Karl E. Misulis, MD, PhD
CHAPTER CONTENTS
•Acute and Subacute Cognitive Disorders
◦First Recognition of Dementia During Hospitalization
◦Hospitalization of the Patient with Dementia
◦Dementia with Lewy Bodies and Parkinson Disease with Dementia
OVERVIEW
Dementia is usually evaluated and managed in the outpatient arena, but hospital-based neurologists often deal with patients with dementia. These may be either patients with dementia whose condition is exacerbated by concurrent illness and hospitalization, or patients with hospital-acquired delirium in whom there is a suspicion of dementia. Patients with dementia are less likely to return to home care following hospitalization.
ACUTE AND SUBACUTE COGNITIVE DISORDERS
Delirium
The differential diagnosis and presentation of delirium in the hospital setting were discussed in Chapter 5. This discussion of the management of hospitalized patients with dementia overlaps that of Chapter 5. Patients more likely to develop delirium in the hospital are those with advanced age, dementia, and sensory deprivation (visual/hearing loss). Patients are also predisposed by sleep deprivation in the hospital caused by the disturbances of ongoing care (medications, presence of equipment and lines).
PRESENTATION is with acute to subacute cognitive change that can be hyperactive or hypoactive.
DIAGNOSIS is suspected when a patient develops confusion, agitation, or lethargy. Brain imaging for stroke, edema, or other structural etiology is often appropriate. Labs should include examination for increased WBC, for urinary tract infection (UTI), and for metabolic disorders including renal, hepatic, and perhaps thyroid dysfunction. If there is concern over a malnourished or an alcoholic state, then studies should include thiamine levels; on suspicion, we consider giving thiamine without laboratory or historical confirmation.
MANAGEMENT is difficult. We try to avoid sedative-hypnotics if possible. Nonpharmacological therapy can include sitters, minimizing interventions at night to maintain sleep, and a quiet environment. Some patients are reassured by a few personal items from home, such as pictures.
Metabolic Encephalopathy
Metabolic encephalopathy is commonly encountered in hospital neurology practice. This was discussed in Chapter 5, but is detailed further here.
PRESENTATION is usually with confusion or lethargy, but delirium with agitation can occur. Focal findings are not expected and would point to a pre-existing lesion or another acute diagnosis.
DIAGNOSIS is established by absence of other causes and identification of responsible cause(s); we usually find metabolic encephalopathies to be multifactorial. Imaging is needed, magnetic resonance imaging (MRI) of the brain is preferable to computed tomography. Electroencephalogram (EEG) shows diffuse slowing, often with a polymorphic appearance. CSF analysis may be needed if there are inflammatory markers or seizures. Among the causes we often identify are:
•Renal insufficiency: New or worsening
•Hepatic failure: New or worsening
•Sepsis/Systemic inflammatory response syndrome (SIRS)
•Medication (e.g., cefepime); or altered metabolism increasing levels of an old medication (e.g., phenytoin with renal failure)
•Withdrawal state, from substance which was stopped or reduced (e.g. benzodiazepine, ethanol)
MANAGEMENT is by correction of the defects, if possible. Withdrawal of any offending medications is recommended if possible.
Transient Global Amnesia
Transient global amnesia (TGA) is the acute onset of short-term memory difficulty without other findings. Cause is uncertain but may be related to migraine or vascular disease; there may be multiple causes for the same presentation.
PRESENTATION is with acute onset of memory loss from the onset forward; in other words, antegrade. Patients are often aware of the deficit and anxious because of it. They may function relatively normally during the event (e.g., driving without incident). Exam is otherwise normal.
DIAGNOSIS is suspected when a patient presents with acute memory loss and the absence of encephalopathy or focal signs. The awareness and anxiety suggests TGA rather than psychogenic amnesia. The otherwise normal demeanor and cognitive function in other areas differentiates TGA from toxic, metabolic, and infectious encephalopathies. Imaging with MRI is preferential to CT and is usually normal, but occasionally there is restricted diffusion in the hippocampus on one or both sides. EEG is normal or shows mild nonspecific slowing, but there have been reports of epileptiform discharges; we believe this is rare, and TGA is typically not a seizure.
MANAGEMENT is supportive. The symptoms resolve within hours, usually less than 12 but almost always less than 24 hours. If vascular risk factors are identified during the evaluation, these are addressed even though the link to the presentation is uncertain.
Syncope
Syncope was discussed in Chapter 5 regarding differential diagnosis, which is expansive. Here, we discuss a few selected syncopal disorders seen in hospital practice. Syncope can be recurrent and lead to serious injury, so we advise patients with syncope that if they feel presyncopal to lower their head to the floor; we have seen multiple patients with damage or death due to injury from syncope.
Neurocardiogenic syncope: Also called vasovagal syncope, is drop in blood pressure usually triggered by an event such as fright or a bowel movement. If recurrent, avoiding precipitating events may help. If autonomic insufficiency is suspected, this should be evaluated with autonomic testing.
Cough syncope: This condition presents with syncope precipitated by coughing fits, most commonly seen in patients with COPD. Association with cough might not be recognized by the patient and should be asked about. Clonic activity is common and raises the concern for seizures. Treatment is focused on the cough.
Micturition syncope: Micturition causes hypotension, particularly when standing, resulting in syncope. Patients usually are aware of the trigger and learn to sit while urinating.
CHRONIC COGNITIVE DISORDERS
First Recognition of Dementia During Hospitalization
Patients with dementia have an increased incidence of hospital-acquired delirium, so it is expected that a significant proportion of patients with delirium have historical evidence to suggest pre-existing incipient dementia or mild cognitive impairment.
DIAGNOSIS of dementia is similar to that in the outpatient arena, with brain imaging (MRI is preferable to CT) and basic labs including thyroid function tests, B12 level, and other studies as indicated. EEG is usually not needed, but hospitalized patients with prominent mental status change should have EEG performed to look for nonconvulsive seizure activity. Lumbar puncture (LP) should be considered when the patient has a subacute or acute change in mental status that is not explained by labs or imaging findings.
Neuropsychological testing is commonly performed in the outpatient arena, but this is not best performed when the patient is confused in the hospital. It is better to perform the neuropsychological testing as an outpatient, after the patient has improved to a baseline. Unfortunately, many patients with delirium have residual cognitive impairment after the illness.1–2
Hospitalization of the Patient with Dementia
Patients with dementia are hospitalized at a greater rate than are people without dementia of similar age. This is likely due to comorbid conditions that predispose to dementia including hypertension, diabetes, obesity, congestive heart failure, and other concurrent disorders. Potential for exacerbation of dementia and hospitalization psychosis should be anticipated and prepared for.
Patients with a baseline Mini-Mental State Exam (MMSE) score of 24 or less have the greatest risk for development of delirium in the hospital, which suggests early dementia is the major risk factor.3
The prescription of sedative-hypnotics should be avoided if possible, and management should rely on nonpharmacological therapy where possible. Unfortunately, although the literature is replete with opinions that neuroleptics and related agents are never needed, this is not the case. While these agents are certainly overused, judicious use when other nonpharmacological measures have failed is appropriate. Haloperidol (especially IM) and lorazepam are both effective, but it is not clear that the combination works better than either alone. Oral haloperidol carries a high risk of extrapyramidal reactions and parkinsonism in elderly patients, and lorazepam can exacerbate confusion. Newer, atypical antipsychotic agents such as quetiapine and olanzapine are often used, especially in nighttime doses.
Alzheimer Disease
Alzheimer disease (AD) is the most common dementia, responsible for at least half of cases. Vascular risk factors predispose to AD. These include obesity, diabetes, hypertension, hyperlipidemia, atrial fibrillation, obstructive sleep apnea, and stroke. This blurs the distinction between AD and vascular dementia.
PRESENTATION begins with memory loss, confusion, and judgment errors. Noncognitive deficits are not expected early in the disease. With advanced AD, ambulation, continence, and swallowing are affected.
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