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Conference Roundup
The diagnosis of EoE is based on clinical presentation, histological findings, and the exclusion of other gastrointestinal diseases.3 The diagnosis of EoE should be considered in patients presenting with clinical symptoms of esophageal dysfunction, such as dysphagia, heartburn, chest pain, strictures, and food impactions, and an EGD should be considered to view the mucosa and collect multiple biopsies. In patients with EoE, these biopsies commonly will reveal eosinophilia with 15 or more eosinophils per high-power field (hpf).1,3 Patients with suspected EoE should be given a trial of high-dose PPIs for 8 to 12 weeks followed by repeat EGD. If the patient is still symptomatic and biopsies reveal more than 15 eosinophils per hpf, then a diagnosis of EoE can be established.3 If both symptoms and esophageal eosinophilia improve after the PPI trial, then other disorders such as GERD or PPI-responsive esophageal eosinophilia (PPI-REE) should be considered.
Differentiating EoE From PPI-REE Proton pump inhibitor-responsive esophageal eosinophilia is a relatively new disorder that is genetically and phenotypically indistinguishable from EoE.5,6 Although PPI-REE can be clinically and histologically identical to EoE, patients with PPI-REE can achieve complete remission after high dose-PPI therapy.3 Given the similarities between EoE and PPI-REE, it is important that all patients with suspected EoE be given a PPI trial to rule out PPI-REE. Patients with PPI-REE should continue PPI therapy, tapered down to the lowest possible dose depending on clinical symptoms.5 Follow-up endoscopy should be performed 1 year after diagnosis to ensure continued histological remission.5
Referral for Allergy Testing in EoE
Once a diagnosis of EoE has been established, patients should be referred to an allergist for testing and determination of food allergens.1 When food triggers are identified and removed from the diet, patients should experience an improvement of symptoms.1 Common diet modifications include the targeted elimination and empiric 6-food elimination diets.1 The targeted elimination diet uses skin patch testing to determine which foods need to be removed from the diet. The empiric 6-food elimination diet focuses on eliminating major food allergens, such as milk, eggs, wheat, soy, peanut and tree nuts, and all seafood, from the diet.7 Although both of these dietary modification strategies are very effective, it is important that providers ensure that patients adhere to the diet. The patient in this case was prescribed a targeted elimination diet but experienced a recurrence of symptoms due to nonadherence.
For patients who are nonadherent or whose symptoms are not well controlled with diet alone, providers should consider initiating corticosteroid therapy, such as fluticasone and budesonide.6 Although they are not indicated for EoE, corticosteroids are useful in the resolution of EoE symptoms because of their ability to reduce inflammation in the esophagus and suppress eosinophil production.6 Corticosteroids can be prescribed in a liquid or nebulized form. Nebulized corticosteroids are puffed into the mouth and swallowed, not inhaled, to coat the entire esophagus. Educating patients about how to appropriately use these medications is vital to ensure therapeutic efficacy. It also is necessary to inform patients about the possible side effects of swallowed steroid therapy, such as dry mouth, local candida infections, adrenal axis suppression, glaucoma, and bone demineralization.6
Along with diet modification, this patient was prescribed a daily PPI for the management of EoE. Although PPIs are not considered first-line therapy, they may be prescribed for symptomatic treatment. These medications can help reduce acid production, providing relief from heartburn, regurgitation, and dysphagia.6 Although PPIs are helpful in the resolution of these symptoms, they are also effective in treating the underlying inflammatory process and can be used as monotherapy.4
In some cases, patients with EoE can suffer from esophageal strictures and food impactions. Esophageal dilation is used for the immediate relief of symptoms in these patients.1 Understanding when dilation should be performed is an important aspect of managing patients with EoE.8 ■
Karmen Elsen, MPA, PA-C, works in the Digestive Health Center at Augusta University in Augusta, Georgia.
References
1. Merves J, Muir A, Chandramouleeswaran PM, Cianferoni A, Wang ML, Spergel JM. Eosinophilic esophagitis. Ann Allergy Asthma Immunol. 2014;112(5):397-403. 2. Park H. An overview of eosinophilic esophagitis. Gut Liver. 2014;8(6):590-597. 3. Kia L, Hirano I. Distinguishing GERD from eosinophilic oesophagitis: concepts and controversies. Nat Rev Gastroenterol Hepatol. 2015;12(7):379-386. 4. Dellon ES, Jensen ET, Martin CF, Shaheen NJ, Kappelman MD. Prevalence of eosinophilic esophagitis in the United States. Clin Gastroenterol Hepatol. 2014;12(4):589-596.e1. 5. Molina-Infante J, Rodriguez-Sanchez J, Martinek J, et al. Long-term loss of response in proton pump inhibitor-responsive esophageal eosinophilia is uncommon and influenced by CYP2C19 genotype and rhinoconjunctivitis. Am J Gastroenterol. 2015;110(11):1567-1575. 6. Furuta GT, Katzka DA. Eosinophilic esophagitis. N Engl J Med. 2015;373(17):1640-1648. 7. Greenhawt M, Aceves S. Non-IgE medicated food allergy: eosinophilic esophagitis update on the pathogenesis, clinical features, and management of eosinophilic esophagitis in children. Curr Pediatr Rep. 2014;2(2):127-134. 8. Al-Hussaini A. Savary dilation is safe and effective treatment for esophageal narrowing related to pediatric eosinophilic esophagitis. J Pediatr Gastroenterol Nutr. 2016;63(5):474-480.
The occurrence rate of BIA-ALCL following breast augmentation with textured implants is variable, ranging from 1 in 355 to 1 in 86,029 patients.
© PDSN / MEDICALIMAGES.COM
Almost 300,000 breast implant surgeries were performed in 2019.
An estimated 1.5 million breast augmentation surgeries are performed worldwide each year, typically for aesthetic or reconstructive purposes.1 In the United States, breast augmentation surgery ranked as the most commonly performed cosmetic procedure in 2019, with 299,715 surgeries reported.2 Because of the cancellation of elective surgeries during the early months of the COVID-19 pandemic, the number of breast augmentations performed in 2020 decreased to 193,073.3
Recent studies have implicated breast implants in the development of breast implant-associated anaplastic large cell lymphoma (BIA-ALCL).4-6 The first documented case was described in 1997; as of January 5, 2020, the US Food and Drug Administration (FDA) had received a total of 733 global and US medical device reports associated with BIA-ALCL, with 36 of those resulting in death.4,5 Of global cases in which a manufacturer was listed, 90.4% involved an Allergan implant, 7.3% involved Mentor implants, 1.5% involved Sientra implants, and 0.9% involved other manufacturers.6
In February 2019, the FDA issued a “Letter to Health Care Providers” to increase awareness of BIA-ALCL, its clinical presentation, and diagnostic recommendations in order to raise awareness of this potentially fatal condition. On July 24, 2019, the FDA asked Allergan to remove Natrelle BIOCELL textured breast implants and tissue expanders from the market.7
Epidemiology
Recent studies have shown variability in the occurrence rates of BIA-ALCL with the reported lifetime risk ranging from 1 in 355 to 1 in 86,029 persons depending on the population and type of textured implant studied.6,8 For implants with a textured outer shell, the risk in the US is estimated at 1 in 30,000 persons.6,8 In general, the number of reported cases has dramatically increased in the past decade as more cases are appropriately identified, although epidemiologic statistics may not be accurate due to underreporting.8,9 Among the medical device reports submitted to the FDA as of January 5, 2020, the median age of BIA-ALCL diagnosis is 52 years (range, 37-83 years); 36% of these cases occurred in the United States.5
BIA-ALCL has predominantly been reported in women, but there have been 3 cases reported in transgender maleto-female individuals who received breast implants.9 Some studies have shown that the majority of cases have occurred in Australia and New Zealand, while the lowest number of cases have occurred in Europe, Brazil, and China. Ethnicity may also play a role in conferring risk as there have been very few cases reported in patients of Scandinavian, Asian, African, and Native American descent.8
Pathophysiology
BIA-ALCL has been classified as a rare, peripheral form of non-Hodgkin T-cell lymphoma. Although the formal etiology is unknown, the risk of developing BIA-ALCL is related to the characteristics of the external surface of the implant: cases reported to the FDA have mostly occurred in women whose implants have a textured outer shell vs a smooth outer shell.5
For those cases that have developed in conjunction with a smooth implant, the patient typically reported a history of previously removed textured implants. The inner fill material of the implant does not appear to confer an independent risk as BIA-ALCL has developed with both saline and siliconefilled implants.5
It is theorized that insertion of a breast implant may trigger an inflammatory response with chronic T-cell stimulation; subsequent cell differentiation then results in malignant cell formation.10 Friction generated by the natural movement of textured implants within their surrounding fibrous capsules may contribute to this chronic inflammation.11
In addition, Pseudomonas aeruginosa and Ralstonia pickettii have been found on the surface of implants, demonstrating the potential for implants to chronically harbor bacteria that may cause further recruitment of lymphocytes, particularly CD4+ and CD30+ T cells.9,12,13 In‐vitro bacterial attachment studies show a linear relationship between surface area/roughness and bacterial attachment/growth, supporting the hypothesis that the uneven surfaces of textured implants are more conducive to bacterial growth.10,13 In an editorial, Santanelli di Pompeo et al have noted the possibility of genetic susceptibility, but chronic inflammation and infection remain the most widely accepted causes of BIA-ALCL.11
Clinical Presentation
BIA-ALCL typically develops approximately 8 to 13 years after the implant is inserted.7,14,15 The most common presentation is a unilateral malignant effusion containing liquefied lymphoma cells and high protein levels. In most cases, the lymphoma cells are contained within the fibrous capsule that forms around the implant (Figure), although approximately 5% of reported cases have shown bilateral effusion.16-18 The effusion frequently causes the affected breast to become edematous with or without associated pain. A solid tumor occurs in about 30% of cases, with or without effusion, and is palpable along the contour of the implant by the patient.16
Skin induration or rashes overlying the effusion may occur but are not common. Other reported signs include axillary or infraclavicular lymphadenopathy, or contractures of the fibrous capsule surrounding the affected implant with associated distortion of the overlying breast shape.12,16 A minimal number of cases have been diagnosed incidentally during an unrelated breast surgery and were asymptomatic or presented with small effusions.16
Differential Diagnosis
Implant rupture must be ruled out in the presence of a large fluid effusion surrounding the implant. Effusions that develop within 1 year of surgery may indicate a postsurgical hematoma or effusion, but periprosthetic fluid collection that
FIGURE. Axial MRI T2-weighted image demonstrating a large fluid collection (red arrows) surrounding an intact right breast implant capsule (blue arrow).
WOMEN’S HEALTH: BREAST IMPLANT-RELATED COMPLICATIONS Breast implant-associated anaplastic large cell lymphoma typically develops approximately 8 to 13 years after the implant is inserted.
has developed more than 1 year after surgery may indicate BIA-ALCL.16 BIA-ALCL can typically be di erentiated from other breast masses based on physical examination and history of breast augmentation surgery. Fibrocystic breast disease may present with multiple bilateral round or rope-like masses that uctuate in size with hormonal stimulation associated with menstrual cycles. Primary breast malignancies tend to present as a hard irregularly shaped mass, nipple retraction, or bloody nipple discharge.
Diagnosis
Initial diagnostic testing could include imaging such as ultrasound or magnetic resonance imaging (MRI) of the a ected breast and ipsilateral axilla to assess for e usion and lymphadenopathy.19 Mammography has not been shown to be superior to ultrasound or MRI.16,19 If uid is found, a ne needle aspiration (>50 mL) should be performed to collect a sample for cytologic pathology.16,19 Likewise, uid can be collected during a capsulectomy procedure. Cells that have invaded the surface of the capsule, breast parenchyma, or regional lymph nodes can be collected for tissue sampling.
On cytology analysis, the cells will appear as large, pleomorphic cells with large nuclei and an increased amount of cytoplasm.9 All ALCL lymphomas, including BIA-ALCL, can usually be distinguished by the presence of “hallmark” cells, which are cells with horseshoe-shaped nuclei.9
A key di erentiating factor between BIA-ALCL and other forms of non-Hodgkin lymphoma is that BIA-ALCL is negative for anaplastic lymphoma kinase (ALK), while most other forms of non-Hodgkin lymphoma are ALK-positive.9 The most common marker for BIA-ALCL is an increased CD30 count, often with CD43 and CD4 elevated as well, which can be noted with immunophenotyping.9 Other markers expressed with BIA-ALCL include T-cell intracellular antigen 1 (TIA-1), granzyme B, and epithelial membrane antigen.20 In addition, BIA-ALCL will not have Reed-Sternberg cells, which are pathognomonic for Hodgkin lymphoma.9
Treatment
Once BIA-ALCL is diagnosed, the recommended treatment is to remove the implant with a total capsulectomy and removal of any associated solid tumors.19 In a total capsulectomy, both the implant and the entire surrounding brous capsule are removed to help prevent reoccurrence or continued symptomatology. Removal of the contralateral implant should also be strongly considered.21 A study by Clemens et al demonstrated that in the absence of a tumor mass, total capsulectomy resulted in complete remission in 93% of cases at 3 years.21
Cases of reoccurrence or metastasis are most commonly related to an incomplete or partial capsulectomy. In uncomplicated cases, surgery is the only treatment indicated. If the disease has metastasized to regional lymph nodes, chemotherapy treatment is warranted in the form of CHOP, which includes cyclophosphamide, doxorubicin, vincristine, and prednisone.17,22 Radiation therapy may also be considered as adjuvant treatment. Total mastectomy is not required as the lymphoma cells do not invade the surrounding breast tissue.23
The Ann Arbor staging system is utilized to predict lymphoma disease prognosis. As BIA-ALCL typically remains contained to the surrounding brous capsule, about 85% of cases are staged as IE.23 About 15% of cases will indicate spread beyond the brous capsule into regional lymph nodes and will be staged as IIE.23 It is very rare for the disease to spread outside of the regional lymph nodes. If the disease is con ned to the capsule and appropriately excised, the 5-year survival rate is approximately 90%.17 An updated staging system for malignant lymphoma based on Lugano classi cation also is available.24
Conclusion
Nurse practitioners and physician assistants working in aesthetic or reconstructive surgical specialties should educate patients
POLL POSITION
Which of the following is not linked to the etiology of BIA-ALCL?
■ Implant with textured outer shell
■ Bacterial infection within the implant ■ Chronic friction related to implant ■ Silicone- lled implant 34%
13% 12%
41%
For more polls, visit ClinicalAdvisor.com/Polls.
Continues on page 32
WOMEN’S HEALTH: BREAST IMPLANT-RELATED COMPLICATIONS Initial diagnostic testing could include imaging such as ultrasound or MRI of the affected breast and ipsilateral axilla to detect effusions.
about BIA-ALCL during presurgical counseling sessions and incorporate this risk into shared decision-making when selecting implant type. The cause of BIA-ALCL appears to be multifactorial; more research should be done to confirm true incidence rates and explore possible pathways of development. It is prudent to continue recommending against textured implants and to investigate any case of breast edema or effusion occurring in relation to implant insertion as the prognosis is most favorable with early and complete surgical intervention. ■
Kristen Grippe, MPAS, PA-C, is an associate professor in the Physician Assistant Department at Gannon University in Erie and works at Spartansburg Medical Center in Spartansburg, Pennsylvania. Elisabeth Duer, MPAS, PA-C, currently works at Rehabilitation and Fitness Consultants, PLLC, and at AdventHealth Altamonte Springs Hospital in Florida.
References
1. Cook JA, Sasor SE, Tholpady SS, Chu MW, Momeni A. Complexity of health news reporting on breast implant‐associated anaplastic large cell lymphoma. Breast J. 2019;25(1):163-165. 2. American Society of Plastic Surgeons. 2019 national plastic surgery statistics. Published 2019. Accessed February 25, 2021.https://www.plasticsurgery. org/news/plastic-surgery-statistics 3. American Society of Plastic Surgeons. 2020 national plastic surgery statistics. Published 2019. Accessed May 3, 2021. https://www.plasticsurgery. org/news/plastic-surgery-statistics 4. Swerdlow SH, Campo E, Pileri S, et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood. 2016;127(20):2375-2390. 5. US Food and Drug Administration. Medical device reports of breast implant-associated anaplastic large cell lymphoma. Published July 24, 2019. Accessed February 25, 2021. https://www.fda.gov/medical-devices/breastimplants/medical-device-reports-breast-implant-associated-anaplastic-largecell-lymphoma 6. Clemens M. BIA-ALCL resources: by the numbers, and what they mean. American Society of Plastic Surgeons. Published February 24, 2020. Accessed February 25, 2021. https://www.plasticsurgery.org/for-medical-professionals/ health-policy/bia-alcl-physician-resources/by-the-numbers 7. US Food and Drug Administration. The FDA requests Allergan voluntarily recall Natrelle BIOCELL textured breast implants and tissue expanders from the market to protect patients: FDA safety communication. Published July 24, 2019. Updated June 1, 2020. Accessed February 25, 2021. https://www.fda. gov/medical-devices/safety-communications/fda-requests-allergan-voluntarilyrecall-natrelle-biocell-textured-breast-implants-and-tissue 8. Collett D, Rakhorst H, Lennox P, Magnusson M, Cooter R, Deva A. Current risk estimate of breast-implant associated anaplastic large cell lymphoma in textured breast implants. Plast Reconstr Surg. 2019;143(Suppl 3):30S-40S. 9. de Leval L. Breast implant-associated anaplastic large cell lymphoma and other rare T-cell lymphomas. Hematol Oncol. 2019;37(Suppl 1):24-29. 10. Turner S, Inghirami G, Miranda R, Kadin M. Cell of origin and immunologic events in the pathogenesis of breast-implant associated large-cell lymphoma. Am J Pathol. 2020;190(1):2-10. 11. Santanelli di Pompeo F, Sorotos M. EURAPS editorial: BIA-ALCL, a brief overview. J Plast Reconstr Aesthet Surg. 2018;71(6):785-787. 12. Ramos-Gallardo G, Cuenca-Pardo J, Rodríguez-Olivares E, et al. Breast implant and anaplastic large cell lymphoma meta-analysis. J Invest Surg. 2017;30(1):56-65. 13. Jones P, Mempin M, Hu H, et al. The functional influence of breast implant outer shell morphology on bacterial attachment and growth. Plast Reconstr Surg. 2018;142(4):837-849. 14. Ghione P, Cordeiro PG, Ni A, et al. Risk of breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) in a cohort of 3546 women prospectively followed after receiving textured breast implants. Hematol Oncol. 2019;37(52):97-98. 15. de Boer M, van Leeuwen FE, Hauptmann M, et al. Breast implants and the risk of anaplastic large-cell lymphoma in the breast. JAMA Oncol. 2018;4(3):335-3341. 16. Quesada A, Medeiros LJ, Clemens MW, Ferrufino-Schmidt MC, PinoOviedo S, Miranda RN. Breast implant-associated anaplastic large-cell lymphoma: a review. Mod Pathol. 2019;32(2):166-188. 17. Clemens M, Jacobsen E, Horwitz S. 2019 NCCN consensus guidelines on the diagnosis and treatment of breast implant-associated anaplastic largecell lymphoma (BIA-ALCL). Aesthet Surg J. 2019;39(Suppl 1):S3-S13. 18. Letter H, Rop B, Edison MN, Turner P. Breast implant-associated anaplastic large cell lymphoma: a case report and literature review. Cureus. 2016;8(3):e546. 19. Kricheldorff J, Fallenberg EM, Solbach C, Gerber-Schäfer C, Rancsó C, von Fritschen U. Breast implant-associated lymphoma. Dtsch Arztebl Int. 2018;115(38):628-635. 20. Dashevsky BZ, Gallagher KM, Grabenstetter A, et al. breast implant‐ associated anaplastic large-cell lymphoma: clinical and imaging findings at a large US cancer center. Breast J. 2019;25(1):69-74. 21. Clemens MW, Medeiros LJ, Butler CE, et al. Complete surgical excision is essential for the management of patients with breast implant-associated anaplastic large-cell lymphoma. J Clin Oncol. 2016;34(2):160-168. 22. Hallquist Viale P. Breast implants and lymphoma: what is the risk for your patient? J Adv Pract Oncol. 2017;8(6):565-567. 23. DePaola NE, Coggins H. Breast implant-associated large-cell lymphoma: what we know. J Adv Pract Oncol. 2019;10(1):54-61. 24. Munakata W, Terauchi T, Maruyama D, Nagai H. Revised staging system for malignant lymphoma based on the Lugano classification. J Clin Oncol. 2019;49(10):895-900.
Alcohol Withdrawal: Individualized Care and Pharmacologic Treatment
More than 50% of patients with alcohol use disorder develop alcohol withdrawal symptoms within hours of discontinuing alcohol use.
© TOMMASO79 / GETTY IMAGES
Alcohol withdrawal occurs within 12 hours of last drink.
Alcohol use disorder (AUD) is a leading risk factor for premature death and disability in the US and worldwide.1,2 In the US, nearly 15 million people aged 12 years and older had AUD in 2019 and excessive alcohol use is responsible for approximately 95,000 deaths per year.1,3
Previously described as separate disorders in the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM-IV), the DSM-5 combines symptoms of both alcohol dependence and alcohol abuse into 1 disorder — AUD — and classi es the disorder as mild, moderate, or severe.2,4,5
Providing individualized care to patients with AUD who seek treatment is challenging. Patients with a history of heavy drinking for a prolonged period who signi cantly reduce their alcohol consumption or abruptly stop drinking can develop alcohol withdrawal syndrome. This typically occurs within 4 to 12 hours of the last drink with symptoms lasting for up to 5 days.2 More than 50% of patients with AUD develop alcohol withdrawal symptoms when discontinuing or decreasing alcohol use.6
Symptoms of alcohol withdrawal range from anxiety, agitation, tremor, insomnia, nausea, and hallucinations to potentially life-threatening seizures and delirium tremens (DTs; Table 1, page 34).2,5-8 In patients with unsuspected or untreated DTs, mortality rates are reported to be up to 37%.6
TABLE 1. DSM-5 Criteria for Alcohol Withdrawal Syndrome5,8
Cessation of or reduction in prolonged, heavy alcohol use
Development of ≥2 of the following symptoms within hours or days of alcohol use cessation or reduction: • Autonomic hyperactivity (sweating or pulse rate >100 bpm) • Increased hand tremor • Insomnia • Nausea or vomiting • Transient visual, tactile, or auditory hallucinations or illusions • Psychomotor agitation • Anxiety • Generalized tonic-clonic seizures
Signs or symptoms above cause clinically significant distress or impairment in social, occupation, or other important areas of functioning
Signs or symptoms above are not attributed to or better explained by another medical condition or mental disorder such as intoxication or withdrawal from another substance
bpm, beats per minute
Pathophysiology of Alcohol Withdrawal Syndrome
The effects of alcohol on the central nervous system are linked to the gamma-aminobutyric acid (GABA)-chloride channel receptor complex.9,10 GABA is the main inhibitory neurotransmitter and glutamate is the primary excitatory neurotransmitter in the brain.10,11 The GABA receptor is a pentameric protein, comprised of 5 subunits – 2 alpha, 2 beta, and 1 gamma (Figure).10 In between the alpha and beta subunits lies the binding site for GABA.9,10 Ethanol readily binds to the receptors on the GABA protein complex because of its high affinity for ethanol.12 As a positive allosteric modulator, alcohol acts as a central nervous system depressant because of its inhibitory effect on N-methyl-D-aspartate (NMDA) receptors leading to sedative and anxiolytic effects.9,11
Alcohol withdrawal causes a significant decrease in GABA levels, which subsequently causes a hyperactive response in the nervous system.11 Withdrawal also causes activation of glutamate, which enhances the function of the NMDA receptors.11,13,14
Detecting Alcohol Withdrawal Syndrome
The American Society of Addiction Medicine (ASAM) recommends universal screening for unhealthy alcohol use in medical settings using validated scales to help identify patients with or at risk for AUD and alcohol withdrawal.8
Some of the screening questionnaires for AUD that can be used in both the inpatient and outpatient setting include the following11,15: • Alcohol Use Disorders Identification Test-Consumption (AUDIT-C) • Cut-Down, Annoyed, Guilty, and Eye-Opener (CAGE) • Munich Alcoholism Test (MALT)
Alcohol dependence should be considered in women who report more than 1 drink daily or more than 7 drinks per week, and in men who average more than 2 drinks daily or more than 14 drinks per week.16,17 Patients’ average daily and/or weekly alcohol intake, history of previous cessation attempts, history of previous alcohol withdrawals, presence of concurrent medical or psychiatric conditions, and concurrent drug abuse should be taken into consideration as clinicians assess for the presence of withdrawal symptoms.17
The Clinical Institute Withdrawal Assessment for Alcoholrevised (CIWA-Ar) is a 10-item assessment tool that can evaluate the presence of withdrawal symptoms, quantify the severity of symptoms, and individualize treatment selection (Table 2).11,18 Each item is evaluated independently, with all components then aggregated to yield a score correlating with the severity of alcohol withdrawal.11 Each component is scored on a scale from 0 to 7, except for orientation and sensorium, which is scored from 0 to 4. In patients who score less than 8, the presence of alcohol withdrawal symptoms is suggested to be absent or minimal. Patients scoring 8 to 20 are noted to be in mild to moderate withdrawal, and those scoring greater than 20 are considered to be experiencing severe withdrawal symptoms. Patients with scores of 10 or less typically do not need pharmacologic treatment.18
alpha subunit beta subunit gamma subunit
Benzodiazepine binding site
GABA binding site CI− channel
extracellular domain
transmembrane domain
GABA binding site
Superior View Lateral View
FIGURE. Subunits of the GABA receptor.10
