Nutritional Status During Inpatient Alcohol Detoxification

Marie-Astrid Gautron; Frank Questel; Michel Lejoyeux; Frank Bellivier; Florence Vorspan

Disclosures

Alcohol Alcohol. 2018;53(1):64-70. 

In This Article

Abstract and Introduction

Abstract

Aims As low rates of thiamine are thought to be implicated in alcohol-related cognitive disorders, we wanted to assess patients with alcohol use disorders (AUD) during detoxification for their nutritional status and test if vitamins blood levels were associated with a surrogate of cognitive impairment.

Methods We performed a retrospective chart review of medical records of 94 consecutive patients hospitalized for alcohol detoxification in a specialized addiction medicine department. Nutritional status was assessed with Body Mass Index (BMI). Vitamins blood levels were available for 80 patients, but thiamine only for 52 patients. The Montreal Cognitive Assessment (MoCA) score was used to screen for cognitive impairment at Day 10 of entry and was available in 59 patients. A binary logistic regression was performed to identify factors associated with MoCA scores below the threshold (26 points).

Results The mean BMI was 23.28 ± 3.78 kg/m2 and 8.79% of weighted patients qualified for malnutrition. The mean MoCA score was 22.75 ± 4.88 points, and 66% of tested patients were below the threshold of suspected cognitive impairment. No low blood thiamine level was found. In multivariate analysis, BMI, but not vitamins blood rates, was significantly associated with a pathological MoCA screening test.

Conclusion Clinical examination is more sensitive than biomarkers to determine malnourished AUD patients who are at-risk for cognitive impairment. Malnourished patients with AUD should receive a full neuropsychological testing.

Summary This retrospective chart review study screened for cognitive disorders during alcohol inpatient detoxification with the MoCA test. Body mass index, but not vitamins blood rates, was associated with a pathological MoCA. Clinical examination is more sensitive than biomarkers to determine malnourished AUD patients who are at-risk for cognitive impairment.

Introduction

The scientific literature reports high rates of dementia in patients with alcohol use disorders (AUD), up to 24% when all types of severe cognitive impairment are considered (Ridley et al., 2013). Previously, two main disorders were described: Wernicke-Korsakoff syndrome (WKS) and alcohol-related dementia (ARD) (Ridley et al., 2013). Now, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders introduces major neurocognitive disorder as an alternative term to dementia, with a subtype related to substance and/or medication use (Sachdev et al., 2014). WKS and ARD could be a direct result of alcohol neurotoxicity, or the consequence of a co-occurring underlying pathology (such as thiamine deficiency) or both (neurotoxicity associated with nutritional deficiencies) (Ridley et al., 2013). Wernicke's encephalopathy (WE), which can lead to WKS, seems to be underdiagnosed, with a higher prevalence of WE lesions in autopsy studies (0.8–2.8%) than predicted in clinical studies (0.04–0.13%) (Sechi and Serra, 2007). But major neurocognitive disorder is now regarded as the emerged part on the iceberg, the final stage of a long lasting continuous process at work in patients with AUD who display several dimensions of cognitive impairment several years before the diagnosis of major neurocognitive disorder (Brion et al., 2014).

Even mild alcohol-related cognitive disorders that do not qualify for a severe neurocognitive disorder diagnosis have an impact on daily functioning and treatment access. Indeed, the behavioral changes in alcohol habits needed to reach and maintain abstinence or low-risk alcohol consumption are more difficult to achieve in individuals with alcohol-related cognitive impairment, and far more difficult in those who qualify for ARD. Patients with ARD display several alterations in cognitive functions, such as a decrease in information processing speed, or dysexecutive syndrome associating flexibility, inhibition, planning, manipulation in working memory and conceptualization alterations (Vabret et al., 2016). ARD is poorly identified and treated, partly because of frequent social isolation suffered by patients with AUD. This is why it seems important to screen and identify those patients as early as possible, for example, if they are hospitalized (Ridley et al., 2013). In order to enhance diagnosis, the classic triad of clinical criteria for Wernicke's encephalopathy (oculomotor abnormalities, cerebellar dysfunction and either altered mental state or mild memory impairment), was modified to include the presence of dietary deficiencies. The clinical diagnosis requires now two signs instead of three (Caine et al., 1997). Several tools are also developed to screen for cognitive impairment in patients with AUD even before a full neuropsychological testing procedure can be performed, such as the Montreal Cognitive Assessment (MoCA) test (Copersino et al., 2009; Alarcon et al., 2015). In patients with Substance Use Disorders, the MoCA is thought to be more sensitive than the MMSE (Folstein et al., 1975) because it has items testing executive functions, especially a short trail making test and a clock drawing test. The main objective of this study was to assess nutritional and cognitive status in patients hospitalized in an addictology-oriented internal medicine ward for alcohol withdrawal. The secondary objective of this study was to determine whether there was a relationship between nutritional status and cognitive impairment in those patients.

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