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The Impact of Purging on the Body

By Dennis Gibson, MD, FACP, CEDS

Purging and Eating Disorders

Compensatory behaviors are an essential criterion present in several eating disorder classifications. Purging is a compensatory behavior, but not all compensatory behaviors are purging. Compensatory behaviors are divided into two categories: purging behaviors and non-purging behaviors. Purging behaviors involve elimination in order to compensate for food intake. The most common form of purging include self-induced vomiting, laxative misuse, diuretic misuse and enemas. Non-purging behaviors include any type of compensatory behavior that does not involve purging, which may include food restriction, excessive exercise or diet pills.

Purging in Diagnostic Criteria

There are several eating disorders that feature purging within the diagnostic criterion, including bulimia nervosa, the binge eating/purging subtype of anorexia nervosa and other specified feeding or eating disorder.

Bulimia Nervosa

Purging is most often associated with bulimia nervosa. Bulimia nervosa (BN) is an eating disorder characterized by cyclical episodes of binge eating and compensatory behavior. A binge eating episode is eating an amount of food in a discreet amount of time that is definitively larger than what most individuals would eat in a similar period of time under similar circumstances while also feeling that one cannot stop eating or control what or how much they are eating. Individuals with BN will engage in recurrent inappropriate compensatory behaviors in order to prevent weight gain, including purging. The binge eating and compensatory behaviors occur, on average, at least once a week for 3 months.

Anorexia Nervosa Binge Eating/Purging Subtype

Anorexia nervosa (AN) is an eating disorder categorized by:

  • Restriction of energy intake relative to requirements, leading to a significant low body weight in the context of the age, sex, developmental trajectory, and physical health
  • Intense fear of gaining weight or becoming fat or persistent behavior that interferes with weight gain
  • Disturbed by one’s body weight or shape, self-worth influenced by body weight or shape, or persistent lack of recognition of seriousness of low bodyweight

Anorexia nervosa further divided into two subtypes: restricting type (AN-R) and binge-eating/purging type (AN-BP). AN-BP is categorized by the above criteria, combined with regularly engaging in binge-eating or purging within the last 3 months.

Other Specified Feeding or Eating Disorder (OSFED)

According to the DSM-5, the category of other specified feeding or eating disorder (OSFED) is applicable to individuals who are experiencing significant distress due to their disordered eating but who do not meet the full criteria for a diagnosis of AN, BN, or ARFID.

Purging Disorder

Purging disorder (PD) is characterized by individuals engaging in purging behaviors such as self-induced vomiting or laxative misuse, without experiencing eating binges or being underweight. Purging disorder is not an independent diagnosis but is often used to describe purging behavior that doesn’t align with independent eating disorder diagnoses.

Complications from Purging: Head to Toe

Purging can cause complications in many of the body’s organ systems, ranging from clinically insignificant presentations in the eyes to serious and deadly gastrointestinal and metabolic complications.

Ophthalmological Complications

Subconjunctival Hemorrhage (red eyes)

Forceful vomiting can cause the blood vessels of the eye to break. During purging, the acute increase in pressure of the eye causes the blood vessels to rupture, causing the white of the eye to appear bright red.

Oral Complications

Purging through self-induced vomiting causes various oral complications. Unlike many complications seen in eating disorder patients, some of the oral complications are irreversible and will require further intervention to restore function and/or improve appearance.

Sialadenosis  

Also known as parotid gland enlargement or colloquially as “chipmunk cheeks,” sialadenosis is a hallmark of purging. It typically occurs 3-4 days after purging has ceased. Sialadenosis causes bilateral enlargement of the parotid glands, and in rare cases, other salivary glands. It is thought to occur due to either a backup of saliva that is no longer needed, cholinergic stimulation of the glands or hypertrophy of the glands to help meet demands of increased saliva production. Treatment includes cessation of vomiting and supportive care until the salivary gland hypertrophy normalizes.

Hyperamylasemia

Patients who experience sialadenosis may also experience hyperamylasemia. Amylase is produced by the salivary glands and pancreas, and it can be indicative of vomiting behaviors.  

Gingivitis & Periodontitis

Purging through self-induced vomiting can cause gum disease (gingivitis). Chronic irritation from the low-pH (acidic) gastric contents can cause inflammation and pain of the gums. Gingivitis can also be caused by dry mouth (xerostomia) in patients who purge.If gingivitis goes untreated, it can develop into more serious periodontal disease. This can lead to a degradation of the jawbone (periodontitis), causing the teeth to become loose or fall out. The space around loose teeth can foster bacteria and lead to infection. Unlike gingivitis, periodontitis is less reversible.

Enamel Erosion (Perimylolysis) & Tooth Damage

Chronic regurgitation of stomach acid can cause dental erosion, which is the most common oral manifestation of people who purge through self-induced vomiting. Repeated exposure to vomitus erodes the lingual (facing toward the tongue) surfaces of the teeth, most notably the maxillary teeth.

Deterioration of the enamel can lead to brittle and week teeth, tooth hypersensitivity and dental caries; however, restriction of nutritional also may increase the risk for dental caries (cavities). When the enamel of the teeth wears away and exposes the dentin, continued exposure to vomitus can cause infection, discoloration, or pulp death of the teeth.

Soft Tissue Damage

Pressure from vomiting can cause blood vessels in the mouth to burst, causing the palate and tongue to turn an orange-yellow color. The act of inserting a hand or object into the mouth to induce vomiting can cause redness, cuts, scratches or bleeding lesions in the soft tissue of the mouth.Frequent vomiting may also increase risk of development of canker sores, due to the contact of the acidic vomitus with the mucosa.

Other Oral Complications

Several other oral complications include:

  • Chronic dry mouth (xerostomia)
  • Bad breath
  • Dry, cracked and inflamed lips

Gastrointestinal Complications

Gastrointestinal complications are numerous in eating disorder patients. Self-induced vomiting causes serious stress on the gastrointestinal tract, leading to numerous complications of the esophagus and the colon.

Cathartic Colon

Excessive and chronic misuse of stimulant laxatives can cause colonic inertia, also known as cathartic colon, a condition whereby the colon becomes incapable of moving stool forward. It is suspected that this is due to direct damage to the gut myenteric nerve plexus. While it was uncertain whether this condition was associated with eating disorders, a recent pilot studies suggest that cathartic colon can develop as a result of abuse of stimulant laxatives.It is imperative to stop using stimulant laxative as this condition is believed to be reversible with cessation of stimulant laxatives.

Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is a chronic condition characterized by the reflux of stomach contents into the esophagus. In a healthy esophagus, the lower esophageal sphincter prevents gastric contents and acid from moving upwards into the esophagus. Over time, recurrent self-induced vomiting can weaken the lower esophageal sphincter, causing contents to flow upwards into the esophagus.

Barrett’s Esophagus

Because the esophageal mucosa of patients who self-induce vomiting is frequently exposed to acidic vomitus, there may be an increased risk of developing Barrett’s esophagus. Barrett’s esophagus is a condition in which the lining of the esophagus becomes more like the lining of the small intestine rather than the esophagus due to repeated exposure to stomach acid.This is a pre-cancerous condition and requires treatment of the underlying cause (i.e. reflux) to help reduce the progression to a cancerous state.

Mallory-Weiss Syndrome

In rare instances the sudden rise in pressure in the stomach or the lower part of the esophagus during vomiting can cause a tear in the lining in the upper gastrointestinal tract and cause bleeding. Vomitus will often appear blood-streaked.

Boerhaave Syndrome

Boerhaave Syndrome is a rare condition of high mortality resulting in spontaneous perforation of the esophagus due to, usually, severe straining or vomiting. It creates a hole through which contents of the esophagus can pass into the chest (mediastinum), putting patients at risk of infection (mediastinitis) and other complications.

Other Gastrointestinal Complications

There are other miscellaneous complications that can occur independently, alongside or as a consequence of the aforementioned complications:

  • Difficulty swallowing (dysphagia)
  • Sensation of having a lump or something stuck in the throat (globus sensation)
  • Chronic cough
  • Hoarseness and sore throat
  • Indigestion
  • Esophageal cancer
  • Pain with swallowing (odynophagia)
  • Irritation of the esophagus (Esophagitis)
  • Esophageal erosions and ulcers
  • Melanosis coli (black discoloration of the intestine)
  • Rectal prolapse (can develop from just restriction without purging as well)

Pulmonary Complications

Pneumonitis and Pneumonia

The greatest risk to the lungs during purging is aspiration, or the inhalation of foreign materials. Inhalation of vomit during purging can cause inflammation of the lung tissue (pneumonitis) or infection of the lung tissue (pneumonia).Aspiration confers high mortality in those with eating disorders.

Pneumothorax

Pneumothorax, or collapse of the lung, can develop from both purging and restricting behaviors. This can present with shortness of breath and can be a medical emergency.

Pneumomediastinum

The increased intrathoracic and intra-alveolar pressures, due to retching, can cause pneumomediastinum, a condition in which air is present within the chest cavity, or the mediastinum.Research also suggests that this air may originate from the intestines and travel up to the chest cavity.

Metabolic & Electrolyte Disturbances

Many of the metabolic and electrolyte disturbances can be attributed to dehydration and malnutrition. Patients with a history of purging should be screened regularly, up to daily, for serum electrolyte disturbances. The severity of electrolyte abnormalities increases with the frequency of purging.

Hypokalemia (low potassium)

Hypokalemia occurs with all three forms of purging. Hypokalemia from purging develops for two reasons. First and most obviously, potassium is lost through vomiting, excessive bowel movements from laxative abuse or through urine from diuretic abuse.

Second, chronic purging also results in the loss of intravascular fluid, which causes hormonal changes in the kidneys that ultimately result in increased production of aldosterone and development of pseudoBartter syndrome. Aldosterone causes the distal convoluted tubules and cortical collecting ducts to resorb sodium and chloride to help combat severe dehydration, hypotension, or fainting. Aldosterone also promotes renal secretion of potassium into the urine, resulting in hypokalemia. The effects of aldosterone are the more significant contributor toward development of the hypokalemia.

Hypokalemia can cause many complications, including:

  • Muscle weakness
  • Cardiac arrhythmias
  • GI dysmotility
  • Death
Metabolic Alkalosis

Metabolic alkalosis and hypokalemia are interrelated. Low hydrogen levels (alkalosis) causes potassium to move into the cells, which drops the serum potassium.

Purging leads to the development of metabolic alkalosis, largely through the action of aldosterone, which causes loss of potassium and hydrogen (acid) in the urine. The loss of hydrogen in the urine maintains the alkalemic state.Vomiting itself can also contribute to development of an alkalotic state through the loss of hydrogen in the emesis.

Pseudo-Bartter Syndrome

All forms of purging cause dehydration, which contributes toward the development of pseduo-Bartter syndrome. This chronically dehydrated state causes an upregulation of aldosterone, which acts to retain water and salt, thereby increasing the blood volume/blood pressure and helping reduce risk for syncope (good). However, the salt and water retention contributes to edema formation (bad), which frequently persists for weeks after cessation of purging and optimization of fluid status. This volume overload is not only distressing to the patient but can also contribute to increased stress on the heart, necessitating proactive treatment.

 

Cardiovascular Complications

Repeated purging can result in dehydration and hypokalemia, which can lead to decreased cardiovascular function and arrhythmias.

Hypotension & Tachycardia

Dehydration from purging decreases the overall blood volume, leading to a drop in blood pressure and a subsequent increase in heart rate (tachycardia). Low blood pressure can contribute to numerous symptoms:

  • Blurred vision
  • Dizziness and lightheadedness
  • Fainting
  • Fatigue
  • Difficulty concentrating
  • Nausea and other GI symptoms
QT Prolongation

Electrolyte abnormalities from purging, specifically hypokalemia, can lead to QT prolongation, which predisposes to more sinister arrhythmias. The QT segment on the cardiac tracing refers to the amount of time it takes the heart to contract and then relax. This time period prolongs with hypokalemia, due to the effects this has on the ion channels located in the myocytes. Many of the medications used to treat comorbid mental health diagnoses and the medical complications of malnutrition also can cause QT prolongation. It is necessary to treat the underlying cause of QT prolongation to avoid development of other arrhythmias. The malnutrition itself is an unlikely contributor to QT prolongation.

Torsades de Pointes

Long QT interval (QT prolongation) puts patients at risk for a life-threatening arrhythmia known as Torsades de pointes, which is a type of polymorphic ventricular tachycardia. Females in general tend to be at higher risk for development of this arrhythmia. Hypomagnesemia, which can be seen with alcohol and diuretic misuse as well as from refeeding, can also predispose toward this arrhythmia. Torsades de pointes does not seem to be inherently related to anorexia nervosa and weight loss.

Emetine Toxicity

Patients who use ipecac to induce vomiting may experience cardiac complications due to chronic ingestion of emetine, ipecac’s active ingredient. Emetine has a long half-life and accumulates in the body, causing irreversible damage to cardiac myocytes, leading to severe congestive heart failure, ventricular arrhythmias and sometimes death.  

Dermatological Signs

Eating disorders have many cutaneous manifestations which can help suggest this diagnosis. While most of them are associated with low weight and restriction, several of them are directly associated with purging.

Periorbital Petechiae & Facial Purpura

Self-induced vomiting can cause small red dots or purple splotches around the face. Purging can cause the capillaries in the face to burst, causing red speckles (petechiae) around the eyes or larger spots of blood pooled under the skin of the face (purpura).

Russell’s sign

Russell’s sign develops from the repeated action of inserting the dominant hand into the mouth and scraping the knuckles across the teeth during self-induced vomiting, causing skin abrasions and calluses to form on the dorsal aspect (backside) of the hand.

Resources

  1. Abebe, D. S., Lien, L., Torgersen, L., & Von Soest, T. (2012). Binge eating, purging and non-purging compensatory behaviours decrease from adolescence to adulthood: A population-based, longitudinal study. BMC Public Health, 12(1). https://doi.org/10.1186/1471-2458-12-32

  2. Nitsch, A., Dlugosz, H., Gibson, D., & Mehler, P. S. (2021). Medical complications of bulimia nervosa. Cleveland Clinic Journal of Medicine, 88(6), 333–343. https://doi.org/10.3949/ccjm.88a.20168
  3. Mehler, P. S., & Andersen, A. E. (2017, November 29). Eating Disorders: A Guide to Medical Care and Complications (third edition). Johns Hopkins University Press.
  4. American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Washington, DC: APA.
  5. Keel, P. K. (2019). Purging disorder. Current Opinion in Psychiatry, 32(6), 518–524. https://doi.org/10.1097/yco.0000000000000541
  6. Panico, R., Piemonte, E., Lazos, J., Gilligan, G., Zampini, A., & Lanfranchi, H. (2018). Oral mucosal lesions in Anorexia Nervosa, Bulimia Nervosa and EDNOS. Journal of Psychiatric Research, 96, 178–182. https://doi.org/10.1016/j.jpsychires.2017.09.022
  7. Smith, B. L. (1972). Pathology of Cathartic Colon. Proceedings of the Royal Society of Medicine. https://doi.org/10.1177/003591577206500329
  8. Gibson, D., Benabe, J., Watters, A., Oakes, J. L., & Mehler, P. S. (2021). Personality characteristics and medical impact of stimulant laxative abuse in eating disorder patients—a pilot study. Journal of Eating Disorders, 9(1). https://doi.org/10.1186/s40337-021-00502-9
  9. Denholm, M., & Jankowski, J. (2011). Gastroesophageal reflux disease and bulimia nervosa - a review of the literature. Diseases of the Esophagus. https://doi.org/10.1111/j.1442-2050.2010.01096.x
  10. Auger, N., Potter, B.J., Ukah, U.V., et al. Anorexia nervosa and the long-term risk of mortality in women. World Psychiatry 2021;20(3):448-49.
  11. Strumia, R. (2005). Dermatologic Signs in Patients with Eating Disorders. American Journal of Clinical Dermatology, 6(3), 165–173. https://doi.org/10.2165/00128071-200506030-00003

Last Reviewed: December 2023 by Dennis Gibson, MD, FACP, CEDS

Written by

Dennis Gibson, MD, FACP, CEDS

Dennis Gibson, MD, FACP, CEDS serves as the Clinical Operations Director at ACUTE. Dr. Gibson joined ACUTE in 2017 and has since dedicated his clinical efforts to the life-saving medical care of…

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