DEMENTIA: ACETYLCHOLINESTERASE INHIBITORS 225 HOW TO Treat with acetylcholinesterase inhibitors Introducing and monitoring acetylcholinesterase inhibitors is a specialist area, usually un dertaken by psychogeriatric teams, or by geriatricians or neurologists working in the setti ng of a memory clinic. In general, acetylcholinesterase inhibitors should not be initiated in inpatient medical or rehabilitation settings, as the effects of environ- mental changes, physical illness or dr ugs may dominate those of the acetylcholinesterase inhibitor, rendering assessment of effec t impossible. It is preferable to initiate treatment when the patient is physically well an d living in their own home. Where given for behavioral disturbance or non-cognitive symptoms (eg hallucinations), acety lcholinesterase inhibitors may be initiated more urgently in an institutional setting. Before treatment \200 Consider the relative risks and bene \201 ts and discuss them with patient and carer Explain that the drugs do not provide a cure, and may reasonably be deferred until symptoms worsen Consider how concordance can be assured \200 Check for relative contraindications, eg bra dycardia or heart block Treatment trial \200 There are signi \201 cant side effects, com monly gastrointestinal (nausea, dyspepsia, diarrhea, anorexia). These occur especially duri ng the dose titration phase at higher doses, are often short lived \200 An acetylcholines terase inhibitor should be given for an initial treatment period of 2 \200\2233 months. If there is no effect at maximum tolerated dose, th e drug should be discontinued. There is probably little bene \201 t from trying other acet ylcholinesterase inhibitors if one has failed Assess impact using \200 Clinician \200\231s subjective global assessment, based on the v iews of relative(s) or carer(s) and serial clinical observations The results of cognitive tests, eg MMSE, clock-drawing test Continuing therapy \200 If be ne \201 t appears to have occurred, the drug should be continued at that dose. Bene \201 t may be absolute, or relative: a small decline would be expected during the 2 \200\2233-mo nth evaluation period, so an absence of deterioration may be attributed to drug bene \201 t Acetylcholinesterase inhibitors can be given inde \201 nitely, but can be withdrawn period ically (18 months) to determine whether bene \201 t continues. If the patient deteriorates promptly after drug withdrawal (within weeks, thus probably secondary to drug withdrawal r ather than disease progression), acetylcholinesterase inhibitors are restarted. The evidenc e for acetylcholinesterase inhibitors in advanced dementia is weak, and they are generally withdrawn at this point As more patients are given an acetylcholinesterase inhibitor at an earlier stage of disease , monitoring may fall more to primary care 226 CHAPTER 9 Psychiatry Dementia: other drug treatments Memantine \200 This is a blocker of N -methyl- D -asparta te (NMDA) receptors that may reduce glutamate-mediated destruction of cholinergic neurons It appears to have a bene \201 cial effect in severe dementia of Alzheimer \200\231s or vascular etiology and may be used in those with behavioral disturbance Recommended by NICE for moderate Alzheimer \200\231s where the patient cannot tolerate acet ylcholinesterase inhibitors, and in severe disease \200 It is well tolerated. Uncommon si de effects include hallucinations and worsening confusion Avoid in severe renal failure \200 Memantine enhances the effect of levodopa and dopamine agonists Other drugs to prevent progression No drugs have been proven to slow or halt progression, a lthough dementia is seen as so catastrophic, the following are often used: \200 Vascular secondary prevention : eg aspirin, lipid-lowering drugs, ACE- inhibitors and other antihype rtensives. For patients with vascular dementia and mixed (Alzheimer \200\231s \200\223vascu lar) dementia, aggressive risk factor modi \201 cation and tailored drug treatment akin to that following stroke is logical but is without evidence. There is better evidence for pri mary prevention, eg in those with hypertension Vitamin E . High doses (eg 400 \200\223800IU bd) are widely used by patients, and have been supported by some doctors, but recent evidence is much less convincing than earlier studie s of an effect in either primary prevention or on slowing of progression. In conjunction wi th recent evidence suggesting no bene \201 t in cardiovascular disease, high-dose vitamin E supplementation cannot be recommended Ginkgo biloba . A supplement widely used by people with memory impairment or dementia to en hance memory and other cognitive functions, but not convincingly supported by trial evidenc e. Preparations are expensive, vary in strength, and have antiplatelet activity \200\224 c aution with anticoagulants DEMENTIA: OTHER DRUG TREATMENTS 227 HOW TO Manage patients with dementia in hospital 2Beware iatrogenic deterioration. Mo dest behavioral deterioration in a patient with moderate dementia at home may lead to hospi tal admission, with a loss of all familiar routine, physical environment, and caregivers. T hus further behavioral decline, administration of sedatives, and further worsened confusion . Over a fourth of UK hospital beds house patients with dementia. Patients with dementia stay in hospital longer than patients with similar problems but without cognitive impairment an d often leave hospital in a worse physical and mental state than when they arrived. \200 Where appropriate, manage the patient at home, with a brief but thorough outpatient attenda nce if there is concern about physical precipitants. Community outreach may be available to help avoid unnecessary admissions If hospital admission is required then if possible admit them directly to a ward with experience managing patients with cognitive impairment Try to minimize disorientation by: Avoiding admission and ward moves at night \200 Avoiding multiple changes of location/war d \200 Quiet room with window (so daylight seen) \200 Minimal distractions (eg turn off background radio/TV) \200 Visible clocks and calendars \200 Well labeled facilities, e g toilets \200\224 images often better \200 Regular ward routine \200 Restricting fami ly visiting unnecessarily Actively ascertain and treat symptoms such as pain or shortness of breath which patients may not spontaneously describe Good nursing management of hydration, nutrition, continence (avoid constipation), pressure areas, falls prevention Where psychoactive medication is required use it sparingly for short courses. Remember that sedation is a side effect and NOT the desired outcome (which is beha vior modi \201 cation) Take time to communicate with the patient and their relatives \200 Minimize the length of admission with proactive early discharge planning Further reading Alzheimer \200\231s Society . Counting the cost: caring for people with dem entia. Online: M http:// alzheimers.org.uk . 228 CHAPTER 9 Psychiatry Dementia: managing behavioral problems Behavioral problems include agitation, anxiety, phob ias, irritability, wan- dering, hoarding, aggression, socially inappropriate behavior (eg s exual disinhibition, inappropriate urination, attention-seeking), hallucinations, and delus ions. These are common in dementia, including Alzheimer \200\231s, and may occur early in the dis ease. Often it is behavioral problems rather than cognitive impairment that lead to institu tionalization; managing them successfully may enable a patient to remain in their own home. General \200 Consider whether acute illness (eg sepsis), pain (eg urinary retention), or changes in drug treatment (eg anticholinergics) have contributed, especially if behavior ha s deteriorated rapidly Consider whether agitation or aggression is a manifestation of depression (consider an SSRI) or of fear (which may respond if care is given in a non-chall enging way by a familiar team) Medication may not be needed if symptoms are transient, do not cause the patient signi \201 cant distress, and are not threatening care of the patient in the current environment Non-drug management These are preferred, and may alone be suf \201 cient \200 Avoid prec ipitants \200 Effective therapies include music, bathing, exercise, pets, art therapy, aromatherapy, etc. The environment should be home-like, familiar and interesting \200 Activities may reduce boredom, wandering, and aggression \200 Delusions and hallucinations may be helped by dis traction and reassurance Anxiety may respond to relaxation, or a discussion of worries \200 The psychogeriatric te am will be able to offer helpful advice Drug treatment The best drug is that which, for that patient with that problem, has worked well previously. For agitation , anxiety , and irritability : Benzodiazepines, eg lorazepam, are often successful but long-term treatment should be avoid ed due to side effects and dependence If depression is prominent, try an SSRI such as citalopram \200 If this fails, or side ef fects (usually oversedation) occur, introduce an atypical antipsychotic such as quetiapine, but be aware that atypical antipsychotics eg quetiapine should be avoided \200\224if consi dered necessary use lowest dose for shortest period possible. Risperidone and olanzapine ar e now rarely recommended because of the increased risk of stroke, IHD, and death Haloperidol and phenothiazines are slow acting and have many side effects so should be avoi ded in the absence of psychotic symptoms Memantine can be used with good effect in extreme agitation DEMENTIA: MANAGING behavioral PROBLEMS 229 For problematic psychotic symptoms (delusions, hallucinations, paranoia): \200 Cholineste rase inhibitors may improve behavior as well as cognition. They have few side effects, and may be given \200\230 \201 rst-line \200\231, especially if symptoms are moderate and not acute in onset Atypical antipsychotics, eg quetiapine should be used at the lowest dose that is effective Trazodone, an antidepressant, may be useful especially where sleep disturbance is a problem and aggression is only verbal In dementia with Lewy bodies, use antipsychotics with great caution, in low dose, under clo se supervision, and only when other non- pharmacological and pharmacological measures have been exhausted. Atypical antipsychotics are preferred Review drug use regularly, being aware of potential side effects such as falls, immobility, or confusion. Behavioral problems are often periodic, so con- sider trials off treatment, especially in those whose behavioral disturbance was not severe and has responded to treatm ent. 230 CHAPTER 9 Psychiatry Compulsory detention and treatment Older people in need of medical assessment, treatment, o r continuing care commonly lack the capacity to judge the risk and bene \201 t of interven - tions. They may therefore refuse care when its bene \201 t is clear to others. In the UK, there are several legal procedures which may support a doctor in the compulsory treatment, admission, or detention of patients. Mental Capacity Act (2005) The most commonly used legal support for actions when the patien t lacks capacity to make a certain decision (see b \200\230The Mental Capacity Act 2005 \200\231, p.656). Actions may include: \200 Admission to hospital \200 Treatment and de tention on a ward or within a hospital \200 Treatment in the home (eg in delirium seconda ry to infection, but refusing antibiotics) Detention in the home (eg wandering presents danger to the patient) Actions should be: Justi \201 able, reasonable, and proportionate to the situation. Based on a consideration of the risks/bene \201 ts for that patient, and their likely wishes were they competent. C onsider alternatives and always opt for the least restrictive ( see b \200\230Deprivation of Liberty Safeguards \200\231, p.657) Carefully documented and reviewed regularly Section 5 (2) of the Mental Health Act (1983) \200 This permits the detention of an inpat ient in a general or psychiatric hospital for up to 72hr after submission of a report, while their mental health needs are a ssessed. Outpatients or DH patients do not fall within this section It should be considered if a patient is highly resistive to treatment or restraint, formalizing actions taken under common law It is sensible to seek the advice of a psychogeriatrician to con \201 rm that it is approp riate, and during the 72-hr period to perform assessment and help guide further management Detention is authorized when the registered medical practitioner in charge of treatment or a fully registered deputy (ie consultant or fully registered juni or doctor; not pre-registration junior) completes a report ( \200\230Form 12 \200\231) and submits it to the duty hospital manager Section 2 of the Mental Health Act (1983) \200 This permits the admission to hospital and detention of a patient for assessment and treatment The patient must have a mental disorder that warrants detention in the interests of the patient or for the protection of others Application is made by a relative or approved social worker, and supported by two registered medical practitioners The assessment period is up to 28 days and is not renewable Deprivation of Liberty Safeguards \200 This code of practice was published in 2007 and pr ovides supplementary guidance to the Mental Capacity Act (2005). It lays down a framework for when and how Deprivation of Liberty (DoL) may be authorized. (See b \200\230Deprivation of Lib erty Safeguards \200\231, p.657) COMPULSORY DETENTION AND TREATMENT 231 The impetus for these guidelines arose out of a well-publicized case dating back to 1997 in which an autistic patient who was incompetent was detained informall y in Bournewood Hospital for assessment. The \200\230Bournewood Gap \200\231 was identi \201 ed as a gap in the law by the European Court of Human Rights. Incompetent patients who were sectioned were subject to stringent rules (Mental Health Act) while \200\230informal patients \200\231 held under the common law of necessity did not have similar protective m echanisms and regulations and potentially could be held for inde \201 nite amounts of time DoLS are applicable in hospitals and care homes. There are detailed requirements about asse ssment, authorizing detention, renewing, and challenging decisions The underlying principle is that a patient should be detained in the least restrictive manner that is practical Despite the huge number of patients who potentially come under these legal safeguards in acute geriatric medicine wards most remain under simple common la w. DoLS teams provide assessment, and support decision making and documentation when the de privation is particularly stringent, longstanding, or is challenged by family or friends HOW TO Manage the older person refusing treatment In practice, compulsion is possible only in hospital. Brief interventions against a patient \200\231s will are sometimes possible at home (eg restraint to prevent dangerous wandering ; forced administration of antibiotics in a sepsis with delirium), but can rarely be sustai ned because of resource restraints and staff feeling legally and physically vulnerable. Use guidance from the Mental Capacity Act to admit to acute medical ward in cases of: \200 Dementia with acute physical illness \200 Delirium with moderate behavioral disturbance Use the Mental Health Act to admit to psychiatric wards in cases of: \200 Dementia, with risk to self, eg dangerous wandering, but alternatives must be explored and considered Delirium with severe behavioral disturbance (to psychiatric or medical or geriatric ward) Psychotic state, severe with risk to self or others, eg severe depression with psychosis or risk of self-harm Compulsory admission is not justi \201 ed and/or not legal in cases of: \200 Physical il lness, refusing treatment without psychiatric illness \200 Psychotic state or other psych iatric illness of moderate severity, without signi \201 cant risk to self or others These are guidelines. If in any doubt, seek emergency advice from the local psychogeriatric team. 232 CHAPTER 9 Psychiatry Psychosis Psychotic symptoms, eg delusions and hallucinations, are common in older people, particularly in those who are acutely unwell, hospitalized, or in care homes. Symptoms rang e from benign and non-distressing to those that cause anxiety among patients, caregivers, a nd often indicate important, treatable disease. What is psychosis? A state of severe impairment of assessment of reality. The results inclu de \200 Distortions of perception eg illusions (misperceptions: distortions of actual per ceptions) and hallucinations (perceptions not the result of external stimulus) Distortions of thought content ie delusions \200\224 beliefs held with great conviction despite contrary evidence. These are usually secondary, ie a response to abnorma l occurrences such as hallucinations or low mood Causes of psychotic symptoms in older people The most common causes are \200\230organic \200\231. In order of frequency: \200 Dementia \200 Depression \200 Delirium \200 D rugs, eg levodopa \200 Other neurological causes, eg cerebrovascular disease, brain tumor Less common causes are \200\230functional \200\231 or \200\230non-organic \200\231, eg: \200 Persistence into late life of chronic schizophrenia \200 Delusional disorder of lat er life ( \200\230late paraphrenia \200\231) \200 Psychotic presentation of affective dis order (mania or depression) Treatment of patients with psychotic symptoms \200 Can usually be managed on the general medical wards, or at home, but early specialist psychogeriatric team support is advised Avoid reinforcing a patient \200\231s paranoid beliefs: don \200\231t avoid contact, don \200\231t seek rapid transfer from the ward, etc. Make a diagnosis and treat the underlying cause, eg stop drugs leading to delirium Attend to hearing and visual impairments \200 Treat underlying mood disorder \200 In de mentia, especially Alzheimer \200\231s and dementia with Lewy bodies, consider acetylcholinesterase inhibitors If symptoms are distressing and persistent, consider the use of antipsychotics eg haloperidol, risperidone, olanzapine; usually after specialist advice. Be cautious in patients who may have dementia with Lewy bodies On discharge, offer opportunities for social interaction and practical home support This page intentionally left blank 234 CHAPTER 9 Psychiatry Delirium: diagnosis Delirium is a syndrome of disturbance of consciousness accompanied by c hange in cognition not accounted for by pre-existing dementia. The term delirium (acute con fusional state) refers to an acute brain syndrome, effec- tively acute brain failure, chara cterized by impairment of consciousness (however slight). Beware sloppy language \200\224 the term confusion means only that: muddled thinking, or a n inability to think clearly. It is an important symptom of acute \200\230organic \200\231 brain disorders such as delirium but is not con \201 ned to them, ie low speci \201 city . It may also be seen in depression, dementia, and less commonly in some primary psychotic disorders. Use the term confusion when describing a presentation, but never as a diagnosis. Key features \200 A disturbance of consciousness (decreased clarity of awareness of the environment). May be hypoactive, hyperactive or mixed (see Box 9.1 ). Decreased ability to focus, shift or sustain attention. Distractability. Lose thread of conversation. Leads to u ncertainty about time of day. Impairment is often not obvious, especially if onset gradual; but, after recovery, memory for the period will be poor. This feature is not seen in early dementia, or in primary psychotic disorders Change in cognition . Often widespread, eg memory impairment (often recent memory), disorie ntation (time, place; person less common), language disturbance (eg dysgraphia, dysnomia), perceptual impairment (misinterpretations, eg slamming door = gunshot), illusions (usually visual, eg bedclothes animated), hallucinations. Thinking may be slow and muddled, but is o ften rich in content Acute onset, and \202 uctuates . Usual onset over hours or a few days. Sometimes changes are subacute (weeks to a few months) and may be misdiagnosed as dementia. Severity varies d uring the day, eg \200\230sundowning \200\231 is a syndrome of worsening confusion in the later part of the day or at night Other features (not essential to make the diagnosis) These include: \200 Disturbance of t he sleep-wake cycle. May be complete reversal \200 Disturbed psychomotor behavior. May be \200\230up \200\231 (restless, picking, wandering) or \200\230down \200\231 (slow, immobile) Emotional disturbance, eg fear, depression, anger, euphoria, lability. Fear and aggression may be a consequence of threatening hallucinations or delusions. The pa tient may call out, scream, or moan continually. In an institutional setting this may be pr oblematic, especially at night. At a lesser level, the patient may appear simply perplexed and bewildered \200 Delusions (often persecutory) are common, but usually transient and poorly elaborated \200 Poor insight is typical DELIRIUM: DIAGNOSIS 235 Box 9.1 Pitfalls in diagnosis Making the diagnosis can be dif \201 cult but early identi \201 cation is vital as early treatment will improve prognosis. Delirium is a varied syndrome. As well as \202 uctuatin g day-to-day or hour-to-hour, it is variable in nature, manifesting distinctly in different patients, or in the same patient at dif- ferent times. For example, two patterns (ends of a spectrum) have been described: \200 Hyperactive or \200\230Up \200\231: oversensitive to stimuli, psychomotor agitation, repeatedly getting out of bed, noisy, psychotic symptoms , aggression Hypoactive or \200\230Down \200\231: psychomotor retardation, lethargy, quiet, paucity of speech, few psychotic symptoms. This variety is more commonly not recognized and has a wors e prognosis A mixed picture can also occur Delirium may be misdiagnosed when it is not present (eg in d eaf, or blind or dysphasic patients). More commonly, the diagnosis is not made when it is p resent. Therefore screening tests (typically the AMTS and b Appendix, \200\230CAM \200\231 , p.692) are valuable, and should be performed in all cases when delirium is possible \200 \224 certainly at the time of admission, and during admission if changes in clinical condit ion occur. Usually there is evidence of the medical condition that has led to delirium. Although this is not necessary to make the diagnosis, it is necessary to treat it effectively. Ensure you document your assessment and diagnosis well. 236 CHAPTER 9 Psychiatry Delirium: causes A particular case is often multifactorial, ie several factors (individu- a lly modest and alone insuf \201 cient) combine to push a patient across a threshold to fra nk delirium. Chronic factors (eg overt or incipient dementia) may maintain a person closer to that threshold, and impaired homeostasis of older age increases the systemic \200\224 a nd cerebral \200\224 effects of illness. Delirium is therefore especially likely to occur in very elderly people, in the physically frail, or if there is pre-existing dementia, defective hearing or vision, or brain damage o f any kind, eg idiopathic Parkinson \200\231s disease. In these cases more minor acute illn esses may cause delirium. Factors that may contribute to delirium 2Usually, there is evidence from either the history or examination or simple tests, of the factor(s) that have contributed to delirium. These factors include: Infection . Viral or bacterial. Not necessarily severe, especially in those with MCI, demen tia, or other contributory factors. Common sources are chest, urine, skin (cellulitis). Rem ember other infections, eg CNS, endocarditis, biliary infection, diverticulitis, pancreatit is, abdominal perforation, and abdominal or pelvic collection Drug intoxication . Especially anticholinergics, anxiolytics/hypnotics, anticonvulsants, opiates (see Box 9.2 ) Disorders of electrolyte/ \202 uid balance , eg dehydration, uraemia, hypo-/ hypernatraemi a, hypercalcaemia. Modest degrees of hyponatraemia ( > 130mM) are unlikely to be the sole c ause of delirium Alcohol or drug withdrawal \200 Organ failure , eg cardiac, respiratory, liver \200 End ocrine . High or low blood sugar, hypo- or hyperthyroid \200 Epileptic . Post-ictal state following unrecognized seizures. Consider if there has been an unwitnessed \200\230collap se \200\231, with amnesia, and any ictal features (incontinence, tongue biting). If conscio us level is low consider ongoing ictal activity or even non-convulsive status Intracranial pathology , eg, head injury, space-occupying lesion, increased intracranial pr essure of whatever cause, infection, pre-existing cognitive impairment or acute/chronic cer ebrovascular disease. However, acute stroke is rarely the sole cause of delirium Pain These factors may be accentuated on admission to hospital by environmental disorientat ion, a lack of information, sensory over- or under-stimulation, impersonal setting, changes in staff or wards, poorly understood investiga- tions and treatments, and being away from a familiar home and family/carers. DELIRIUM: CAUSES 237 Box 9.2 Drugs causing delirium Drug-induced delirium is common. Incidence of delirium is closely associ- ated with anticho linergic activity. Therefore tricyclic antidepressants and neuroleptics constitute high-ris k groups. Many more are less frequently associated with delirious reactions. \200 Anticho linergics (used for either cardiac or gastrointestinal effects, eg atropine, hyoscine, propantheline) Antipsychotic drugs ( \200\230neuroleptics \200\231) , eg chlorpromazine, tri \202 uoperaz ine, thioridazine Antihistamines , eg chlorphenamine, diphenhydramine \200 Hypnotics/anxiolytics , eg barbi turates, benzodiazepines, \200\230Z-drugs \200\231 (zolpidem etc.) Antidepressant drugs . Especially tricyclics \200 Anticonvulsant drugs , eg phenytoin, ca rbamazepine \200 Opiates and opiate-like drugs , including codeine, dihydrocodeine, and tramadol Corticosteroids including prednisolone \200 Lithium \200 H2 receptor blockers , eg cime tidine (rarely) \200 L -dopa (co-beneldopa, co-careldopa), dopamine agonists . Caution in treating parkinsonism in patients with Lewy body dementia Digoxin \200\230Recreational \200\231 drugs that may cause delirium include alcohol, marij uana, LSD, amphetamines, cocaine, opiates, and inhalants. A drug may be the \200\230 \201 nal straw \200\231 that leads to overt delirium. For exam ple a dry, septic patient who has tolerated co-codamol when well, may become delirious when it is again administered in hospital. 238 CHAPTER 9 Psychiatry Delirium: clinical assessment History and examination \200 Most factors leading to a pres entation with delirium can be identi \201 ed by taking a history and examining the patient . Even confused, forgetful patients report ongoing symptoms (eg pain, dysuria) if asked \200 Always obtain a collateral history, paying careful regard to recent minor/major sympt oms (eg cough), as well as drug history, and an exploration of the nature and duration of m emory/cognitive symptoms Always assess cognition objectively \200\224 eg using the AMTS, MMSE or clock-drawing test. This may yield surprising results (better or worse than expected), and permits tracking of progress If a patient is non-compliant with examination, use distraction (eg chatting whilst examini ng) or complete the examination in sections. Sedation will only rarely be necessary Focus the examination on important areas \200\224 is there evidence of infection (examine all lung areas, abdomen), or of new focal neurology? Is the patient dehy drated or overloaded? Repeat vital signs regularly, especially temperature \200 Check arterial oxygen saturatio n off oxygen \200\224 even modest hypoxaemia (sats (cid:100) 95 % ) may indicate important cardiopulmonary pathology Investigation \200 One contributing factor may be obvious (eg UTI), but do not assume tha t this is the sole \200\224 or even the most important \200\224 factor, until others have been excluded All patients should have some baseline tests (see Box 9.3 ). These will vary according to the clinical picture, the availability of tests, and whether a clear cause is already apparent If the cause remains unclear despite a careful history, examination, and \200\230simple \200\231 tests, then repeat clinical assessment, consider less common causes, and consider more advanced tests such as CT/MRI brain, EEG, or CSF examination DELIRIUM: CLINICAL ASSESSMENT 239 Box 9.3 Baseline investigations in delirium \200 FBC , ESR . Evidence of infection, anemi a (unlikely on its own to cause delirium) U , C + E . Hypo-/hypernatraemia, dehydration, renal impairment \200 Glucose . Hypo-/hype rglycaemia. The sugar may now be normal \200\224 but what was it an hour/day ago? LFTs and amylase \200 TFTs . Hypo- or- hyperthyroidism are common and treatable. Both may contribute to a presentation of delirium CRP . A very useful test, but may be normal early in the course of infection Calcium and phosphate \200 CXR . Clinical examination is relatively insensitive to early/ localized pathology, eg infection ECG . Silent ischaemia/infarction common in older people. Consider troponin Urinalysis urine microscopy and culture . Asymptomatic bacteriuria is common; a positive dipstick may not therefore explain a patient \200\231s delirium. Look for additional cause s Blood culture . Always send before starting antibiotics. Occult bacteraemia is common Blood gasses . Hypoxaemia or hypercapnia may contribute to delirium 240 CHAPTER 9 Psychiatry Delirium: treatment issues 2Initiate treatment early: delirium is a medical emergency. Where to treat? In many cases the patient should be admitted to an acute general hos- pital where there are advanced diagnostic facilities (including CT) and staff trained to manage acute illness. Outside an acute hospital \200\224 in a domestic setting, care home, commun ity or psychiatric hospital \200\224 the medical team must in each case balance the bene \201 ts of advanced diagnostics, treatment and monitoring with the possible detrimental eff ect of transfer. There is little place for a \200\230treat at home and hope \200\231 appro ach, unless: \200 The dominant cause is clear \200 Effective treatment can be given \200 Appropriate care and supervision can be assured \200 The risks of transfer are cons idered to outweigh the bene \201 ts Keep the admission brief. With appropriate support and monitoring, discharge home or transfer to a less acute environment can often be achieved e arly. The underlying cause 2Making the diagnosis of delirium is half the job. The second part is elic- iting and treating the cause(s). \200 However, don \200\231t treat totally blindly, eg there is little place for blind, broad-spectrum antibiotics with the associated risk of Clostridium colitis, unless the patient is very ill and sepsis appears likely \200 Alway s check the drug chart. Consider each drug in turn: at this time, does risk equal or exceed bene \201 t? If so, stop the drug, at least temporarily Ensure adequate \202 uid and nutrition. The patient may not be dry or malnourished on admission (though they commonly are), but may soon become so If alcohol dependency or severe malnutrition is known or suspected, high-dose parenteral vitamin B supplements may be needed \200 Occasionally, the cause of delirium is not apparent. In such cases: \200 Initiate general supportive measures ( \202 uid, pressure care, nutrition, etc.) Continually re-examine and consider more advanced tests Competency Patients with delirium are not usually competent to direct treatment. The law al lows assessment and treatment in their best interests. This may include: \200 Holding wit hin a ward or hospital if a patient attempts to leave \200 Temporary physical restraint ( eg while drugs are administered) \200 Covert administration of essential drugs Clear expl anations should be given to staff and family of the need for such interventions, and their ethical and legal justi \201 cation. Document clearly in the medical notes why the team co nsiders that such measures are neces- sary. Reassess competence continually. Once the acute illness is over a \200\230Deprivation of liberty assessment \200\231 may be needed (see b \200\230Deprivation of Liberty Safeguards \200\231, p.657). DELIRIUM: NON-DRUG MANAGEMENT 241 Delirium: non-drug management Delirious patients feel ill, frightened, bemused, and disorie ntated. There are problems with attention, memory, and perception. Therefore do what you ca n to make life easier for the patient: \200 Provide a quiet environment free from worryin g sounds; appropriate clothes; quality lighting, at an appropriate level for the time of da y; a clock or outside view to aid orientation Optimize visual and auditory acuity by providing spectacles and hearing aids that work Reassure the patient repeatedly and calmly \200 Explain who you are, what you wish to do and con \201 rm understanding \200 Patients will sense a doctor \200\231s manner, partic ularly aggression or frustration. At all times appear relaxed, unhurried and pleasant \200 Use non-verbal communication: sit down, smile and appear friendly rather than professional Don \200\231t argue, or correct delusions \200\224 the product will be aggravation and lesser compliance Educate visitors who are heightening emotion \200\224 ask them to modify their behavior or even asked them to leave Explain to relatives, and enlist their help, in supervising, feeding, and bringing in items familiar to the patient Physical restraint Restraint is terrifying and has adverse mental and physical sequelae. It is only rarely needed, but is sometimes (inappropriately) used as a substitute for supervi sion and guidance by an experienced carer/nurse. In cases of severe aggression, where parenteral drugs are required, brief immobilization of the patient using the minimum force necessary may on balance be in the patient \200\231s b est interests. Recovery phase 2Patterns of recovery from delirium vary. Most patients recover com- pletely in a few days, some take much longer, but some never return to baseline cognitive and/or p hysical function. Delirium can \200\230unmask \200\231 a previ- ously unrecognized dementi a. In those whose functional status declines signi \201 cantly, remember that full recover y may take weeks or months \200\224 beware making irreversible decisions (eg home versus r esidential care) \200\224 before the \201 nal functional level is known. Once a patient is admitted, multiple barriers to discharge often appear: Carers and family will fear that recent deterioration will persist, and may resist discharge Care packages may be canceled, taking weeks to restart \200 Therapists may assess functio n as suboptimal in the unfamiliar hospital environment, judging that discharge is unsafe Therefore once the acute event has been diagnosed and treatment begun, encourage the team t o begin promptly to plan for home. Delay in discharge leads to increased prescription of ps ychotropic drugs, institutionalization and care home placement. 242 CHAPTER 9 Psychiatry Delirium: drug treatments Drugs are needed only when the agitation that accompanies deliriu m is: \200 Causing signi \201 cant patient distress \200 Threatening the safety of the patient or others \200 Interfering with medical treatment (eg pulling out of iv lines, a ggression preventing clinical examination) Having decided that drug treatment is in the patient \200\231s interests, remember that: \200 Drugs should complement, not replace, non-drug approaches \200 The correct dose is the minimum effective dose \200 The response (adverse and bene \201 cial) and prescripti on must be reviewed regularly It is preferable to use only one drug, starting at low dose, and increasing the dose increm entally at intervals of 30 \200\22360min Delirium can resolve quickly so avoid regular prescription \200\224 each dose should be as needed (prn). The relative merits of differing drug classes and drugs are debated, but a reasonable conse nsus is presented in b \200\230HOW TO Prescribe sedating drugs in delirium \200\231, p.243. In cases where behavior remains problematic, seek urgent advice from the local psychogeriatric team. DELIRIUM: DRUG TREATMENTS 243 HOW TO Prescribe sedating drugs in delirium Short-acting benzodiazepines (eg lorazepam) \200 Have recently replaced antipsychotics as \201 rst-line treatments. Useful if sleep disturbance is prominent, or for severe distre ss or agitation \200 Short-acting benzodiazepines are preferred, eg lorazepam orally (po) , im, or sublingual repeated as necessary/tolerated Dependence and tolerance is possible, so review regularly and discontinue as soon as possib le. Avoid inclusion on \200\230to take out \200\231 (TTOs) if possible Long-acting benzodiazepines are especially useful for the treatment of delirium caused by a lcohol or benzodiazepine withdrawal. Use chlordiazepoxide, in reducing dose In extreme cases only (eg severe distress/agitation, with imminent danger to self/others), consider giving a small intravenous dose of a short-acting benzodiazepine (eg midazolam), c arefully titrated to response. Monitor closely both clinically and with oximetry \200\224 the major risk is respiratory depression Typical antipsychotics (eg haloperidol) \200 Compared with low-potency antipsychotics, th ere are fewer side effects (eg sedation, hypotension, anticholinergic) Begin with a small dose, eg 0.5mg orally, as tablet or liquid, as required. Repeat doses after 1 \200\2232hr, and increase the dose size as needed and tolera ted. Total daily oral dose is usually 0.5 \200\2234mg \200 Response is idiosyncratic: som e patients are very sensitive to low dose, others only to very large doses In older people the half-life of haloperidol may be as long as 60hr. Dosing can be cumulati ve. Failure to titrate the dose correctly may render the patient semi-conscious for days The oral liquid formulation of haloperidol is colorless and odorless, aiding covert administration (eg in a drink) if required \200 In the very agita ted consider haloperidol 1 \200\2232mg im repeated after 1hr (approximately 2:1 oral to int ramuscular dose equivalence) The incidence of extrapyramidal side effects is high. Avoid haloperidol in dementia with Lewy bodies and in all causes of severe parkinsonism Atypical antipsychotics (eg olanzapine, risperidone) \200 The place of the newer atypical antipsychotic medications remains unclear, following concerns of increased risk of stroke Should be considered when response to other strategies is poor \200 Risperidone liquid ca n be diluted in water, black coffee, or orange juice \200 Risperidone 0.5mg has similar p otency to haloperidol 1mg Combination treatment Benzodiazepines and antipsychotic medicatio ns are sometimes combined in the management of delirium symptoms, generally under specialis t advice. Stopping treatment Once behavior has improved, consider stepwise dose reduction, aiming to stop the drug as soon as possible without prompting relapse.