Ophthalmic manifestations of Eating Disorders

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Disease Entity

Epidemiology/Etiology

The term “eating disorder” encompasses a wide range of psychiatric illness, including but not limited to anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED).[1] In the United States, lifetime prevalence of AN is 0.80%, BN is 0.28%, and BED is 0.85%, with the majority occurring in females.[2] Eating disorders are multisystem illnesses that permeate many body systems, including the eye. Common eye manifestations include dry eyes, lagophthalmos, acute and chronic visual loss (e.g., nutritional amblyopia), nystagmus, ophthalmoplegia (e.g., Wernicke encephalopathy), and rapid weight changes associated with intracranial hypertension.[1][3][4] Consequently, ophthalmic manifestations can arise in both the active disease state as well as the treatment phase.

Pathology

The various pathologies of ocular abnormalities related to eating disorders are as numerous as the classifications of eating disorders. Hence, only the common manifestations mentioned above will be covered.

1. Lagophthalmos, the inability to completely close the eyelids, often occurs due to orbital fat atrophy, particularly seen with AN.[1][5]

2. Acute visual loss associated with eating disorders is multifactorial and can include decreased retinal nerve fiber layer thickness (RNFL), as well as cotton wool spots and intraretinal hemorrhages neighboring the optic disc.[3][6]

3. Vitamin B1 deficiency, manifesting as Wernicke encephalopathy, can cause both nystagmus and ophthalmoplegia in AN via enzymatic blockades. Other vitamin deficiencies can manifest as parts of eating disorders.[1][4]

4. IIH, also known as pseudotumor cerebri, following weight gain can surface during the course of an eating disorder or during the therapeutic stage.[7][8] For BN and BED, increased weight from eating habits predisposes individuals to develop IIH.[8] In the case of AN, IIH may follow refeeding syndrome if intentional weight gain is not closely monitored and causes rapid shunting of vital nutrients out of the circulation.[7]

5. Chronic bilateral symmetric central visual loss (visual acuity and central/cecocentral scotoma) with secondary optic atrophy OU.

Diagnosis

History

Presenting symptoms and history will be dependent on which form of eating disorder an individual has. For AN, there is often a record of restricted food intake and excessive exercise in an attempt to maintain a low body weight and body mass index.[4] As far as ocular disturbances, there may be a history of lagophthalmos, dry eyes, or decreased visual acuity – this is typically subacute and painless.[1][3][5] If AN has caused vitamin B1 deficiency, the patient may report symptoms of ataxia, confusion, or nystagmus/ophthalmoplegia, the classic triad of Wernicke syndrome.[4] In BN, patients have a history of self-induced vomiting or laxative abuse. The increased pressure created by the vomiting can cause pinpoint subconjunctival hemorrhages, which are painless and often only noted when looking in a mirror or by family/friends.[9] Finally, individuals with BED have a history of binge eating episodes not followed by compensatory actions, such as purging. These individuals may complain of headaches and cranial nerve palsies produced by IIH in the setting of weight gain (typically CN VI).[8] If a patient currently is recovering from an eating disorder, especially AN, and present with the same symptoms, one should also consider IIH because of refeeding syndrome.[7] What is particularly challenging is that eating disorder behaviors are not mutually exclusive and patients may have an intricate history composed of certain aspects of each psychiatric illness.

Physical Exam

As with the history, physical exams of patients with eating disorders will vary depending on the type. AN typically presents as a thin individual, often female, with obvious signs of malnutrition.[1] Physical exam of the eye may show lagophthalmos with narrowing of the palpebral fissures and keratoconjunctivitis sicca, or dry eye.[5] Additionally, visual acuity may be decreased depending on the extent and duration of the disease.[3][6] As mentioned in the history, vitamin B1 deficiency due to AN can present on physical exam with Wernicke triad.[4]

The physical exam of someone with BN can be more challenging, as the person often appears well-nourished. However, subconjunctival hemorrhages may be present.[9] Papilledema or optic disc atrophy, signs of increased intracranial pressure, may be seen on physical exam of an individual with BED if the binging has caused rapid weight gain and secondary IIH.[10][11][12] Refeeding syndrome following AN, if precipitating IIH, can look similarly on physical exam, and thus history will be used to distinguish between the two.[7][11] Nutritional optic neuropathy from B9 (folate) or B12 deficiency typically presents as bilateral, painless, progressive, loss of vision in both eyes (central/cecocentral scotoma) and eventual optic atrophy OU.

Diagnostic Procedures

For the diagnosis of AN itself, a BMI of < 18.5 kg/m2 is needed.[2] As for eye manifestations, optical coherence topography (OCT) can be utilized to diagnose decreased RNFL thickness, and fundoscopy can visualize any signs of retinopathy, such as cotton wool spots or intraretinal hemorrhages, leading to decreased vision.[3][6] There is not typically a diagnostic ophthalmic procedure for BN, as the only sign is often conjunctival pinpoint hemorrhaging that can be seen with the naked eye. Magnetic resonance imaging (MRI) of the brain and magnetic resonance venography (MRV) are useful in BED and can show features of intracranial hypertension secondary to rapid weight gain caused by binge eating episodes.[8][9]MRI and MRV are also recommended to exclude other pathologies that could lead to increased intracranial pressure, such as a mass lesion, stroke, or hematoma.[13] Additionally, if dural venous sinus stenosis, scleral flattening, or an empty sella turcica are seen on imaging, these may suggest increased intracranial pressure (although some features are non-specific, and these features do not specifically mean the patient has IIH).[13] A lumbar puncture (LP) could then be considered to look for an opening pressure of > 25 cm H2O, which in the absence of alternative etiologies, and assuming normal cerebrospinal fluid content, would meet diagnostic criteria for IIH.[8][11] MRI, MRV, and LP might also be considered in a suspected case of refeeding syndrome following an eating disorder as it will present similarly to IIH in BED.[7]

Laboratory Testing

For most eating disorders, there are no specific laboratory tests that can conclusively identify the disease. However, there are certain tests that are supportive. In a suspected Wernicke disease case associated with AN, vitamin B1 levels can be directly checked or quantified by measuring transketolase activity.[4][14] A 25% stimulation of transketolase activity following thiamine pyrophosphate (TPP) addition indicates B1 deficiency.[14] Metabolic alkalosis, defined as elevated serum bicarbonate levels and a high pH, may be seen on arterial blood gas (ABG) or suggested on venous blood gases in a bulimic patient. In cases of laxative abuse, ABG more often shows metabolic acidosis due to the bicarbonate wasting in the stool.[1][9] Complete blood count (CBC) and urinalysis can be utilized for most eating disorders to check for anemia, electrolyte abnormalities, liver enzymes, elevated lipids, and other lab abnormalities. BED, specifically, tends to have an elevated lipid profile due to altered metabolism from increased food consumption.[15] Monitoring for refeeding syndrome with electrolytes including phosphate should be performed when patients are undergoing supervised nutrition plans for eating disorder management – any phosphate level below 0.8 mmol/L should trigger consideration of more aggressive management to prevent permanent brain and muscle damage.[1][7] Serum levels of vitamin A (e.g., nyctanopia), C (dry eye), B1 (nystagmus, ophthalmoplegia), B9 and B12 (central visual loss) should be considered in these cases. Serum homocysteine levels and methylmalonic acid are more representative of long term B9 and B12 deficiency.

Management

General

Management of eating disorders often includes a complex combination of pharmacotherapy, behavioral therapy, and nutritional therapy that is outside the purview of this article.[16] Instead, the surgical and medical approaches of the various ophthalmic manifestations will be covered. However, the importance of controlling the underlying eating disorder cannot be understated, as perpetual disordered eating will only further exacerbate the ocular abnormalities. Vitamin supplementation and restoration of normal diet are the first steps in treating neuro-ophthalmic effects of eating disorders.

Surgery

The surgical treatment of lagophthalmos, often precipitated by AN, typically begins with tarsorrhaphy, the partial sewing of the eyelids together in order to narrow the excess eyelid opening.[12] Additionally, gold or platinum weights inserted into the upper eyelid utilize gravity to pull said eyelid downward.[12] In the case of IIH following BED or refeeding syndrome, acetazolamide therapy is recommended to relieve increased intracranial pressure.[7] An optic nerve sheath fenestration (ONSF) or cerebrospinal fluid (CSF) diversion procedure may be necessary for patients who fail, are intolerant to, or non-compliant with maximum medical therapy.[10]

Medical Approach

A number of pharmacotherapies, like selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors (SNRIs), can be prescribed for eating disorders.[16] Treatment of the ophthalmic manifestations depends on the presentation. Any case of suspected Wernicke encephalopathy in someone with an eating disorder should be treated empirically with high dose (e.g., 500 mg IV thiamine three times a day) and magnesium as soon as concerns for the diagnosis are made. Prophylactic thiamine can also be given to minimize the risk of Wernicke syndrome.[14] B12 and B9 supplements should be considered in deficient symptomatic individuals. IIH is typically treated with weight loss, however this may not be beneficial to someone suffering from an eating disorder. Therefore, in IIH due to BED or refeeding syndrome, acetazolamide is often the drug of choice.[13]

Follow-up

Follow-up is needed for both the eating disorder itself, as well as any ocular findings. Regular targeted ophthalmic evaluations to the manifestations the patient has is recommended.[4][10] As relapses are common for eating disorders, regular psychiatric follow up is also recommended.[2]

Complications

The complications regarding eating disorders are two-fold – disorder-related and treatment-related. Since the ocular complications have already been discussed, the non-ocular will be mentioned here. Those with AN and BN can experience abnormalities throughout every single body system, including skin, cardiac, gastrointestinal, hematologic, and endocrine, owing to the poor eating habits they participate in and inadequate nutritional intake.[1][9] The complication of IIH following BED or refeeding syndrome has already been stated and can be found above.

Prognosis

The prognosis of the ophthalmic manifestations of eating disorders is in part contingent on the control of the underlying illness. If the eating disorder is detected early and the patient engaged and compliant with their treatment plan, the physical and visual complications can often be minimized. For AN, studies have demonstrated that only 50% of cases are diagnosed and anywhere from 20-73% of patients withdraw from treatment, dependent on inpatient or outpatient setting.[17] Meta-analysis has shown that prognosis is generally better for BN and BED, although the mechanism behind the improved outcomes is not well known.[18]

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Gibson D, Workman C, Mehler PS. Medical Complications of Anorexia Nervosa and Bulimia Nervosa. Psychiatr Clin North Am. 2019;42(2):263-274. doi:10.1016/j.psc.2019.01.009
  2. 2.0 2.1 2.2 Udo T, Grilo CM. Prevalence and Correlates of DSM-5-Defined Eating Disorders in a Nationally Representative Sample of U.S. Adults. Biol Psychiatry. 2018;84(5):345-354. doi:10.1016/j.biopsych.2018.03.014
  3. 3.0 3.1 3.2 3.3 3.4 Caire-Estévez P, Pons-Vázquez S, Gallego-Pinazo R, Sanz-Solana P, Pinazo-Durán MD. Restrictive anorexia nervosa: a silent enemy for the eyes and vision. Br J Ophthalmol. 2012;96(1):145. doi:10.1136/bjophthalmol-2011-300957
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Oudman E, Wijnia JW, Oey MJ, van Dam MJ, Postma A. Preventing Wernicke's encephalopathy in anorexia nervosa: A systematic review. Psychiatry Clin Neurosci. 2018;72(10):774-779. doi:10.1111/pcn.12735
  5. 5.0 5.1 5.2 Gaudiani JL, Braverman JM, Mascolo M, Mehler PS. Lagophthalmos in severe anorexia nervosa: a case series. Arch Ophthalmol. 2012;130(7):928-930. doi:10.1001/archophthalmol.2011.2515
  6. 6.0 6.1 6.2 Karasu B, Gunay BO, Erdogan G, Kardes E, Gunay M. Purtscher-Like Retinopathy Associated with Anorexia Nervosa. Case Rep Ophthalmol Med. 2016;2016:1934091. doi:10.1155/2016/1934091
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 Sundström N, Brorsson C, Karlsson M, Wiklund U, Koskinen LD. Refeeding syndrome: multimodal monitoring and clinical manifestation of an internal severe neurotrauma [published online ahead of print, 2020 May 4]. J Clin Monit Comput. 2020;1-8. doi:10.1007/s10877-020-00513-y
  8. 8.0 8.1 8.2 8.3 8.4 Raggi A, Curone M, Bianchi Marzoli S, et al. Impact of obesity and binge eating disorder on patients with idiopathic intracranial hypertension. Cephalalgia. 2017;37(3):278-283. doi:10.1177/0333102416640514
  9. 9.0 9.1 9.2 9.3 9.4 Mehler PS, Rylander M. Bulimia Nervosa - medical complications. J Eat Disord. 2015;3:12. Published 2015 Apr 3. doi:10.1186/s40337-015-0044-4
  10. 10.0 10.1 10.2 Rigi M, Almarzouqi SJ, Morgan ML, Lee AG. Papilledema: epidemiology, etiology, and clinical management. Eye Brain. 2015;7:47-57. Published 2015 Aug 17. doi:10.2147/EB.S69174
  11. 11.0 11.1 11.2 Spennato P, Ruggiero C, Parlato RS, Buonocore MC, Varone A, Cianciulli E, Cinalli G. Pseudotumor cerebri. Childs Nerv Syst. 2011;27(2):215-235. doi:10.1007/s00381-010-1268-x
  12. 12.0 12.1 12.2 Fu L, Patel BC. Lagophthalmos. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 10, 2020.
  13. 13.0 13.1 13.2 Boyter E. Idiopathic intracranial hypertension. JAAPA. 2019;32(5):30-35. doi:10.1097/01.JAA.0000554732.85914.91
  14. 14.0 14.1 14.2 Wiley KD, Gupta M. Vitamin B1 Thiamine Deficiency. [Updated 2020 Jun 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.
  15. Nakai Y, Noma S, Fukusima M, Taniguchi A, Teramukai S. Serum Lipid Levels in Patients with Eating Disorders. Intern Med. 2016;55(14):1853-1857. doi:10.2169/internalmedicine.55.5632
  16. 16.0 16.1 Gorla K, Mathews M. Pharmacological treatment of eating disorders. Psychiatry (Edgmont). 2005;2(6):43-48.
  17. Jagielska G, Kacperska I. Outcome, comorbidity and prognosis in anorexia nervosa. Psychiatr Pol. 2017;51(2):205-218. doi:10.12740/PP/64580
  18. Graves TA, Tabri N, Thompson-Brenner H, et al. A meta-analysis of the relation between therapeutic alliance and treatment outcome in eating disorders. Int J Eat Disord. 2017;50(4):323-340. doi:10.1002/eat.22672