July 23, 2019

Home Sweet Nursing Home

Every year, about one-quarter of the 1.4 million American nursing home residents are hospitalized. Most of them survive the experience and go back to the same nursing home from whence they came. But like their community-dwelling counterparts, they often suffer from one or more adverse events after discharge, despite the documentation that is supposed to travel with them from the hospital to the nursing home, and despite the nursing staff that cares for them on their return and the physicians who attend to them shortly after their arrival. How often do they experience such adverse events? How serious are they? And can they be prevented? A new study in JAMA Internal Medicine attempts to provide the answers.

To analyze what happens when nursing home residents travel from the hospital back to their nursing home of origin, the authors of the study sampled 32 nursing homes from the 762-member New England Nursing Home Quality Collaborative. They identified all residents who made the nursing home-to-hospital-and back-journey over a nearly two-year period ending on December 31, 2017. They hired and trained nurse reviewers to study the records of these patients and, after further physician review, came up with 379 adverse events.

Classifying these episodes on a four-part scale ranging from not serious to fatal, they found that fully 38 percent were serious, another 7 percent were life-threatening, and 2 percent proved fatal. In terms of the type of episode, over half (52 percent) were related to “resident care,” i.e. involved a pressure ulcer, skin tear, or fall. The biggest chunk were due to heath care acquired infections (29 percent), with medication-related episodes accounting for 17 percent. In the judgment of the physician reviewers, fully 70 percent were either preventable or ameliorable.

What’s going on here? Why did so many long-term care residents suffer an adverse event after hospitalization? Clearly, this is a very vulnerable population. The patients tend to be very old and very frail, otherwise they wouldn’t live in a nursing home. That means they are particularly susceptible to common health care acquired infections such as c. difficile. Often weak before their hospitalization, they are typically weaker—and at greater risk of falling and of skin tears—after being ill, with associated immobility and poor nutrition. Is there a fix? Are many of these events truly preventable or at least ameliorable?

Most likely, improving this sad situation will require additional effort by both hospital and nursing home personnel. At the hospital level, early mobilization is essential, as is adequate attention to nutrition. Avoiding high risk medications, whether those predisposing to c diff or those apt to trigger delirium, is of utmost importance. At the nursing home level, assuming that whatever-worked-before-will-work again is probably the major impediment to change. Simply re-instituting the previous regimen—the same diet and the same degree of independent ambulation—or mindlessly accepting the new medication list sent over from the hospital predisposes to problems. 

As is so common in geriatrics, we may know what to do but don't make the effort to do it. To incentivize the relevant staff to do what’s necessary, we may need to design a system in which facilities are paid extra to go the extra mile. Maybe nursing homes that take their residents back from the hospital without an intervening skilled nursing facility (“rehab”) stay should be paid extra for the days they should be functioning more like a short stay SNF. Maybe Medicare payments to hospitals should be adjusted to account for frailty, with hospitals whose nursing home patients do well after discharge getting a bonus for outstanding care. Perhaps hospitals and nursing homes need to take shared responsibility for the welfare of long-term care residents, using a shared electronic medical record system, “warm” hand-offs, and even shared staff. If we really want to improve a manifestly improvable system, maybe we should do all the above.

July 01, 2019

The Dirt on Drugs

Several months ago, in writing about Katy Butler’s generally admirable new book, The Art of Dying Well,I questioned her uncritical acceptance of claims that certain drugs, the anticholinergics, caused dementia. That drugs such as antihistamines and some antidepressants cause delirium, or acute confusion, is well-established. But dementia? A large, well-conceived study just published in JAMA Internal Medicine provides additional evidence that they may well result in dementia. Previous studies were tainted because they tended to be small, observational studies that lumped many different anticholinergic drugs together, some of which are known to be far more potent than others. So how does the new study fare by comparison?
The recent analysis is still an observational study—it is impossible to randomize patients into those who receive anticholinergics and those who do not and then follow them for years—but it is very large, it analyzes different classes of anticholinergics separately, and it focuses on the cumulative anticholinergic exposure over a period of many years. While not perfect, it is probably the best we are going to get and it provides strong, although not definitive, evidence that anticholinergics are a risk factor for dementia.
This “nested case control study” allowed the authors to identify just under 59,000 people over age 55 with dementia from a British data base of 30 million. For each case, they found 5 controls matched along four discrete dimensions. The main variable of interest was the total, cumulative anticholinergic exposure which they calculated according to a well-established protocol that allows standardization across drugs with different dosage regimens. The authors also decided in advance to study the association between the total standardized daily dose (TSDD) for each type of anticholinergic: antihistamines, antidepressants, antipsychotics, antiparkinsonian drugs were considered both separately and collectively. Finally, the study repeated the analysis for patients diagnosed with Alzheimer’s disease, those diagnosed with vascular dementia, and those with some other form of dementia. So what did they find?
The main finding was that the adjusted odds ratio associated with low anticholinergic exposure was 1.06, while the ratio associated with the highest degree of anticholinergic exposure was 1.49, a highly significant difference. Also interesting was the observation that only certain groups of anticholinergics increased the risk of developing dementia. In particular, antidepressants, antipsychotics, antiepileptics, and drugs used to treat Parkinson’s and incontinence were the main offenders (and antihistamines, which geriatric physicians inveigh against as potential causes of delirium, had no effect). Curiously, the effects were more dramatic in patients with vascular dementia than in those with Alzheimer’s disease, a novel finding. Finally, the strongest association was found in people diagnosed before age 80.
As the authors are quick to point out, associations do not demonstrate causality. They can’t. Researchers simply cannot exclude the possibility that some of the drug use in fact reflected early, preclinical effects of as yet undiagnosed dementia. For example, many people with dementia are depressed; it is entirely possible that the depression manifests itself before a formal diagnosis is made, at a time when patients are beginning to detect subtle but disturbing changes in their memory and problem-solving ability. But if anticholinergics are causative, then they may well be responsible for as much as 10 percent of all dementia. The evidence is sufficiently suggestive and the magnitude of the danger sufficiently great that it’s time to be very wary of these drugs, especially in people under age 80.