Research in Eating Disorders and Treatment Paper you will select 2-3 published journal articles (original research, not review articles) related to topics

Research in Eating Disorders and Treatment Paper you will select 2-3 published journal articles (original research, not review articles) related to topics from the course and then write a paper that includes a summary of the methods and findings of the research described in the articles, as well as a discussion of how the findings might have implications for eating disorder treatment. Papers must be double-spaced, with 1.0 line spacing, no spacing before and after paragraphs, 12-point Times New Roman, and 1-inch margins on all sides. A separate title page and reference page (with APA-formatted references for the articles) are also required, and do not count towards the 4-5 page total. Your writing should be well organized;the threee articles are listen below Mehler and Rylander Journal of Eating Disorders (2015) 3:12
DOI 10.1186/s40337-015-0044-4
REVIEW
Open Access
Bulimia Nervosa – medical complications
Philip S Mehler1,2*† and Melanie Rylander1†
Abstract
As with anorexia nervosa, there are many medical complications associated with bulimia nervosa. In bulimia nervosa,
these complications are a direct result of both the mode and the frequency of purging behaviours. For the
purposes of this article, we will review in detail the many complications of the two major modes of purging,
namely, self-induced vomiting and laxative abuse; these two account for more than 90% of purging behaviours
in bulimia nervosa. Some of these complications are potentially extremely dangerous and need to be well
understood to effectively treat patients with bulimia nervosa. Other methods of purging, such as diuretic abuse,
are much less frequently utilized and will only be mentioned briefly. In a subsequent article, the treatments of
these medical complications will be presented.
Keywords: Bulimia nervosa, Medical, Complications, Self-induced vomiting
Background
Self-induced vomiting is the most frequently used purging method which patients with eating disorders revert
to in order to compensate for binging behaviour and in
order to lose weight. The medical complications of selfinduced vomiting come to clinical attention in a variety
of ways and manifest themselves through physical exam
findings as well as unique laboratory anomalies. This
section of the article will review the medical complications of self-induced vomiting. Some of the following information is based on expert clinical opinion, with some
based on cohort studies.
of starvation including alopecia, xerosis, hypertrichosis
lanuginose, cheliosis, carotenoderma, pruritis, and nail fragility [1,2]. These changes are most apparent when the
body mass index (BMI) drops below 16 [2].
Patients who induce vomiting will often do so mechanically by inserting their fingers into their mouths. Over
time, introduction of the hand into the mouth results in
repetitive trauma and skin abrasions to the hand, ultimately resulting in callous formation on the dorsal aspect
of the hand. This characteristic finding is referred to as
Russell’s sign [3].
Eyes, ears, and nose
Review
Cutaneous manifestations
The cutaneous effects of self-induced vomiting are either a reflection of starvation or the act of inducing emesis. Where empirical evidence (e.g., from randomised
controlled trials) is lacking, information is based on
other levels of evidence including open cohort studies
and experienced clinical opinion. Patients at sufficiently low
body weight may demonstrate dermatologic manifestations
* Correspondence: PMehler@dhha.org
†
Equal contributors
1
Department of Medicine, University of Colorado Health Sciences Center,
ACUTE at Denver Health, Denver, CO, 777 Bannock Street, MC4000, Denver,
CO 80204, USA
2
Department of Medicine, University of Colorado Health Sciences Center,
Eating Recovery Center, 7351 E Lowry Blvd, Suite 200, Denver, CO 80230,
USA
Self-induced vomiting may result in subconjunctival
haemorrhage or recurrent epistaxis [4]. Subconjunctival
haemorrhage consists of red patches in the white of the
eyes, and although worrisome in appearance, is actually
a benign finding. Recurrent bouts of epistaxis should
prompt inquiry about purging.
Dental
A patient’s dentist may be the first one to see signs of
self-induced vomiting. Several abnormalities in the oral
cavity have been reported including dental erosion, reduced salivary flow rate, tooth hypersensitivity, dental
caries, periodontal disease, and xerostomia (dry mouth)
[5-10]. Dental erosions typically occur on the lingual
surface of the maxillary teeth. Though mandibular teeth
may also be affected, they are believed to be somewhat
© 2015 Mehler and Rylander; licensee BioMed Central. This is an Open Access article distributed under the terms of the
Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public
Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this
article, unless otherwise stated.
Mehler and Rylander Journal of Eating Disorders (2015) 3:12
protected, from gastric acid exposure, by the tongue
[5,11]. Erosions may be apparent as early as six months
after onset of regular self-induced vomiting [6]. The rate
and severity of erosions may ultimately be determined
by duration of illness, types of food consumed, oral hygiene, frequency of vomiting, and baseline quality of the
tooth structure [11]. Increased frequency of dental caries
has been reported as a consequence of binging on high
carbohydrate-content foods, increased consumption of
carbonated beverages, poor oral hygiene, in addition to
acid exposure [7-9]. Gingivitis (gum disease) and periodontal disease may result from repeated exposure to
gastric acid. This causes chronic gum irritation and
bleeding. Xerostomia is encountered in patients with
self-induced vomiting; it is hypothesized to relate to reduced salivary flow rates [10].
Other abnormalities, besides those affecting dentition,
occur in the oral cavity as a consequence of self-induced
vomiting. Sialadenosis, or hypertrophy of the salivary
glands, has been reported in 10-50 percent of patients
with self-induced vomiting [11]. It is generally bilateral
and only minimally tender. Though the pathogenesis of
this phenomenon is unclear, pathologic examination reveals a non-inflammatory process. Reductions in salivary
flow have been observed but the electrolyte and protein
composition of saliva does not differ between patients
and controls [10]. It has been hypothesized that sialadenosis may be the result of either regurgitation of acidic
contents, consumption of carbohydrate dense foods over
a short period of time (binges), or the result of pancreatic proteolytic enzymes coming back into the mouth
during vomiting and stimulating lingual receptors [12].
The bilateral parotid glands are the glands most commonly involved, but submandibular enlargement may
also be seen [13,14]. This “chipmunk-type” facies generally occurs 3-4 days after the cessation of self-induced
vomiting. The enlargement of salivary glands has been
correlated with elevations in serum amylase levels. Kinzle, et al, found that 61 percent of bulimic patients, purging via self-induced vomiting, had elevated serum
amylase levels [15]. Isoenzyme studies further demonstrate that the elevations in serum amylase originate
from salivary glands as opposed to the pancreas [15-17].
Levels generally rise within 1-2 days of said purge episode and normalize within one week [11,17].
Page 2 of 5
repeated sore throats [18,19]. A study of eight singers
with bulimia found that their throat examinations demonstrated some or all of the following: post cricoid
edema, vocal fold edema, thick mucus covering the
larynx, posterior commissure hypertrophy, ventricular
obliteration, telangiectasia and polypoid changes in 50-100
percent of such patients [19].
Gastrointestinal
Patients who induce vomiting will commonly complain
of symptoms consistent with gastroesophageal reflux
(GERD), dysphagia, and odynophagia [20,21]. These
complaints generally imply abnormalities of the esophagus. With repetitive vomiting, the esophageal epithelium suffers repeated abnormal exposure to acidic
gastric contents and microtrauma. Consequences of this
can include esophagitis, esophageal erosions and ulcers,
Barrett’s esophagus and bleeding. Barrett’s esophagus
refers to a condition in which there is a change in the
mucosal lining type due to chronic and repetitive abnormal acid exposure to the esophagus. It is a known risk
factor for esophageal carcinoma. While the criteria to
screen, via endoscopy, for Barrett’s esophagus have been
recently loosened, screening may perhaps be indicated
for bulimic patients with chronic esophageal reflux
symptoms whose symptoms are difficult to control with
acid reduction therapies [22]. The most severe, albeit
very rare, acute consequence of self-induced vomiting,
is Boerhaave’s syndrome (esophageal rupture); it is a
surgical emergency [11,20]. This syndrome manifests
with chest pain, shortness of breath, and the very
unique complaint of painful yawning in a patient who is
tachypneic, tachycardic and appears to be in significant
distress. Overall, despite the potential frequency of complaints in these patients, endoscopic evaluation is generally normal or only demonstrates mild esophagitis [23].
Upper endoscopy may be indicated for those patients
with bulimia who have purged excessively for years and
for any bulimic patients with clear new symptoms of
dysphagia. Esophageal motility studies typically have not
demonstrated significant differences between patients
and controls [20]. Why the frequency of gastrointestinal
complaints does not correlate with objective endoscopic
findings is not currently known.
Electrolytes
Throat
Acid reflux, as a result of frequent bouts of self-induced
vomiting and damage to the esophageal sphincters,
affect areas of the pharynx and larynx and is referred to
as laryngopharangeal reflux (LPR). Regurgitated acidic
contents may come into contact with the vocal chords
and surrounding areas, resulting in hoarseness, dysphagia, chronic cough, a burning sensation in the throat or
Repeated episodes of vomiting can lead to dehydration
and subsequent upregulation of the secretion of the
renin-angiotensin-aldosterone steroid hormone system.
Aldosterone is secreted by the adrenal glands and results
in increased renal absorption of sodium and bicarbonate
and subsequent water retention to mitigate against a
propensity towards dehydration, hypotension and volume depletion from recurrent vomiting. This results in a
Mehler and Rylander Journal of Eating Disorders (2015) 3:12
metabolic alkalosis and low serum potassium values
[24]. Taken together, this phenomenon is referred to as
pseudo-Bartter’s syndrome [25]. Aldosterone continues
to be upregulated even after purging ceases. The resultant ongoing avidity toward increased sodium and bicarbonate retention by the kidneys, in the absence of
continued purging, can result in severe peripheral edema
formation especially if the patient with bulimia is given
intravenous saline-containing fluids in a rapid manner to
correct dehydration or electrolyte abnormalities [4,26].
Additional potassium losses emanate from the actual
vomitus. Though low serum potassium may be specific
marker for the self-induced vomiting of bulimia, it is not
sensitive [27,28]. The majority of patients with bulimia,
who vomit only occasionally, will have normal serum
electrolytes, in contrast to those who vomit excessively
or those who do so very regularly for a protracted course
of time.
Cardiac
Dehydration as a result of repeated episodes of emesis
can result in both resting and exertional sinus tachycardia, hypotension, and orthostasis. The resultant hypokalaemia can result in a prolonged QTc interval putting the
patient at risk for significant arrhythmias resulting in
syncope and palpitations. The most severe of these is a
specific type of ventricular tachycardia known as torsades
de pointes that can be fatal [29].
Though patients will often use their fingers or an object to induce emesis, some may revert to use of ipecac,
a syrup previously used to treat acute toxic ingestions.
Patients with bulimia who engage in self-induced vomiting may abuse this medication. The active ingredient of
ipecac is emetine which has a long half-life and consequently can accumulate to toxic levels with chronic
ingestion. Emetine toxicity can result in irreversible
damage to cardiac myocytes resulting in severe congestive heart failure, ventricular arrhythmias, and sudden
cardiac death [11,29].
Reproduction
While not a direct result of self-induced vomiting, it is
worth briefly mentioning that reproductive health outcomes are compromised in patients with bulimia. Although normal weight bulimics do not incur the
difficulties with fertility experienced by patients with
anorexia nervosa, bulimia nervosa has been associated
in smaller cohort series with an increased risk of miscarriages [30].
Pulmonary
In patients who purge via self-induced vomiting, aspiration of regurgitated food is a possibility. Thus, in an
otherwise healthy young adult with sudden onset
Page 3 of 5
respiratory distress and lower lobe opacities on chest
radiography, self-induced vomiting with aspiration
should be considered. Another pulmonary complication of self-induced vomiting is pneumomediastinum,
which is the dissection of air through the alveolar
walls, due to retching [31]. Finally, the presence of an
unusual foreign body in the esophagus or stomach on a
chest radiograph, may be due to the accidental ingestion of an object like a toothbrush used to induce
vomiting [32].
Laxative abuse
While less common than self-induced vomiting, abuse of
laxatives is the second most commonly utilized mode of
purging in patients with bulimia nervosa. Laxatives can
be grouped into five major classes, depending on their
mechanism of action: bulk laxatives, osmotics, surfactants, emollients, and stimulants. Of the various classes
of laxatives, the ones most abused by bulimic patients,
and the ones associated with most of the medical complications, are the stimulant laxatives, including compounds containing phenolphthalein, senna, bisacodyl
or anthraquinone. They act rapidly and directly to
stimulate colonic motility, producing a large volume of
watery diarrhea.
The medical complications of laxative abuse can be
divided into two main categories, those due to effects
on the gastrointestinal system along with the systemic
effects, of hypovolemia and those due to electrolyte
disturbances. The gastrointestinal effects of laxative
abuse include melanosis coli, cathartic colon, and functional impairment. Melanosis coli is a dark brown
discoloration of the colonic mucosa. Microscopic melanosis can be seen in about half of patients taking
anthraquinone-based laxatives. There is no indication
that melanosis coli has any significant pathophysiologic consequences.
In contrast, the cathartic colon syndrome is a serious
entity, involving loss of normal colonic peristalsis because of long-term habituation to stimulant laxatives.
The result is a dilated, atonic colon, which is incapable
of propagating fecal material, typically defined on the
basis of radiologic findings. A barium enema reveals that
the colon loses the normal haustral markings and is dilated. Cathartic colon is suggested, on an abdominal
radiograph, when an ahaustral colon is present with increased submucosal fat [33]. These changes arise from
inflammation of the mucosa, alterations in muscular
layers of the colon, and degeneration of the myenteric
and Auerbach’s nerve plexi caused by a direct toxic
effect from the stimulant laxatives. Microscopically, the
colon shows thinning of the microvilli and abnormalities
within cytoplasmic organelles. As a result of these
changes, slowed or absent transit occurs through some
Mehler and Rylander Journal of Eating Disorders (2015) 3:12
Page 4 of 5
Table 1 Common electrolyte changes with different purging modes
Purging mode
Sodium
Potassium
Chloride
Bicarbonate
Diuretics
Decreased or normal
Decreased
Decreased
Increased
Laxatives (short-term)
Decreased or normal
Decreased
Increased
Decreased
Laxatives (long-term)
Decreased or normal
Decreased
Decreased
Increased
Vomiting
Decreased or normal
Decreased
Decreased
Increased
or all segments of the colon, leading to hard, infrequently passed stools and refractory constipation
wherein the colon is converted to an inert tube. There
is marked variation in individual susceptibility to these
effects of stimulant laxatives and a true prevalence of
this devastating disorder in bulimia, is not known.
With truly prolonged abuse of these laxatives, the
cathartic colon syndrome is potentially irreversible.
Loss of normal colonic function can become so severe
that resultant ostomy is needed to treat intractable
constipation with resultant ostomy. A history of
prolonged laxative use may also produce a more innocuous reflex constipation. This constipation can be
bothersome during withdrawal from laxatives, making
it somewhat difficult to terminate laxative abuse, but it
is usually transient if patience prevails.
The systemic effects of laxative abuse emanate from
the hypovolemia and electrolyte disturbances that develop as a result of the diarrhea and the body’s compensatory mechanisms. Electrolytes lost through laxative use
include chloride, calcium, bicarbonate, and potassium.
The hypokalemia leads to further slowing of intestinal
motility [34,35]. Moreover, the risk for severe edema formation with abrupt cessation of purging via laxatives
can again occur with abrupt cessation of the laxatives
[24]. Chronic diarrhea, like self-induced vomiting produces a hypochloremic, hypokalemic metabolic alkalosis
attributable to hypovolemia-induced hyperaldosteronism, but acute diarrhea of shorter duration results in a
hyperchloremic metabolic acidosis, without an increased
anion gab (Table 1).
Because of the relatively high prevalence of laxative
abuse in patients with bulimia, such abuse should be
suspected and appropriate questions directed to these
patients because bulimic persons are often of normal
body weight and may not admit to their disorder or their
laxative abuse. In suspected cases, laxative abuse can
also be detected by ordering toxicological assays of the
feces or urine, a way to establish a suspected diagnosis
of laxative abuse beyond doubt. In addition, surreptitious
laxative abuse should be suspected in those patients
complaining of chronic diarrhea without an obvious
source. In one study of patients being evaluated for diarrhea, the prevalence of laxative use was 15%, despite patients’ denying any laxative ingestion [36]. Restoration of
normal bowel function may take weeks.
Conclusions
Similar to anorexia nervosa, bulimia nervosa is associated with many different medical complications. These
are dependent on the mode and frequency of purging.
Diuretic abuse very closely mimics the acid-base and
electrolyte abnormities seen with self-induced vomiting.
Overall, some of these complications can be quite serious and can cause permanent adverse sequelae.
Abbreviations
BMI: Body mass index; GERD: Gastroesophageal reflux;
LPR: Laryngopharangeal reflux.
Competing interests
Dr. Philip S. Mehler and Dr. Melanie Rylander declare that they have no
significant competing financial, professional or personal interests that might
have influenced the performance or presentation of the work described in
this manuscript.
Authors’ contributions
Both authors read and approved the final manuscript.
Acknowledgements
The authors acknowledge the superb administrative support of Ms. Adrianna
Padgett.
Received: 16 December 2014 Accepted: 24 February 2015
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