Dementia

Get a cognitive baseline on the record - More than 20% of patients over 65 arriving for surgery already have cognitive deficits, and the PACU exam is unreadable without knowing what normal looks like for this person. Outside emergencies, run a brief cognitive screening tool — Mini-Cog or MMSE — and document the result. Then get function from the caregiver in concrete terms: does the patient manage their own medications, dress and feed themselves, live alone?

Treat the history as incomplete until a caregiver confirms it - Incomplete and inaccurate histories and medication lists are where dementia bites, and they are how anesthetic considerations get missed. Reconcile the list against a pharmacy record, the facility MAR, or the caregiver before induction rather than accepting what the patient reports.

Reduced anesthetic requirement - Most of these patients are old, and the age effect alone is large: MAC falls about 6% per decade, and geriatric brains are roughly 30% more sensitive to propofol on EEG suppression. Cut the propofol bolus by 40% to 50% (about 1 to 1.75 mg/kg), give it over 30 seconds, and cut the maintenance infusion by 30% to 50%. Etomidate is the induction agent of choice with poor cardiac reserve at a reduced 0.2 mg/kg rather than 0.3 to 0.4. Opioids are more potent and longer-lasting with a blunted hypoxic and hypercarbic drive, so start small and titrate. Lower anesthetic doses are themselves associated with less postoperative delirium.

Emergence runs long - Increased body fat and a larger volume of distribution mean more accumulated lipid-soluble volatile agent to wash out, and reduced hepatic and renal clearance slows everything else. Plan for a slower, later wake-up rather than treating it as a new neurologic event, and know that closing capacity now exceeds FRC, so these patients desaturate faster during any apneic period.

Cholinesterase inhibitors change the block in both directions - Donepezil, rivastigmine, and galantamine inhibit the same cholinesterase that hydrolyzes succinylcholine, so the depolarizing block is prolonged — in a reported case, no twitches at 20 minutes and four twitches with fade only at 50 minutes after a single standard dose. The prolongation is usually under an hour, which still makes succinylcholine a poor choice for a short case. Nondepolarizers have gone the other way: a reported patient broke through 0.6 mg/kg of rocuronium during laryngoscopy and then needed higher-than-expected vecuronium throughout. The literature here is case reports, not trials, so use a twitch monitor and expect either direction rather than predicting one.

Whether to hold the cholinesterase inhibitor - Usually it is continued and the altered blockade simply anticipated. If it is held, that is a preoperative-clinic decision, not a morning-of one: donepezil's half-life is about 70 hours and closer to 100 hours in older patients, and the manufacturer's insert recommends stopping at least 2 weeks before a scheduled operation. There is a reason to lean toward continuing — perioperative rivastigmine reduced postoperative delirium incidence in older patients with cognitive dysfunction in a 2016 study. Memantine is an NMDA antagonist with no cholinesterase activity, so none of this applies to it; it can be continued.

Cholinesterase inhibitors are vagotonic - They suppress sinoatrial activity and can produce sinus bradycardia and any degree of AV block, in patients with and without known conduction disease, and the effect is additive with beta blockers, carvedilol, and diltiazem. Read the preoperative ECG for baseline conduction delay. Symptomatic bradycardia is treated by stopping the agent and giving IV atropine.

Neuromuscular blockade lasts longer than you expect - Neurotransmitter and receptor availability falls with normal aging and falls further in the setting of neurologic disease, which prolongs the duration of most nondepolarizing agents. Favor drugs that do not depend on organ clearance — cisatracurium, atracurium, mivacurium. Confirm full recovery of neuromuscular function before extubation: pharyngeal muscles are already weak and the cough reflex already blunted, so even minimal residual block raises the risk of aspiration pneumonia.

Anticholinergic load is subtracted from a deficit - Cortical acetylcholine is already low in the aging brain and lower still in dementia, which is why the drugs that get reflexively reached for are the wrong ones here. The potentially inappropriate medications anesthesia providers most often give are diphenhydramine, scopolamine, benzodiazepines, metoclopramide, meperidine, and NSAIDs. Skip the scopolamine patch and the diphenhydramine.

Rethink the anxiolytic premed - Benzodiazepines show a marked increase in duration of action in older patients, and the long-acting ones — lorazepam, diazepam — are associated with delirium. Meperidine significantly raises postoperative delirium risk, and ketamine is rarely used in older patients for the same reason. The better premedication is usually a familiar caregiver, an unhurried explanation, and a quiet holding area.

A familiar caregiver is a clinical intervention, not a courtesy - Delirium-prevention programs that work (HELP and its variants) are built on reorientation, family visits, and socialization, and caregiver training in de-escalation — distraction, simple choices, clear single-step instructions — reduces behavioral symptoms. Environmental factors do real work in both directions: sensory over- or under-stimulation and a room that is too hot, cold, or loud all worsen agitation. Keep the caregiver in holding through induction and get them into PACU early.

Glasses and hearing aids stay on as long as possible - Sensory thresholds are already raised by aging, and vision and hearing protocols plus provision of sensory aids are among the measures shown to lower delirium rates. A patient who cannot see or hear the person reorienting them is not being reoriented. Leave the aids in place into the room, and get them back on before the patient wakes.

The pain you will not be told about - Painful conditions are present in at least 49% of patients with dementia, yet only 20% to 40% receive analgesics compared with 60% to 80% of similar patients without dementia — under-reported by the patient and under-recognized by us. Difficulty communicating pain also delays diagnoses, including the acute abdomen. Score it with a validated observational tool, PAINAD or FLACC, instead of asking for a number, and ask the caregiver what this patient's nonverbal pain looks like. Scheduled acetaminophen (maximum 3 g/day in the frail elderly) is a reasonable base layer.

Agitation in PACU is a differential, not a diagnosis - Work through the treatable causes before reaching for a drug: pain, a distended bladder, constipation, hypoventilation, an uncomfortable position, a room that is too loud or too cold. Antipsychotics in dementia carry an increased risk of death (3.5% vs 2.3%, largely cerebrovascular events and infection), so they belong late in the sequence, not first.

Dysphagia and aspiration in advanced disease - Dementia is a recognized adult cause of chronic aspiration: swallowing muscle weakness worsens with neurologic decline, and silent aspiration is the rule rather than the exception. Patients with dysphagia have triple the pneumonia rate and a 2.9% absolute increase in in-hospital mortality, and aspiration pneumonitis carries over 20% mortality in older patients. Ask the caregiver the questions that actually predict it — coughing or choking with meals, thickened liquids, a modified diet, an existing feeding tube — because those answers, not the NPO time, decide whether this is an RSI. A formal speech and swallow study is the study to order when there is time.

Relationship to postoperative delirium and cognitive dysfunction - Pre-existing dementia is the strongest predisposing factor for delirium, and the combination has its own name: delirium superimposed on dementia, reported in 22% to 89% of hospitalized and community-dwelling patients and routinely missed. Part of why it is missed is that hypoactive delirium is the most common form and looks like a quiet, sleepy patient — in one study only 21% of nursing staff recognized it. POCD is separate and slower, affecting about 10% of patients over 60 at three months after noncardiac surgery, with underlying dementia named among its causes. Both have their own entries in this library — see Postoperative Delirium (POD) and Postoperative Cognitive Dysfunction (POCD) rather than re-deriving the prevention bundle here.

Capacity is a snapshot, and someone has to sign - A dementia diagnosis does not by itself remove capacity. Capacity is decision-specific and valid only for the time, place, and situation in which it was assessed — the same patient may be lucid today and unable to participate two weeks from now. The exam that establishes it is the mental status exam: level of consciousness, orientation, attention, short-term memory, insight, and judgment, testing whether the patient can understand the information, appreciate how it applies to them, reason about it, and express a choice. Only a licensed physician, PA, or NP can make and document that determination — it is not a job for nursing or support staff — and it has to be documented, because until it is, treating without consent is neither ethical nor legal. Where capacity is absent, consent goes to the medical durable power of attorney.

Severe neuroleptic sensitivity in Lewy body disease - Severe antipsychotic sensitivity is a defining feature of dementia with Lewy bodies, so the reflex antipsychotic for postoperative agitation is the wrong drug here. In DLB and Parkinson disease dementia, avoid every antipsychotic except quetiapine, pimavanserin, and clozapine — the rest worsen the motor disease. The feared reaction is neuroleptic malignant syndrome (NMS): altered mental status, muscle rigidity, hyperthermia, and autonomic instability developing over one to three days, with mortality of 5% to 20%, most deaths from complications of the rigidity. Treat by stopping the offending agent, cooling and fluid resuscitation, and dantrolene 0.25 to 2 mg/kg IV every 6 to 12 hours (max 10 mg/kg/day) or bromocriptine 2.5 mg PO every 6 to 8 hours (max 40 mg/day), with ICU admission. Delayed treatment leaves residual parkinsonism, catatonia, and renal or cardiopulmonary morbidity.

Antiemetic choice in Lewy body and Parkinson dementia - The same dopamine blockade that makes an antipsychotic dangerous sits in your PONV drawer. Metoclopramide, promethazine, and prochlorperazine are dopamine antagonists that produce extrapyramidal reactions and can precipitate NMS; prochlorperazine is a first-generation antipsychotic in everything but how we think of it. Default to a 5-HT3 antagonist in these patients, and note that any butyrophenone or other antipsychotic used for agitation or nausea falls under the DLB avoid-list above.

Antiparkinsonian dosing schedule - Levodopa/carbidopa runs 300 to 1200 mg daily split across 3 to 12 doses, and the benefit wears off between them. Abrupt withdrawal or dose reduction of levodopa is itself a cause of NMS, as is rapidly switching one Parkinson drug for another. Give the morning dose with a sip of water, hold the home interval through the perioperative period, and restart as early as the airway and gut allow. There is no IV levodopa — if the oral route will be down, the alternatives are the inhaled formulation or nasojejunal infusion. If NMS does develop from withdrawal, treatment is replacing levodopa at the prior doses plus aggressive ICU supportive care. Protein-containing and high-fat meals compete with and delay absorption by up to two hours, so a postoperative diet advance can masquerade as a failed dose.

Autonomic dysfunction and orthostasis - Orthostatic hypotension shows up early in Lewy body dementia and is standard in the Parkinson-plus syndromes, so expect an exaggerated fall on induction and with every position change. Many of these patients are already on fludrocortisone or midodrine for it. Have a vasopressor drawn before induction and move the table slowly.

Fluctuating cognition confounds the delirium exam - DLB brings fluctuating cognition, episodes of diminished responsiveness, and recurrent visual hallucinations that look exactly like postoperative delirium. The distinguishing feature is onset — Lewy body fluctuations come on gradually, delirium abruptly. Establish the baseline from the caregiver preoperatively: what this patient's ordinary attention, hallucinations, and responsiveness look like on a normal day. Without that, the PACU exam is unreadable.

Vascular dementia flags the arteries - The diagnosis means established cerebrovascular and atherosclerotic disease with hypertension, diabetes, hyperlipidemia, and smoking behind it, and cardiovascular death is the common endpoint. Read a baseline ECG for atrial fibrillation and prior infarct, and pull the existing head CT or MRI for stroke burden and carotid disease — these patients have usually already been imaged. Coexisting coronary artery disease, atrial fibrillation, and ischemic heart disease drive the intraoperative plan more than the cognitive impairment does.

Antithrombotics in vascular dementia - Secondary prevention in vascular dementia means antiplatelet agents, warfarin, or a prior carotid endarterectomy, so assume the patient is on something and confirm the agent and last dose. ⚠ Neuraxial timing intervals for antiplatelet and anticoagulant therapy are not resolved in this entry — check current ASRA guidance against the specific drug rather than working from a remembered interval.

Blood pressure target - Hypertension is the one risk factor that matters most in vascular dementia, and it is usually long-standing and treated. ⚠ No perioperative numeric pressure target for this population is established in the grounding sources — use the patient's own preoperative baseline as the reference and avoid the swings rather than chasing a fixed MAP number.

Frontotemporal dementia - FTD is the most common dementia under 60, so don't discount cognitive impairment in a 55-year-old. Behavioral disinhibition and loss of social decorum make cooperation with an awake or regional technique, and with holding-area instructions, unpredictable. Dysphagia is common and drives the pneumonia and respiratory failure that kill these patients. Ask specifically about an overlapping motor neuron disease syndrome (FTD-MND): lower motor neuron disease makes succinylcholine a hyperkalemia risk, prolongs and destabilizes the response to nondepolarizers, and adds bulbar aspiration risk on top.

Relationship to POD and POCD - Dementia is one of the named predisposing factors for delirium alongside age over 70, with medications, acute illness, and infection as the usual precipitants. When delirium lands on top of dementia — delirium superimposed on dementia, DSD — it buys a longer stay, accelerated cognitive and functional decline, higher cost, and increased mortality. Both have their own entries in this library: see Postoperative Delirium (POD) and Postoperative Cognitive Dysfunction (POCD) rather than re-deriving the prevention bundle here.

Prefer glycopyrrolate over atropine or scopolamine - Older patients are more vulnerable to anticholinergic effects because of changes in metabolism, excretion, and the CNS itself. Glycopyrrolate's quaternary ammonium group keeps it out of the brain; atropine and scopolamine are tertiary amines that cross lipid barriers easily. Scopolamine specifically raises the risk of central anticholinergic syndrome, so skip the PONV patch in a demented patient and reach for glycopyrrolate when you need an antisialagogue or a reversal partner.

Capacity, and who signs - A dementia diagnosis does not by itself remove capacity. Capacity is decision-specific and can fluctuate within a single day, so assess it at the moment of consent against the four elements: the patient understands the situation, appreciates the consequences, reasons consistently with their own stated values, and can communicate a choice. Capacity is not competence — competence is a judge's ruling, and a patient ruled incompetent may still retain capacity for a given medical decision. If capacity is absent, the healthcare surrogate (healthcare power of attorney or proxy) holds exactly the authority the patient would have had; where none was designated, state law sets the order, commonly legal guardian, spouse, adult child, then parent. Pull the advance directive and any POLST/MOLST or DNR order before the case — those are active medical orders, and perioperative suspension has to be discussed explicitly, not assumed.

Dementia — major neurocognitive disorder in DSM-5 — is an acquired, persistent, progressive decline in one or more cognitive domains: memory and learning, complex attention, executive function, language, perceptual-motor, and social cognition. The decline has to represent a change from the patient's own prior level and has to cost them function, first the instrumental activities of daily living (managing money, managing medications) and later basic ones (grooming, feeding). It is not diagnosed on the basis of an episode of delirium alone. Patients frequently have little or no insight into their deficits, and no cause of dementia currently has a cure.

It is a syndrome, not a disease, and one patient can carry more than one cause. Alzheimer disease is by far the most common, at roughly 70% to 80% of cases; vascular dementia accounts for about 15%, Parkinson disease dementia about 10%, and Lewy body dementia about 5%. Prevalence rises steeply with age — dementia is rarely diagnosed before 65, but around 60% of people are affected by age 90.

What the anesthesia provider inherits is shared across every subtype: a brain with reduced neuronal and neurotransmitter reserve — cortical acetylcholine falls the most — inside a body that is usually old. That combination produces a lower anesthetic requirement, prolonged drug effect, a low threshold for postoperative delirium, an unreliable history and medication list, and a patient who often cannot tell you they are in pain.

Dementia is a syndrome, not a single disease, and the subtype changes the anesthetic. Vascular dementia is second only to Alzheimer disease and accounts for roughly 15% to 17% of dementia syndromes. It comes from ischemic injury to the brain and shares its risk factors with atherosclerosis — hypertension, diabetes, hyperlipidemia, smoking — so these patients carry coexisting atherosclerotic disease, and death from cardiovascular causes is common.

Lewy body dementia covers two entities: dementia with Lewy bodies (DLB) and Parkinson disease dementia (PDD), separated by an arbitrary 12-month rule — parkinsonism present a year or more before cognitive decline is PDD, a shorter interval is DLB. Both are alpha-synuclein disorders marked by intraneuronal Lewy body inclusions. The acetylcholine deficit is more pronounced than in Alzheimer disease and dopamine falls as well. The clinical picture is fluctuating cognition with episodes of diminished responsiveness, recurrent visual hallucinations, delusions, parkinsonian rigidity and bradykinesia, REM sleep behavior disorder, autonomic dysfunction with early orthostatic hypotension, unexplained falls, and sensitivity to antipsychotic medication.

Frontotemporal dementia (FTD, Pick disease) is the most common dementia in patients under 60. It presents either as a behavioral variant with disinhibition and loss of social decorum or as primary progressive aphasia, and it overlaps with motor neuron disease, progressive supranuclear palsy, and corticobasal syndrome. Dysphagia drives the pneumonia and respiratory failure that are a significant cause of death.

Mixed dementia is common enough that a clean subtype label often is not available — vascular pathology coexists with Alzheimer pathology, and the vascular diagnosis itself is acknowledged to be imprecise. When the chart says only "dementia," plan for the features of more than one.