Anorexia Nervosa: Medical Management Richard A, Lenon, MD Abstract ‘The major medical issues in anorexia ner~ ‘yosa are assessment of risk and the manage ment of refeeding. Responsibility for risk assessment will generally be shared by the internist and the psychotherapist; both cur- rent medical condition and spticipated ‘behavior must be taken into account. This paper begins with a discussion of the medical ‘consequences of starvation in anorecties, and proceeds to offer suggestions on medical assessment of the individual patient. An ‘argument is then made for the desirability of earlfer and ongomg medical assessment, with close collaboration between the interm= ist and the psychotherapist. Finally, the management of refeeding is discussed. Medical Consequences of Starvation in Anorexia Nervosa Anorexia nervosa is clearly a disease associated with considerable morbidity and mortality. Death rates from 0 to 19% have been reported (Baker & Lyen, 1982), with much of the variance undoubtedly attributable to dif- ferences in patient populations and follow-up. Voluntary programs with strict admission enteria and short follow-up predictably report low mortality. Some programs do not readtrit their own faifures, Programs with a high pro portion. of involuntary patieats and previous treatment failures would be expected to have highes mortality. An interesting statistical argu- ment has been ‘made chat the superiority of results reported by experienced, highly siruc- tured programs can be adequately explained by their patient selection (Goldberg, Ecker, Casper, Halmi, Davis & Roper, 1980). While the overall mortality of anorexia nervoss is unknown, the mortality of ongoing starvation will eventually be 100%, 2 Starvation in initiolly healthy amorecies is ferent from that seen in other citoustances. Most anorectic cat enough to slow protein loss dramatically, making them unlike the strict hhunger-srikers, who generally died in SO to 80 ays, Famines are generally not subject to sophisticated medical observation, but what ine formation we do have from such setings has infeetion playing a much more significant role than it does in fatal anorexia. Protein- conserving mechanisms are much more effec- tive im the absence of severe infection or maligaaney: failing cancer patients rerely sur- Sive lose of more then 308 of initial weight, while anorexies ean often lose $0% or more (Donaldson & Lenon, 15779). When anorecties develop a medical condition that announces its presence, they will generally receive prompt cffective treatment, Fatal outcomes in anorexia are usally relatively sudden and without ob- vious prior warring. ‘Cause of death in anorexia is often debatable. Nine series, inchuding. 654 patients and 38 deaths, were reviewed hy Baker and T yen ({882), Bight ofthese deaths were reporied as suicides; but most oF the rest were open to ques thon, Bight were attributed 10 “starvation,"" ‘without further explanation, ‘There were an unspecified muber from eardiapolmenary causes and infection. Bight deaths were af ‘ributed to miscellaneous causes, incfuding three with “electrolyte dsturbances."" One was attributed to hypoglycemia. There have been at least three deaths among patients treated at Stanford im te last threc years: one was m= den and unexplained, one was probably a s cide, and the third was of fiver failure in a pa tiem who was also alcoholic. A fourth patient spent four months in te intensive care uni after suffering severe damage during documested hyposlyeemic coma: she survived, but was sig- mfieantly impaired when last’ secn scven ‘rmsacemal Avalos Journalmonths after the insult. The more than eaths reported in patients on protein diets may well be a consequence of voluntary starvation; they remain poorly understor, but arrhythmis are thought to have played a role (Lamtigua, Arvatruda, Bild, Forbes, & Lock wood, 1980}. Significant arrhythmias have been ciserved in anorecticsas well (Gotiliener, Gross, Henry, Borer & Bbert, 1978; Mitchell & Gilium, 1980), Archythimia may well be the cause of many of the sudden deaths seen in anorexia, Elec twolyte disturbances ure not the only possible basis. Sericis ventricular arrhythmias have been observed during protein-sparing niodified fasts (SMF), and in snorectics in the absence ‘of significant serum electrolyte abnorraalitis. “The physiologic basis of these arrhythmias may be simple starvation; lass of eardiae mass dur- ing starvation is well-documented. There is probably considerable variability in the popul tion's sensitivity to starvation-induced ar- rhythmias; 3 of 6 closely monitored patients on 4 PSME (Lantigua, et al, 1980) and 4 of 11 similarly followed anorecties showed serious Ventricular arshythmias (Goudiener, et al, 1978), but the incidence of syncope and sud- den death in such popolations is obviously far lower. The true incidence of arrhythmic deaths in arorectics will not be known until long term monitoring becomes more practical ‘Organic mental impairment is another well- recosnized consequence of starvation. A gross organic brain syndrome is present in the end- stages of starvation: significant impairme begins well before it is clinically obvious Descriptions of starving non-anorectics agree that they are obsessed with thoughts of food, and have little time ar attention for other eon siderations. Attention span and ability 0.eon- centrate are impaired. Irritability and lability increase, Eventually, the victims become in creasingly listless (Leyton, 1946). Convincing documentation of an organic effect in anorec ties is available. Computed tomography was done on 23 anorectic with 2 mean weight love of 16.5 kg: 21 had definite signs of loss of brain tissue mass. Bleven of these patients were restudied four weeks after regaining significant Weight, and showed substantial improvements. Psychometric testing done on the I patients showed parallel improvement in concentration time, perceptual speed, and reaction time: IQ Wo, 43, No, te Jamar 1985 ANOREXIA NERVOSA: MEDICAL MANAGEMENT changes were not statistically significant (Kohlmeyer, Lehmkuhl & Poutska, 1983). While such mental impairment is alarming in its own right, it may well have special impor- tance in making some anorectics less amenable to therapy. At some point, the impairment is severe enough that refeeding becomes a necessary preliminary to psychotherapy. Assessment of Risk ‘The above is sutficient justification for stating that there is significant risk of mortality in fnorexia nervosa, that there are a variety of possible causes, and thatthe specific cause may not announce itself hefore the event. Since we cannot rely on our ability 1 foresee specific ‘aus of death, we must in large degree depend ‘on our assessment of overall damage. What is most needed is a method of assessing risk of death from any and all causes. Baker snd Lyen (1982) regard a history of laxative abuse, diuretic abuse, or “bizarre dictary intake" a associated with increased risk. They also con- sidered degree of weight loss helpful; ofthe 38 dlaths in their 9 series, in 13 cases it was possi- ble to assess weight loss. The mean weight loss was SLT, with a standard ceror of 3.6% Other physical findings they’ mentioned. were hhypotbernia (ess than 95°F), hypotension, and “mental stalus changes suggestive of toxie cencephalopaky.” Laborslory findings men- tioned includ! low serum potassiany, EKG ab- normalities, hypoglycemia, and the absenee of ketonaria despite starvation Baker and Lyen (1982) did not choose to rank the urgency af their ominous signs. It seems possible to suggest at least three levels of tmedical risk; from high, to moderate, to relatively low. High risk patients would be those for whom immediate medical hosptalza- tion should be strongly considered. Mocerate risk patients would be those requiring at least closé medica follow-up. For low risk patients, the role of the internist might be limited to an initial assessment and one oF 140 follow-up Visits, if all goes well ‘The high risk category cerainly includes ps- tients with 50% weight loss, symptoms hypoglycemia, “toxic encephalopathy."” or significant EXG abnormalities. Hypothermia and absence of ketonuria may also warrant a high risk designation. Recent onset of syncope and rapidly progressive weakness were not aRICHARD A, LENON, MD. mentioned by Baker and Lyen (1982), but we regand these also as high Fisk findings. Syn- ‘copal episodes may represent serious ar- rhytimia oF hypoglycemia (Zalin & Lant, 1984). Patients too weak to walk are an obvious ‘easo, Li they cannot stand from ¢ chair without using their hands, hospitalization and ag- gressive altention are indicated. Clumsiness, hystagmus, oF impaired eye movement can herald Wemicke's encephalopathy (Handler & Perkin, 1982); prompt attention is again in- dicated, Wernicke’s is more likely to be seen in patients with “bizarre dietary intake.” Inthe laboratory, low white counts are not uncom ‘man, but an absolute neutrophil count less tha. 1000 should receive prompt attention. Serum albumin ard transferrin are clearly indications fof advanced starvation, but in anorexia they are very insensitive; anorecties ean clearly die of starvation with @ normal serom albumin. ‘The moderate risk category can safely in- ‘clude many patients who abuse laxatives or diuretics, or admit bizarre dietary intake. Blood pressures as Tow as 90 systolic and serum Dorassium values as low as 3.0 meg/l are relatively common, and would wot necessarily demand that medical concerns take precedence over all others. Edema will not always occur inthe course of starvation, and does not always indiewe high risk when present. ILis more fre quent and occurs earkier in patients with a history of laxative or diuretic abuse. Minor liver enzyme abnormalities are fairly common, and do not necessarily disqualify the patient from the moderate risk category. ‘Conservatively, the /ow risk category could include otherwise healthy patients who have lost Jess than 15% of inital body weight, and tare also less than 15% below idcal body weight. Amenorthea does not necessarily disqualify them. ‘The medical assessment of risk in anorectics jg much more sensitive and reliable when pa Gents can be followed over a period of time. Many of the important indicators mentioned above are relatively subjective: deterioration of strength, coordination, and mental functioning are obviously better assessed from a baseline. Even weipht requires subjective interpresation, since changes in total body water can obscure significant changes in body composition. Total body water increases as starvation progresses, ‘especially in patients with a history of diuredie 4 or laxative abuse. Weight can thus actualy in- cxease while starvation proceeds. AL least LO to 15% increase in. water as a percentage of bhady weight is possible before edemn even ‘becomes apparent, since in starved patients, ‘uch of this excess wator will be intracellular (Heymsficid & Dept, of Medicine, Emory Uni- versity, 1952). Measurements of total body water and dry mass are possible using isotope methods; but such measurements are stil cumbersome, expensive, and too insensitive to register changes in individual patients over periods of less then a month or more. Arm eit- cumference measurements can be useful here, singe they are somewhat less affected than ‘weight by fluid gains; they are relatively vscless im anoreetes without baseline values, however ‘As a gross rule of thumb, itis useful to ‘remember that over time an anorectic will lose about 0.2 kg por day on a water-only fast, iF there is no water retention. Conversely, if she cats 3500-4000 calorics, the average gain should be about 0.2 kg per day; “real” weight sain of 0.2 kg requires at least 1800 calories above maintenance. or ahout 4000 calories per pound (Allardyce & Groves, 1974). Larger changes in cither direction can be assuined reflect changes in tal body water, Fluctuations are understandably greater in patierts whose total body water is increased, Rapid aceamuls tion of uid is common in refeeding, and especially severe im laxative abusers; 5-10 ky increases in the first week sre not uncommon In following patients daily, drops of up to a kilogram and more are often unexplained. A sharp dectease in intake may be responsible. ‘When a well-outished person initiates & water- only fast, 35% weight loss in the first 24 to 48 hours is not uncommon. Because thei total body water is high t begin with, sudden decrease in intake can cause an anorectic wo lose even more. One mechenism is salt and water Joss due to impairment of renal function: as soon as the patient takes in more than sbout 100 calories. in. carbohydrate, function will be restored to norml and most ofthe weight loss will be regained (Cahill, 1970). Some loss is also accounted for by food in tansit; every calorie requires the presence of about 1 ec of water. A pariemt who suddenly drops from 4000, calories per day down to 3000 can transiently show a loss of a kilogram. Of course, surrep: titious laxative or diuretic abuse must be con- rawsatonal Anclts Soursidered, Over time, however, fasters tend (0 lose about 0.2 kg per day in ““real’* weight, and a 3500-4000 caloric intake willbe requited for “real” gain at the same rate ‘Though ratc of change in medical status is ‘ powerlul indicator, 2 caution is necessary. It is quite possible to be lulled into a false sense of security when a patient remains stable at very low weight for Jong periods of time, especially if substantially lower weights have been recorded inthe past. The unstated assurnp- ‘ion is thatthe risk of catastrophic events begins at some discreet point, A much stronger case ‘can be mage thal rigk increases more gradually; ‘ovo months at 70% of idex! weight may be ss dangerous as one month as 60%. In any case, the physiology of starvation contributes to mak ing true stbility difficult Zor the anorectic. The ‘uid retention associated with starvation often provokes them to redouble their efforts. ‘Though weight my be stable or even increas ing, total body protein can comtinue to decline. Management of Refeeding ‘the meaical management ot voluntary sefeeding is relatively straightforward. The ‘edema that can occur is wsualy not dangerous, inthe absence of other signs of congestive heart failure. The distress the patient experiences at her “puffiness” and rapid weight gain will ‘often respond fairly well to repeated reassur- ance. Tn some cases, carefully controlled use of diurctics may be justified to help decrease the anxiety. Congestive heart failure can oc~ cur during voluntary refeeding in anorectics, but it is quite uncommon and should give ade~ ‘quate warning ‘When volumiary incake is not sufficient, and ‘decision fas been made that prompt improve ‘mene in nutritional status is imperative, we must choose hetween tube feeding and intravenous hyperalimeniation. Both methods require close medical supervision. In almost all cases, tube feeding will be simpler and safer. Starvation alone virtually never renders the gut unusable (Baker & Lyen, 1982), and there is general ‘agreement among nutritional support specialists thatthe gut should be used in preference to the iniravenous route whenever possible. Patients who vomit can usually be fed distal t9 the pylorus, by pump-controlled continuous infu Sion. The risk oF aspiration is lowest with con- ‘tinuous infusion, but even bolus feeding should VoL 15, No, 1 January 1985 [ANOREXIA NERVOSA: MEDICAL MANAGEMENT: de acceptable in alert patienms who are compe sent to vomit. Tube feeding can certainly cavse _ypophosphatemia or hypokalemia. Both tend +9 occur early in feeding. when demand is especially high. Precipitation of folate hiamine defiieney by the same mechani atleast a theoretical possbily. However, i Aerting a tube is smuch less dangerous tha i serting a central venous eatheter, which can Jead to laceration of the great vessels and/or pneumothorax. Intravenous feeding. is also associated with serious infection, air embolus, _uced thrombosis of the great veins, and reac” live hypoglycemia, Theze isa zeported fatality attributed to hypophosphatemia in an anorec- {ic on intravenous feeding @erschuk, Forster, Burhy, & Mallen, 1981). IFpatiens are going wo tamper with their feeding, cleary the risk oftampering with tube feeding s much Lower The expense of tbe feeding should be at most 20% that of intravenous feeding. Neither is likely to have any significant advantage in efficacy. "There is great deal at stake in the treatment or anorexia, For most patients who achieve and inaintain normal weight the damage wuffered during sn episode of starvation seems to be largely reversible. Resummpion of menses oc- curs to the majority oF sueh patients (Hsu, 1980), though it may be delayed; we have pa- sient with a 15-year history of amenorshea ‘whose menses resumed 3 months afier she achieved normal weight t age 35. Even loss ‘oF cerebral mass Seems to be reversible. The ‘steoporosis that occurs in anorecties has been emphasized only recently (Ayers, Gidwani, Schmid & Gross, 1984): we do not know hew seversibe it will be, While anozectics can be extremely frustrating, the reeaveries possible can be as spectacular as any in medicine, ac ‘quite rewarding tothe inernises involved, as ‘well as tothe psychotberapiss Richard Lenon, MD, is a Palo Alto, Califor- xia, intemist and oncologist. Starvation in cancer patients was an early interest, from ‘which the interest in anorexia evolved. REFERENCES Alar, DB, & Gromen, AD (197A. A coravisons sional pi ring rom anos ael ena Seong Supers, Cyneclogy and Obmerics 730, a 5RICHARD A. LENON, M.D. Ayers AW, Gide, CLP. Seti, EM. GSM "GOis) tegen in tnpige: yng ween Snore nerves. Feri and Sety #224228. Baker Le Lyen, (1982), Anoreia nervosa, Carers ‘Concept arin, 17. 196188, Cai GF (19M Searvaon i ma, New England ror al of Meng, 292, 608-573, Doalion, 5.8, Lamon, RA, (279). 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