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Medical complications in male adolescents with anorexia nervosa
JOURNAL OF ADOLESCENT HEALTH 1995;16:448-453
FELLOWSHIP
FORUM
Medical Complications in Male Adolescents with Anorexia Nervosa J A N E T H. S I E G E L , D.O., D A N I E L H A R D O F F ,
I. R O N A L D
M.D., N E V I L L E H . G O L D E N , M . D . , A N D
S H E N K E R , M.D.
Purpose: Medical information on male anorectics is scant. We present data on 10 males with anorexia nervosa, w h o were treated at our Eating Disorders Center during a twelve-year period. Methods: Retrospective chart review. Results: All patients were malnourished w e i g h i n g 80% or less of their ideal body weight with a mean B.M.I. of 13.5 _+ 2.0. Height below the 50th percentile was evident in 80% of the patients, and was below the 10th percentile in 30% of the patients. Structural brain changes on brain computerized tomography scans were noted in seven out of nine patients and more than 50~4 had mild anemia relative to the Tanner stage. Other findings included a mean presenting heart rate of 68.3 ÷ 17: four out of ten patients had presenting heart rates of 80 or greater and of these, three had serious medical problems and were severely malnourished. Two patients had cardiac complications and one had a lifethreatening electrolyte disturbance. Conclusion: Despite the small number of patients, the proportion of male adolescent anorectics with medical abnormalities seems high, and may be due to difficulties in establishing the diagnosis and delay in seeking medical attention. Patients w h o had heart rates of 80 or greater were perhaps sicker and further along in their development of congestive heart failure, thus explaining their initial relative tachycardia. We suggest a higher index of suspicion for congestive heart failure and closer medical monitoring w h e n a malnourished adoles-
From the Divisio*l ~!fiAdoh'~ccm MediLim', 8chm'ider Childre~l's Hospital qf Lon~.~lslmld Jewish Medaal Center, New Ht/dc Park, New York. amf the Division1 qf Adoh'sce, t Medicine, Department ~!f Pcdiat rics, B',ai Zion Medical Cc,ter. Haffa. Israel. Address correspolafence to: Neville H. Golden, M.D., Divisio, ot Adolescent Medici,e. Schm'ider Children's Hospital, Ixm.1 lslamt low ish Medical Ce~tter, New Hi!de Park, New York 11042. Prescl~h'd m part at the Fifth hltcrlmtioplal Ccmh'rcllcc o~t EatiJ~R Disorders, New York City, April 1992. Mmmscript ~tcccpte~[Jmtuary 5, I ~95.
448 1054-139X/95/$9.50 SSDI 1054-139X(94)00003-B
cent with anorexia nervosa presents with relatively elevated heart rates. KEY WORDS:
Anorexia nervosa Complications Male Congestive heart failure
Introduction
Anorexia nervosa (AN) is an u n c o m m o n clinical condition in males, accounting for 5-10% of patients with this illness (1-3). While medical information on females with anorexia nervosa is available, only a few reports exist on medical complications in males with anorexia nervosa (4-11). Accordingly, we describe the medical findings in ten male patients, representing a p p r o x i m a t e l y 6% of patients with A N of the Eating Disorders Center of Schneider Children's Hospital o v e r a t w e l v e - y e a r period. Schneider Children's Hospital is a tertiary pediatric hospital that serves as a referral center for adolescents with eating disorders.
Materials
and Methods
Charts of all male patients fulfilling DSM-III-R criteria for AN (1) between 1978 and 1990 w e r e retrospectively reviewed. Information w a s obtained on age, race, height, weight, sexual m a t u r i t y rating according to Tanner (12), heart rate, blood pressure and t e m p e r a t u r e , as well as certain hematologic, endocrine and blood chemistry values. Vital signs
© Societyfor AdolescentMedicine, 1995 Publi~ht,d by Elst'xier 5cit'nce [nc 655 Avenueof the Americas,New York,NY 10010 ,
June 1995
were measured in the sitting position. Orthostatic vital signs were not consistently documented. Results of electrocardiograms, echocardiograms, and brain computerized t o m o g r a p h y were obtained from the medical record. CT scans were evaluated for structural brain changes by experienced radiologists using the standards of Huckman, et al. (13). Quantitative brain m o r p h o m e t r y was not available at the time the studies were performed. Normative blood pressure values were from the Task Force on Blood Pressure Control in Children (14). Height percentiles from The National Center for Health Statistics were used (15). Ideal b o d y weight (IBW) was defined as the m e d i a n weight for height, age, and gender. The b o d y mass index (BMI) (16) was calculated from height and weight according to the following formula: BMI = weight in k i l o g r a m s / h e i g h t in meters squared. BMI percentile values were obtained from standardized percentile curves of BMI for children and adolescents (17).
Results Ten male patients with anorexia nervosa were treated at our institution during the stated time interval (Table 1). Our patients ranged in age from 9 years 5 months-22 years 8 months, with a mean of 16.1 _+ 3.7 years. The majority (eight out of ten) were adolescents; one was a pre-adolescent, and the other a y o u n g adult. Eight patients were Caucasian, one was Hispanic, and one was Asian. All patients weighed 80~.>; or less of their ideal b o d y weight. The mean IBW was ~69;, with a range of 43-80%. The mean BMI value was 13.5, with a range of 10.9-16.9 (less than the fifth percentile for gender and age). Nine patients had severe malnutrition warranting inpatient admission. The significant medical complications of our patients, summarized in Table 1, were supraventricular tachycardia (SVT), hypernatremia, and initial cardiop u l m o n a r y arrest with subsequent tachycardic episodes, each in one patient. Cortical atrophy (18-20) was noted in seven out of nine patients on CT scan. The mean heart rate at presentation was 68.3 beats per min + 17 with a range of 42-92. Four out of ten patients had presenting heart rates of 80 or greater. Two of these patients had cardiac complications and one had a life-threatening electrolyte disturbance. Blood pressure recordings were at least 90/50, except for one patient who presented in cardiopulmonary arrest. Electrocardiograms that were obtained did not show serious cardiac pathok)gy, and an echocardiogram of patient S.M., done shortly after his cardiopul-
MALE ADOLESCENTS WITH ANOREXIA NERVOSA
449
monary resuscitation, showed minimal pericardial effusion with resolution on repeat echo. The majority of the patients were hypothermic, with initial temperatures less than 36.6°C. Initial temperatures were not available in two patients, and one patient presented with a temperature of 37.2°C. Eighty percent of the patients were below the 50th percentile for height, and 30% were below the 10th percentile. Mild anemia was present in seven patients, based on normative values for their sexual developmental stage (21).
Discussion The cardiovascular response to prolonged starvation is c o m p e n s a t o r y bradycardia and hypotension (22). An elevated heart rate, a cardiac compensatory mechanism during heart failure (23), has been described during refeeding in both starvation and AN (24,25). In contrast to published reports (5,26-28), which emphasize bradycardia (heart rate < 60 beats/min.) as the main cardiac manifestation in AN, elevated heart rates were noted in 40% of our patients. This differs from reports in adolescent females by Palla and Litt (28), in which 95% of strict dieters and 92<;~ of those who vomit or purge had heart rates less than 60 beats per minute during their hospital stay. A heart rate of 80 beats per minute, although normal for healthy adolescents, is elevated for malnourished individuals with AN. Three of our four male patients with heart rates at or above 80 beats per minute developed life-threatening complications. These three patients had mean BMI values that were at least 2SD less than the mean calculated value obtained by Fohlin et al. (14.1 1.0) (5) and Hay et al. (12.9 _+ 3.0) (7) in their series of male anorectics. None of our patients were hypotensive. The majority of our patients had subnormal body temperatures, as expected for a malnourished population. Therefore, the elevated heart rates could not be ascribed to high b o d y temperature. The relative tachycardia m a y have been a compensatory mechanism for early CHF in our patients. These results suggest that the finding of high heart rate in the presence of severe malnutrition in an adolescent with anorexia nervosa should alert the physician to a patient who m a y be developing CHF. Cardiac abnormalities such as the loss of left ventricular muscle mass (28-31), impaired myocardial contractility (32), and CHF especially during refeeding (25,33), have been d o c u m e n t e d in patients with AN. The m y o c a r d i u m of these patients is less able to withstand the stress of increased metabolic de-
450
SIEGEL ET AL
JOURNAL OF ADOLESCENT HEALTH Vol. 16, No. 6
T a b l e 1. Patient Profiles Medical C o m p l i c a t i o n s
IBW
Patient J.M.
Age 12 vrs 3 mths
HX H i s p a n i c w i t h illness
BMI
'~
HT %
l l.9
68
30
Initial
Short
Tanner
tleart
Stature
Stage
Rate
Cardiac
80
Other
<10~;;
Structural Brain Anemia
ND
Hypernatremic
d u r a t i o n of 8 nlonths
Changes
dehydration (serum sodium - 172 m e q / l )
C.K.
9 vrs 5 mths
Caucasian preadolescent
(%
129
65
93
i
109
76
30
5
5(~
137
7D
15
4
8d
11.5
u7
7
2
5t~
with a 3 m o n i h history ot restrictwe eating b e h a v i o r , e x t r e m e tear of b e i n g tat, and a 13 lb. w e i g h t loss
E.S.
22 v r s 8 mths
C a u c a s i a n athletic Young
+
a d u l t w h o had restrictive e a t i n g b e h a v i o r and w e i g h t loss o v e r t w o years duration
T.F.
16 yrs 5 mths
C a u c a s i a n with a 15 lb. w e i g h t loss o v e r five m o n t h s , and nnc year of restrictive e a t i n g behavior
K.H.
14 vrs 9 mths
Caucasiml with restrictive
SV1
e a t i n g b e h a v i o r resulting
puberty
in a lO lb. weight los', over the preceding eight months S.M.
]9 vrs 6 mths
Caucasian who presented
10.9
43
F,
5
92
l~lOlla YV
cardiopulmonary
arreM,
resuscitation. At o n r
tachvtardic
facilit~ he had m u l t i p l e
episodes
w h i c h resoR ed ~xith rm trifionaI rehabilitation 15 yrs 11 mths
( ardiopul-
to a n o t h e r hospital for
e p i s o d e s of tach,.cardia
R.F.
C a u c a s i a n w h o initially b e g a n to lose w e i g h t to e n h a n c e his athletic abiIities with r e s t r k tive e a t i n g b e h a v i o r leading to a ~0 lb. weight loss o v e r 12 month~. [ ~ e %~a> s u e n
~lS a l l
outpatient and wa~ lost to follow tip
Delayed
15.9
S0
25
42
+
+
+
]t.mc 1995
MALE ADOLESCENTS
WITI-t A N O R E X I A
NERVOSA
451
Table 1. Patient Profiles (coPlttJlltc(t> Medical Complications
IBW Patient
k.I).
,,\ g,_, 17 xrs
1 IX (;aucasian ~ l t l l a 1-~4 lb.
B",'II
';
124
5t~
Ill
';
Initia]
Short
lallner
Heart
Stature
Stage
l£ate
4
45
27
weight io>,~ oxer 2 ','ears and peripheral nau,,~ular
mth~
Cardiac
Other
• l(1G
Structural Anemia
Brain Changes
Neuropathv, netl tropcnia, anemia, t h r o m bocvtopenia
'~\'eakIlebb ~.)II prebt, l l t a t i o n .
Ills s y m p t o m s i m p r o x e d
with 1nutritional rehabilitation and a d i a g n o s i s oI neuro[~athy s e c o l l d a r \ tt~ nutritii)na]
deticit was m,~de J.P
15 ors
(Taucasian of {.;reek ancestry
I ruth
14.9
71
t>5
4
74
14 ()
74
:~
4
t~4
with a 20 lb. ~x'eight h)>> in 3 montln~ and a 4(1 lb total lo~,> k~xer 111 lI'loI/tl/s
tie had re~trl~tixe eating bellat i;~r, extreme body i m a g e diMurtion alld \x',~s ~117t'XCe%%i\ e exerciser. }{t' had ai~ initial ele\ ated ervthro~ vt¢, sedimel?tatit m rate of 27 and a negatixo
medical ~xork u p lt~r o t l l e r Cakl~,e~ tl~ c d k b e x i a
S.S
16 ors
..\,,inn of India11 descent
c~ mths
who initialh begaia ill ltlse "~x'ei~ill to e l l h a l l c e
his athletic abilitie,, 1 li\ egetarian re
N D = not d o n e .
mands, owing to the decreased compliance of the atrophied heart muscle as well as diminished contractility. Cardiac decompensation may result from fluid overload during nutritional rehabilitation, with an increased cardiac output and an increase in metabolic rate that overloads the small left ventricle and results in p u m p failure (33). Electrolyte disturbances, particularly of sodium or potassium, are k n o w n complications of eating disorders (34). The hypernatremia observed in patient J.M. was probably due to water restriction with resultant dehydration. This contrasts with a more c o m m o n finding in females with AN, of hyponatremia owing to self-imposed salt restriction a n d / o r water overloading (34). Nonlife-threatening findings were observed as well. Structural brain changes seen on brain corn-
puterized tomography scans of patients with AN include sulcal widening and ventricular enlargement (18-20). A previous study from our eating disorders unit demonstrated cortical atrophy in 40% of females with AN (18), in contrast to our finding of 70G male anorectics in our series. However, both studies were limited, in that there was no control group. In another study, Krieg et al., (19) showed that 829~ of an almost exclusively female patient population had enlarged external cerebrospinal fluid spaces. These structural brain changes are at least partially reversible after weight gain (19) and there has been no evidence of cognitive deficits associated with the changes (35). Our findings of short stature and anemia are consistent with published data (28,36-39). Prior work done at our institution described short stature
452
SIEGEL ET AL
in females with AN (36). Seventy-six and one-half percent of female subjects fell below the 50% height percentile. Similar height percentiles were noted in our males, suggesting that males with AN also have a higher incidence of short stature than would be expected in a normal population. Hematocrit values increase during puberty in healthy males, owing to the stimulating influence of androgens on hematopoiesis (21). In our male patients with AN, more than 50% had hematocrit values below that expected for their pubertal development. Females with this eating disorder also may develop anemia secondary to malnutrition (28,39). Limitations of our study include its small sample size and retrospective design. Because of the retrospective design, we were unable to determine whether the elevated heart rates were compensatory mechanisms for orthostatic changes, compensatory mechanisms for subtle alterations in hydration, or indications of early CHF.
Conclusion Our data suggest that medical complications are not uncommon in male adolescents with anorexia nervosa. Reasons for the relatively high proportion of patients with medical complications in our series are unclear; however, it is likely that the lack of familiarity with AN in males leads to delay in evaluation, diagnosis, and referral. This may result in male patients with AN who are severely malnourished on presentation and require hospitalization, with a higher risk for developing medical complications. Three out of four patients who presented with heart rates of 80 or greater experienced life-threatening medical complications and may have been in early cardiac failure. Although medical monitoring is indicated for all malnourished patients with AN, we recommend a higher index of suspicion for CHF and a closer level of medical monitoring when a malnourished adolescent with AN presents with relatively elevated heart rates.
References 1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (3rd ed., revised). Washington, DC: 1987.
JOURNAL OF ADOLESCENT HEALTH Vol. 16, No. 6
4. Beaumont PJV, Beardwood CJ, Russell GFM: The occurrence of the syndrome of anorexia nervosa in male subjects. Psycho Med 1972;2:216-31. 5. Eohlin L: Body composition, cardiovascular and renal function in adolescent patients with anorexia nervosa. Acta Paediatr Scand (Suppl.), 1977;268:1-20. 6. Crisp AH, Hsu LKG, Chen CN, et al. Reproductive hormone profiles ill male anorexia nervosa before, during and after restoration of body weight to normal, Int J Eating Disorders 1982;1:3-9. 7. Hay GG, Leonard JC. Anorexia nervosa in males. The Lancet 1979;2:574-9. 8. Anderson AE, Wirth JB, Strahlman ER. Reversible weight-related increase in plasma testosterone during treatment of male and female patients with anorexia nervosa. Int J Eating Disorders 1982;1:74-83. 9. Lemaire A, Ardaens J, Leprete A, et al. Gonadal hormones in male anorexia nervosa. Int J Eating Disorders 1983;2:4,135-44. 10. Hogan WM, Huerta E, Lucas AR. Diagnosing anorexia nerrosa in males. Psychosomatics 1974;15:122-26. 11. Anderson AE, ed. Males with eating disorders. New York: Brunner/Mazel, 1990. 12. Tanner JM. Growth at adolescence, 2nd ed., Oxford, England: Blackwell Scientific Publications, 1962. 13. Huckman MD, Fox J, Topel J. The validity of criteria for the evaluation of cerebral atrophy by computed tomography. Radiology, 1975;116:85-92. 14. Report of the Second Task Force on Blood Pressure Control in Children. Pediatrics 1987;79:1-25. 15. National Center for Health Statistics. Height and Weight of youths 12-17 Years: United States, 1973. Rockville, Md: (Vital and Health Statistics. Series 11, no. 124). 16. Billewicz WZ, Kensley FF, Thomson AM. lndices of adiposity. Br J Prey Soc Med 1962;16:183-88. 17. Hammer LDH, Kraemer HC, Wilson DM, et al. Standardized percentile curves of body-mass index for children and adolescents. Am J Dis Child 1991;145:259-63. 18. Nussbaum M, Shenker IR, Marc J, et al. Cerebral atrophy in anorexia nervosa. J Ped 1980;96(5):867 69. 19. Krieg JC, Brackmund H, Pirke KM. Endocrine, metabolic and brain morphological abnormalities in patients with eating disorders. Int I Eating Disorders 1986;5:99a-1005. 20. Krieg/C, Pirke KM, Lauer C, et al. Endocrine, metabolic, and cranial computed tomographic findings in anorexia nervosa. Biol Psych 1988;23:377-87. 21. Daniel WA. Hematocrit: maturity relationship in adolescence. Pediatrics 1973;52(3):388-94. 22. Keys A, Brozek J, Henschel A, et al. The biology of human starvation, Vol 1, Chapter 28, Circulation and cardiac func~ tion. Minneapolis: The University of Minnesota Press, 1950. 23. Andreoli TE, Bennett JC, Carpenter CC, et al, ed. Cecil Essentials of Medicine. Philadelphia: W.B. Saunders Co., 1993, p. 35. 24. Keys A, Henschel A, Taylor HL. The size and function of the human heart at rest in semi-starvation and in subsequent rehabilitation. Am J Phys 1947;150:153~9.
2. Scott DW. Anorexia nervosa in the male: a review of clinical, epidemiological and biological findings, lnt J Eating Disorders 1986;5:5,799-819.
25. Powers PS. Heart failure during treatment of anorexia nervosa. Am J Psych 1982;139:1167 70. 26. Silverman JA. Anorexia nervosa: clinical observations in a successful treatment plan. J Ped 1974;84(1):68 73.
3. Lucas AR, Beard CM, O'Fallon WM, et al. Fifty year trends in the incidence of anorexia nervosa in Rochester, Minn.: a population-based study. Am J Psychiatry 1991;148:7,917 22.
27. Shocken DD, Hollaway JD, Powers PS. Weight loss and the heart: effects of anorexia nervosa and starvation. Arch Intern Med 1989;149:877-81.
June 1995
MALE ADOLESCENTS WITH ANOREXIA NERVOSA
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28. Palla B, Lift IF. Medical complications of eating disorders in adolescents. Pediatrics 1988;81:613-23.
34. Garfinkel PE, Garner DM. Anorexia nervosa: a multidimensional perspective. New York: Brunner/Mazel, 1982.
29. Moodie DS, Salcedo E. Cardiac function in adolescents and young adults with anorexia nervosa. J Adolesc Health Care 1983;4:9-14.
35. Shenker IR, N u s s b a u m M, Sonnenblick M. Are abnormal C.T. scans in anorexia nervosa associated with cognitive, memory, perceptual-motor or personality aberrations? (Abstract). Ped Res 1982;16:81A.
30. Gottdiener JS, Gross HA, Henry WL, et al. Effects of self-induced starvation on cardiac size and function in anorexia nervosa. Circulation 1978;58(3):425-33. 31. St. John Sutton MG, Plappart T, Crosbv L, et al. Effects of reduced left ventricular mass on chamber architecture, load, and function: a study of anorexia nervosa. Circulation 1985; 72(5):991-1000. 32. Kalagar T, Brubakk O, Bassoe HH. Cardiac performance in patients with anorexia nervosa. Cardiology 1978;63:1-4. 33. Hevmsfield SB, Bethel RA, Ansley JD, et al. Cardiac abnorma~lities in cachectic patients before and during nutritional repletion. Am Heart J 1978;95:584-94.
36. Nussbaum M, Baird D, Sonnenblick M, et al. Short stature in anorexia nervosa patients. J Adolesc Health Care 1985;6:45355. 37. Crisp AH, Toms DA. Primary anorexia nervosa or weight phobia in the male: report on 13 cases. Br Med J 1972;1:33438. 38. Root AW, Powers PS. Anorexia nervosa presenting as growth retardation in adolescents. J Adolesc Health Care 1983;4:2530. 39. Rieger W, Brady JP, Weisberg E. Hematologic changes in anorexia nervosa. Am J Psych 1978;135(8):984-85.
FELLOWSHIP
FORUM
Medical Complications in Male Adolescents with Anorexia Nervosa J A N E T H. S I E G E L , D.O., D A N I E L H A R D O F F ,
I. R O N A L D
M.D., N E V I L L E H . G O L D E N , M . D . , A N D
S H E N K E R , M.D.
Purpose: Medical information on male anorectics is scant. We present data on 10 males with anorexia nervosa, w h o were treated at our Eating Disorders Center during a twelve-year period. Methods: Retrospective chart review. Results: All patients were malnourished w e i g h i n g 80% or less of their ideal body weight with a mean B.M.I. of 13.5 _+ 2.0. Height below the 50th percentile was evident in 80% of the patients, and was below the 10th percentile in 30% of the patients. Structural brain changes on brain computerized tomography scans were noted in seven out of nine patients and more than 50~4 had mild anemia relative to the Tanner stage. Other findings included a mean presenting heart rate of 68.3 ÷ 17: four out of ten patients had presenting heart rates of 80 or greater and of these, three had serious medical problems and were severely malnourished. Two patients had cardiac complications and one had a lifethreatening electrolyte disturbance. Conclusion: Despite the small number of patients, the proportion of male adolescent anorectics with medical abnormalities seems high, and may be due to difficulties in establishing the diagnosis and delay in seeking medical attention. Patients w h o had heart rates of 80 or greater were perhaps sicker and further along in their development of congestive heart failure, thus explaining their initial relative tachycardia. We suggest a higher index of suspicion for congestive heart failure and closer medical monitoring w h e n a malnourished adoles-
From the Divisio*l ~!fiAdoh'~ccm MediLim', 8chm'ider Childre~l's Hospital qf Lon~.~lslmld Jewish Medaal Center, New Ht/dc Park, New York. amf the Division1 qf Adoh'sce, t Medicine, Department ~!f Pcdiat rics, B',ai Zion Medical Cc,ter. Haffa. Israel. Address correspolafence to: Neville H. Golden, M.D., Divisio, ot Adolescent Medici,e. Schm'ider Children's Hospital, Ixm.1 lslamt low ish Medical Ce~tter, New Hi!de Park, New York 11042. Prescl~h'd m part at the Fifth hltcrlmtioplal Ccmh'rcllcc o~t EatiJ~R Disorders, New York City, April 1992. Mmmscript ~tcccpte~[Jmtuary 5, I ~95.
448 1054-139X/95/$9.50 SSDI 1054-139X(94)00003-B
cent with anorexia nervosa presents with relatively elevated heart rates. KEY WORDS:
Anorexia nervosa Complications Male Congestive heart failure
Introduction
Anorexia nervosa (AN) is an u n c o m m o n clinical condition in males, accounting for 5-10% of patients with this illness (1-3). While medical information on females with anorexia nervosa is available, only a few reports exist on medical complications in males with anorexia nervosa (4-11). Accordingly, we describe the medical findings in ten male patients, representing a p p r o x i m a t e l y 6% of patients with A N of the Eating Disorders Center of Schneider Children's Hospital o v e r a t w e l v e - y e a r period. Schneider Children's Hospital is a tertiary pediatric hospital that serves as a referral center for adolescents with eating disorders.
Materials
and Methods
Charts of all male patients fulfilling DSM-III-R criteria for AN (1) between 1978 and 1990 w e r e retrospectively reviewed. Information w a s obtained on age, race, height, weight, sexual m a t u r i t y rating according to Tanner (12), heart rate, blood pressure and t e m p e r a t u r e , as well as certain hematologic, endocrine and blood chemistry values. Vital signs
© Societyfor AdolescentMedicine, 1995 Publi~ht,d by Elst'xier 5cit'nce [nc 655 Avenueof the Americas,New York,NY 10010 ,
June 1995
were measured in the sitting position. Orthostatic vital signs were not consistently documented. Results of electrocardiograms, echocardiograms, and brain computerized t o m o g r a p h y were obtained from the medical record. CT scans were evaluated for structural brain changes by experienced radiologists using the standards of Huckman, et al. (13). Quantitative brain m o r p h o m e t r y was not available at the time the studies were performed. Normative blood pressure values were from the Task Force on Blood Pressure Control in Children (14). Height percentiles from The National Center for Health Statistics were used (15). Ideal b o d y weight (IBW) was defined as the m e d i a n weight for height, age, and gender. The b o d y mass index (BMI) (16) was calculated from height and weight according to the following formula: BMI = weight in k i l o g r a m s / h e i g h t in meters squared. BMI percentile values were obtained from standardized percentile curves of BMI for children and adolescents (17).
Results Ten male patients with anorexia nervosa were treated at our institution during the stated time interval (Table 1). Our patients ranged in age from 9 years 5 months-22 years 8 months, with a mean of 16.1 _+ 3.7 years. The majority (eight out of ten) were adolescents; one was a pre-adolescent, and the other a y o u n g adult. Eight patients were Caucasian, one was Hispanic, and one was Asian. All patients weighed 80~.>; or less of their ideal b o d y weight. The mean IBW was ~69;, with a range of 43-80%. The mean BMI value was 13.5, with a range of 10.9-16.9 (less than the fifth percentile for gender and age). Nine patients had severe malnutrition warranting inpatient admission. The significant medical complications of our patients, summarized in Table 1, were supraventricular tachycardia (SVT), hypernatremia, and initial cardiop u l m o n a r y arrest with subsequent tachycardic episodes, each in one patient. Cortical atrophy (18-20) was noted in seven out of nine patients on CT scan. The mean heart rate at presentation was 68.3 beats per min + 17 with a range of 42-92. Four out of ten patients had presenting heart rates of 80 or greater. Two of these patients had cardiac complications and one had a life-threatening electrolyte disturbance. Blood pressure recordings were at least 90/50, except for one patient who presented in cardiopulmonary arrest. Electrocardiograms that were obtained did not show serious cardiac pathok)gy, and an echocardiogram of patient S.M., done shortly after his cardiopul-
MALE ADOLESCENTS WITH ANOREXIA NERVOSA
449
monary resuscitation, showed minimal pericardial effusion with resolution on repeat echo. The majority of the patients were hypothermic, with initial temperatures less than 36.6°C. Initial temperatures were not available in two patients, and one patient presented with a temperature of 37.2°C. Eighty percent of the patients were below the 50th percentile for height, and 30% were below the 10th percentile. Mild anemia was present in seven patients, based on normative values for their sexual developmental stage (21).
Discussion The cardiovascular response to prolonged starvation is c o m p e n s a t o r y bradycardia and hypotension (22). An elevated heart rate, a cardiac compensatory mechanism during heart failure (23), has been described during refeeding in both starvation and AN (24,25). In contrast to published reports (5,26-28), which emphasize bradycardia (heart rate < 60 beats/min.) as the main cardiac manifestation in AN, elevated heart rates were noted in 40% of our patients. This differs from reports in adolescent females by Palla and Litt (28), in which 95% of strict dieters and 92<;~ of those who vomit or purge had heart rates less than 60 beats per minute during their hospital stay. A heart rate of 80 beats per minute, although normal for healthy adolescents, is elevated for malnourished individuals with AN. Three of our four male patients with heart rates at or above 80 beats per minute developed life-threatening complications. These three patients had mean BMI values that were at least 2SD less than the mean calculated value obtained by Fohlin et al. (14.1 1.0) (5) and Hay et al. (12.9 _+ 3.0) (7) in their series of male anorectics. None of our patients were hypotensive. The majority of our patients had subnormal body temperatures, as expected for a malnourished population. Therefore, the elevated heart rates could not be ascribed to high b o d y temperature. The relative tachycardia m a y have been a compensatory mechanism for early CHF in our patients. These results suggest that the finding of high heart rate in the presence of severe malnutrition in an adolescent with anorexia nervosa should alert the physician to a patient who m a y be developing CHF. Cardiac abnormalities such as the loss of left ventricular muscle mass (28-31), impaired myocardial contractility (32), and CHF especially during refeeding (25,33), have been d o c u m e n t e d in patients with AN. The m y o c a r d i u m of these patients is less able to withstand the stress of increased metabolic de-
450
SIEGEL ET AL
JOURNAL OF ADOLESCENT HEALTH Vol. 16, No. 6
T a b l e 1. Patient Profiles Medical C o m p l i c a t i o n s
IBW
Patient J.M.
Age 12 vrs 3 mths
HX H i s p a n i c w i t h illness
BMI
'~
HT %
l l.9
68
30
Initial
Short
Tanner
tleart
Stature
Stage
Rate
Cardiac
80
Other
<10~;;
Structural Brain Anemia
ND
Hypernatremic
d u r a t i o n of 8 nlonths
Changes
dehydration (serum sodium - 172 m e q / l )
C.K.
9 vrs 5 mths
Caucasian preadolescent
(%
129
65
93
i
109
76
30
5
5(~
137
7D
15
4
8d
11.5
u7
7
2
5t~
with a 3 m o n i h history ot restrictwe eating b e h a v i o r , e x t r e m e tear of b e i n g tat, and a 13 lb. w e i g h t loss
E.S.
22 v r s 8 mths
C a u c a s i a n athletic Young
+
a d u l t w h o had restrictive e a t i n g b e h a v i o r and w e i g h t loss o v e r t w o years duration
T.F.
16 yrs 5 mths
C a u c a s i a n with a 15 lb. w e i g h t loss o v e r five m o n t h s , and nnc year of restrictive e a t i n g behavior
K.H.
14 vrs 9 mths
Caucasiml with restrictive
SV1
e a t i n g b e h a v i o r resulting
puberty
in a lO lb. weight los', over the preceding eight months S.M.
]9 vrs 6 mths
Caucasian who presented
10.9
43
F,
5
92
l~lOlla YV
cardiopulmonary
arreM,
resuscitation. At o n r
tachvtardic
facilit~ he had m u l t i p l e
episodes
w h i c h resoR ed ~xith rm trifionaI rehabilitation 15 yrs 11 mths
( ardiopul-
to a n o t h e r hospital for
e p i s o d e s of tach,.cardia
R.F.
C a u c a s i a n w h o initially b e g a n to lose w e i g h t to e n h a n c e his athletic abiIities with r e s t r k tive e a t i n g b e h a v i o r leading to a ~0 lb. weight loss o v e r 12 month~. [ ~ e %~a> s u e n
~lS a l l
outpatient and wa~ lost to follow tip
Delayed
15.9
S0
25
42
+
+
+
]t.mc 1995
MALE ADOLESCENTS
WITI-t A N O R E X I A
NERVOSA
451
Table 1. Patient Profiles (coPlttJlltc(t> Medical Complications
IBW Patient
k.I).
,,\ g,_, 17 xrs
1 IX (;aucasian ~ l t l l a 1-~4 lb.
B",'II
';
124
5t~
Ill
';
Initia]
Short
lallner
Heart
Stature
Stage
l£ate
4
45
27
weight io>,~ oxer 2 ','ears and peripheral nau,,~ular
mth~
Cardiac
Other
• l(1G
Structural Anemia
Brain Changes
Neuropathv, netl tropcnia, anemia, t h r o m bocvtopenia
'~\'eakIlebb ~.)II prebt, l l t a t i o n .
Ills s y m p t o m s i m p r o x e d
with 1nutritional rehabilitation and a d i a g n o s i s oI neuro[~athy s e c o l l d a r \ tt~ nutritii)na]
deticit was m,~de J.P
15 ors
(Taucasian of {.;reek ancestry
I ruth
14.9
71
t>5
4
74
14 ()
74
:~
4
t~4
with a 20 lb. ~x'eight h)>> in 3 montln~ and a 4(1 lb total lo~,> k~xer 111 lI'loI/tl/s
tie had re~trl~tixe eating bellat i;~r, extreme body i m a g e diMurtion alld \x',~s ~117t'XCe%%i\ e exerciser. }{t' had ai~ initial ele\ ated ervthro~ vt¢, sedimel?tatit m rate of 27 and a negatixo
medical ~xork u p lt~r o t l l e r Cakl~,e~ tl~ c d k b e x i a
S.S
16 ors
..\,,inn of India11 descent
c~ mths
who initialh begaia ill ltlse "~x'ei~ill to e l l h a l l c e
his athletic abilitie,, 1 li\ egetarian re
N D = not d o n e .
mands, owing to the decreased compliance of the atrophied heart muscle as well as diminished contractility. Cardiac decompensation may result from fluid overload during nutritional rehabilitation, with an increased cardiac output and an increase in metabolic rate that overloads the small left ventricle and results in p u m p failure (33). Electrolyte disturbances, particularly of sodium or potassium, are k n o w n complications of eating disorders (34). The hypernatremia observed in patient J.M. was probably due to water restriction with resultant dehydration. This contrasts with a more c o m m o n finding in females with AN, of hyponatremia owing to self-imposed salt restriction a n d / o r water overloading (34). Nonlife-threatening findings were observed as well. Structural brain changes seen on brain corn-
puterized tomography scans of patients with AN include sulcal widening and ventricular enlargement (18-20). A previous study from our eating disorders unit demonstrated cortical atrophy in 40% of females with AN (18), in contrast to our finding of 70G male anorectics in our series. However, both studies were limited, in that there was no control group. In another study, Krieg et al., (19) showed that 829~ of an almost exclusively female patient population had enlarged external cerebrospinal fluid spaces. These structural brain changes are at least partially reversible after weight gain (19) and there has been no evidence of cognitive deficits associated with the changes (35). Our findings of short stature and anemia are consistent with published data (28,36-39). Prior work done at our institution described short stature
452
SIEGEL ET AL
in females with AN (36). Seventy-six and one-half percent of female subjects fell below the 50% height percentile. Similar height percentiles were noted in our males, suggesting that males with AN also have a higher incidence of short stature than would be expected in a normal population. Hematocrit values increase during puberty in healthy males, owing to the stimulating influence of androgens on hematopoiesis (21). In our male patients with AN, more than 50% had hematocrit values below that expected for their pubertal development. Females with this eating disorder also may develop anemia secondary to malnutrition (28,39). Limitations of our study include its small sample size and retrospective design. Because of the retrospective design, we were unable to determine whether the elevated heart rates were compensatory mechanisms for orthostatic changes, compensatory mechanisms for subtle alterations in hydration, or indications of early CHF.
Conclusion Our data suggest that medical complications are not uncommon in male adolescents with anorexia nervosa. Reasons for the relatively high proportion of patients with medical complications in our series are unclear; however, it is likely that the lack of familiarity with AN in males leads to delay in evaluation, diagnosis, and referral. This may result in male patients with AN who are severely malnourished on presentation and require hospitalization, with a higher risk for developing medical complications. Three out of four patients who presented with heart rates of 80 or greater experienced life-threatening medical complications and may have been in early cardiac failure. Although medical monitoring is indicated for all malnourished patients with AN, we recommend a higher index of suspicion for CHF and a closer level of medical monitoring when a malnourished adolescent with AN presents with relatively elevated heart rates.
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JOURNAL OF ADOLESCENT HEALTH Vol. 16, No. 6
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