Program for Positive Aging, Department of Psychiatry and Behavioral Sciences, University of California Davis, Sacramento, CA; Department of Psychiatry, University of Michigan, Ann Arbor, MI.
College of Nursing and Health Professions, Drexel University, Philadelphia, PA.
J Am Med Dir Assoc. 2019 Sep;20(9):1074-1079. doi: 10.1016/j.jamda.2019.05.022. Epub 2019 Aug 6.
Antipsychotic reductions have been the primary focus of efforts to improve dementia care in nursing homes by the Centers for Medicare & Medicaid Services National Partnership. Although significant antipsychotic reductions have been achieved, this policy focus is myopic in 2 ways; there is no evidence for any increases in use of nonpharmacologic interventions, and there are indications for compensatory increases in the use of other (unmeasured) sedating psychotropics. This increased use of other sedating psychotropics is more concerning than the antipsychotics that they replaced, as there is even less support of efficacy for behavioral and psychological symptoms of dementia (BPSD) and ample proof of harms, including mortality. The current paradigm of "assessment" and "treatment" for BPSD is largely cursory and reflexive, with little effort put forth to understand possible underlying causes. This contrasts with the methodical, evidence-based way the field handles other symptoms considered "medical" (eg, shortness of breath). To move beyond this nonmedical approach to BPSD, we suggest a conceptual model that includes putative causal contributors. Although at their core BPSD are caused by brain circuitry disruptions, such disruptions are theorized to increase the person with dementia's vulnerability to 3 categories of triggers: those related to the (1) patient (eg, pain, hunger, and infection), (2) caregivers (eg, competing priorities, unrealistic expectations, and negative communications), and (3) environment (eg, overstimulation and limited light exposure). Assessing modifiable triggers is inherently person-centered as it enables clinicians to select specific nonpharmacologic strategies to mitigate identified triggers. Assessing triggers and selecting strategies, however, is time-intensive and reflects a paradigm shift necessitating a reorganization of dementia care including compensation for time spent elucidating and addressing modifiable triggers, vs unintendedly incentivizing the use of potentially harmful psychotropics. This paradigm shift should also include the measurement and restriction of any sedating medications for BPSD, particularly without assessment of underlying causes.
抗精神病药物的减少一直是医疗保险和医疗补助服务中心国家伙伴关系努力改善疗养院痴呆症护理的主要重点。尽管已经取得了显著的抗精神病药物减少，但这种政策重点在两个方面是狭隘的；没有证据表明非药物干预措施的使用增加，而且有迹象表明其他（未测量的）镇静性精神药物的使用增加。这种其他镇静性精神药物的使用增加比它们所替代的抗精神病药物更令人担忧，因为几乎没有支持痴呆症行为和心理症状（BPSD）的疗效证据，并且有充分的证据表明存在危害，包括死亡率。目前，BPSD 的“评估”和“治疗”范式在很大程度上是草率和反射性的，几乎没有努力去理解可能的潜在原因。这与该领域处理其他被认为是“医学”的症状（例如，呼吸急促）的有条不紊、基于证据的方法形成鲜明对比。为了超越这种非医学方法治疗 BPSD，我们建议采用一种包含假设因果因素的概念模型。尽管 BPSD 的核心是由大脑电路中断引起的，但这些中断被认为会增加痴呆症患者对以下 3 类触发因素的脆弱性：与（1）患者相关的触发因素（例如，疼痛、饥饿和感染）、（2）护理人员相关的触发因素（例如，优先级冲突、不切实际的期望和负面沟通）和（3）环境相关的触发因素（例如，过度刺激和光照不足）。评估可修改的触发因素本质上是以患者为中心的，因为它使临床医生能够选择特定的非药物策略来减轻已确定的触发因素。然而，评估触发因素和选择策略是一项耗时的工作，反映了范式转变，需要重新组织痴呆症护理，包括补偿花在阐明和解决可修改触发因素上的时间，而不是无意中鼓励使用可能有害的精神药物。这种范式转变还应包括测量和限制任何用于 BPSD 的镇静药物，特别是在没有评估潜在原因的情况下。
