Lopez et al., 1985). MARASMUS- 1985 919 Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from

Endocrine changes resulting from poor diets and numerous infections contributed to high infant death rates which were The endocrine glands, particularly the adrenals and comparable to those now encountered in many Asian, the pituitary, appear to atrophy in PEM (Trowell et African and South American towns today. Urban al., 1954) although there is no significant reduction in influences, rapid successive pregnancies, early wean- production of hormones. Thyroid function remains ing, unsound artificial feeding, poor hygiene and normal although thyroid function tests may be altered repeated infections all play a role in the pathogenesis by the alteration in plasma protein binding. Thyrotro- of marasmus. The reason for early weaning may be phin response is normal. Growth hormone level is due to another pregnancy or to the belief that the milk normal and may even be supranormal in marasmus. of a pregnant mother is harmful for the child. Circadian oscillations are abolished but plasma The reasons for inadequate food intake in the UK cortisol level may be elevated and as hypoalbumin- are given in Table III. and feeding difficul- aemia leads to reduced binding ofcortisol, the level of ties may complicate any illness, operation or injury in free cortisol in the plasma may be particularly high. children. There may be associated vomiting and This may contribute to the abnormal glucose tolerance diarrhoea. In addition, metabolic expenditure may be found in patients with marasmus. After an oral considerably increased with negative nitrogen balance glucose load insulin secretion may be low but returns particularly in post-operative cases. The three factors to normal after 3 to 6 weeks of therapy. of impaired intake, malabsorption and increased loss The raised plasma cortisol diverts free amino acids of dietary nutrients often coincide in gastrointestinal from tissue turnover to muscle rather than liver and a tract disease. differential rise in plasma cortisol may be an impor- tant difference between marasmus and kwashiorkor Malabsorption (Lunn et al., 1976). Arateus, in the second century B.C. noted that un- digested food might appear in the stools and that Aetiology copyright. Severe malnutrition leading to marasmus may stem Table m Causes of inadequate nutrition in the UK from inadequate food intake, malabsorption, or poor utilization. However, more than one factor may be Example responsible and infection, particularly ofthe gastroin- Systemic diseases renal or hepatic testinal tract, often plays an important role in the failure, chronic pathophysiology of the condition. infections, congenital PEM is much less common in adults because they do heart disease not need protein for growth. In most normal adults Structural or severe dietary protein provides only 10% of the energy physiological gastroesophageal requirements. abnormalities of the reflux, pyloric http://pmj.bmj.com/ gastrointestinal tract stenosis, Pierre- Inadequate food intake Robin syndrome Non-accidental maternal or Marasmus, together with other forms of PEM, is injury environmental common in areas of the world with insufficient food, deprivation, inadequate knowledge offeeding techniques and poor emotional hygiene. It has been estimated that 100 million chil- deprivation and/or dren under four years of age suffer from moderate or physical injury on October 3, 2021 by guest. Protected severe malnutrition (Bengoa, 1974). A recently grow- Psychosomatic such as anorexia ing problem has been the importation into developing disorders nervosa, bulimia countries of inappropriate western models such as Food fads feeding with manufactured infant milks which have Economic tended to replace the traditional practice ofprolonged deprivation breast feeding. However, family incomes may be insufficient to buy adequate supplies of milk and Neurological cerebral palsy facilities to prepare uncontaminated feeds may be disorders inadequate. This is thought to have resulted in in- Others drugs such as digoxin creased infant morbidity, malnutrition and mortality. and diuretics may During the nineteenth century in the industrial cause vomiting or towns of Europe and North America, marasmus anorexia Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from 920 D. BARLTROP & B.K. SANDHU malnutrition could thus occur. He called this the Other causes of malabsorption, defined as the failure 'coeliac disease of chronic nature' (Adams, 1856). ofthe normal digestive and absorptive functions ofthe In 1888 Samuel Gee described the clinical features small intestine for at least one nutrient (Burke & of coeliac disease and recommended withdrawal of Anderson, 1975), are given in Table IV. flour from the diet: a good example of a gut disorder Children presenting with protracted diarrhoea pose leading to malnutrition and on occasions marasmus particular problems in diagnosis and management. which is reversible on withdrawal of dietary gluten. The diarrhoea may be devastating and the child severely marasmic. The diarrhoea may result from a Table IV Causes of malabsorption wide variety of aetiologies but in a small proportion Example diagnosis cannot be made despite extensive investiga- tions et al., 1977; Sandhu & Milla, Surgical short gut syndrome, (Larcher 1984). post gastrectomy, Hirschprung's disease Treatment Pancreatic cystic fibrosis, insufficiency Schwachmann-Dia- The treatment of marasmus has evolved mond syndrome, present day chronic over the years and as our understanding of the pancreatitis pathophysiology of PEM has improved the treatment Mucosal small coeliac disease, has become more scientifically based. intestinal damage acquired lactose Treatment of severe PEM can be divided into three intolerance, cows' milk protein phases:- resuscitation, stabilization and rehabilita- intolerance tion. During stabilization, if the underlying aetiology is not apparent, investigations may need to be under- Intestinal infections persistent bacterial taken to establish a In the or viral infection, diagnosis. developing parasitic infestation, countries the exact treatment used will depend on the e.g. Giardia lamblia, local facilities and resources available and various

enterocolitis regimes incorporating locally available food sourcescopyright. have been described et Extraintestinal urinary tract (De Meyer al., 1981; Harland, infections infections, recurrent 1983; Vis, 1985). respiratory tract infections, congenital Resuscitation infections, e.g. cytomegalovirus The immediate causes of death in severe PEM are Immune deficiency severe combined dehydration and electrolyte imbalance, infection, hy- states imuno-deficiency poglycaemia and hypothermia and these need urgent attention. Dehydration usually needs to be corrected Abnormal bile ileal disease or with an intravenous isotonic solution. If the child has http://pmj.bmj.com/ acid metabolism resection, bacterial hypovolaemia the ideal initial fluid may be plasma or colonization of small blood (20 ml/kg). Ifintravenous therapy is not availa- intestine ble rehydration may be carried out using an oral Post-enteritis following episode of glucose-electrolyte solution. syndrome acute gastroenteritis The child needs to be nursed in a warm room as Inflammation and Crohn's disease, marasmic children are susceptible to hypothermia. Infection be without if the infiltration ulcerative colitis, may present pyrexia and on October 3, 2021 by guest. Protected amyloidosis child appears septicaemic or critically ill, antibiotics Malignancy need to be given after blood cultures and other lymphomas have been obtained. Venous or constrictive bacteriological specimens lymphatic pericarditis obstruction Stabilization Selective inborn glucose-galactose During this phase of initiation of recovery, mainten- errors of absorption malabsorption, ance amounts of and digestion congenital energy and protein are gradually chloridorrhoea introduced and a steady state achieved (0.6g of protein and 95 cal/kg/day). Too rapid an introduction Miscellaneous lethal familial of protein may produce liver failure and coma, too protracted diarrhoea high an energy or sodium intake may lead to cardiac laxative abuse failure. Oral feeding is usually started as frequent Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from MARASMUS- 1985 921 small boluses ofmilk, the first few feeds may be diluted teraction needs to be encouraged and improved. 1:1 with water. If there is lactose malabsorption, a Developmental delay and apathy characteristic of the lactose-free formula is usually necessary. The maras- malnourished child can be reversed if stimulation and mic infant is prone to prolonged non-specific diarr- play are provided (Grantham-McGregor et al., 1980). hoea. In children who have severe protracted diarr- hoea and temporary multiple food intolerance, the Prognosis usual practice in the UK is to use an oligoallergenic formula consisting of comminuted chicken with car- The mortality figures from various units around the bohydrate added as a glucosepolymer (Francis, 1974). world vary considerably but it is apparent that over Gradually long chain fatty acids, triglycerides, the last 30 years the mortality rate from severe PEM vitamins and mineral supplements are added. Alter- has decreased from approximately 50% to as low as natively a formula based on a casein hydrolysate, may 1%. The long term morbidity will depend on the be used or introduced after the child has been underlying cause and the environment to which the stabilized on a comminuted chicken mix. child returns. In the majority of cases if the environ- Ifthere is not a rapid response to dietary manipula- mental circumstances are favourable, normal stature tion and the child continues to lose weight, parenteral and health can be obtained (Keet et al., 1971). nutrition is normally started at an early stage and may Although it is often stated that malnutrition in early be life saving. Otherwise a vicious cycle with persistent life permanently impairs intellectual development, diarrhoea, and failure to replace depleted tissues will there is little evidence to support this proposition predispose to overwhelming infection, septicaemia (WHO, 1974) and environmental factors probably and death. The only way to interrupt this cycle is to play a considerable role in the ultimate intellectual provide adequate energy and protein intravenously. achievement of each child. The intravenous solutions contain amino acids, dex- trose, electrolytes, minerals and vitamins. The amount Prevention given is gradually increased and a fat emulsion can be added to the regime. Severe PEM is closely associated with infection and is

In the less developed countries peripheral alimenta- more prevalent where poverty, social inequality, poor copyright. tion has been found to be more successful than the hygiene and ignorance coexist. Marasmus has almost central venous route because of the high incidence of been eliminated in the more developed countries over septicaemia associated with central venous catheters the last century due to improvements in living stan- in malnourished children nursed in poorly staffed dards, health education and improved hygiene. units unfamiliar with parenteral feeding. Peripheral Similar improvements are needed elsewhere in the alimentation may be continued for two to three weeks world. Practical strategies to alleviate malnutrition while oral feeds are gradually being introduced. If the and infection include adequate food supply, uncon- diarrhoea still poses a serious problem, particularly if taminated drinking water, improved waste disposal, the small intestine is in a secretory state, phar- primary health care, control of communicable dis- macological agents with antisecretory properties may eases, and the promotion of breast feeding. There is http://pmj.bmj.com/ be helpful (Sandhu et al., 1981, 1983). also a need for the detection of mild and moderate PEM, whether due to malnutrition or underlying Rehabilitation organic disease, so that the treatment can be initiated before a life threatening condition has developed. After stabilization the child is ready to start the Our understanding of the pathophysiology of process of repair and growth. This demands not only marasmus and other forms of PEM has increased adequate provision of energy and protein but also considerably over the last 50 years and the mortality on October 3, 2021 by guest. Protected vitamins (A, B, D, C and folic acid), essential minerals due to severe PEM has decreased markedly. However, and trace elements. The energy needs for growth are many fundamental questions, such as why a child with approximately 5 cal/g of tissue. A child weighing 6 kg severe PEM may present with marasmus and another and a weight of 60 per cent of the expected weight for from the same family with kwashiorkor, and what is his age and height needs 4,000 x 5 = 20,000cal in the precise pathogenesis of the so called post-enteritis addition to maintenance for catch-up growth. Rapid syndrome, remain unanswered. rehabilitation requires 150 to 200cal/kg (Ashworth, 1980). This can be accomplished using milk or milk substitute with added vegetable oil and a diet planned with the help of a dietician with the child feeding according to appetite. The voluntary intake falls to normal values as the expected weight for height is approached. During rehabilitation mother-child in- Postgrad Med J: first published as 10.1136/pgmj.61.720.915 on 1 October 1985. Downloaded from 922 D. BARLTROP & B.K. SANDHU

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