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EOL Neurological symptoms NS MOM
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Efforts are made to ensure the accuracy and agreement of these guidelines. However, we cannot guarantee this. This guidance does not override the individual responsibility of healthcare professionals to make decisions appropriate to the circumstances of the individual patient, in consultation with the patient and/or guardian or carer, in accordance with the mental capacity act, and informed by the summary of product characteristics of any drugs they are considering. Practitioners are required to perform their duties in accordance with the law and their regulators and nothing in this guidance should be interpreted in a way that would be inconsistent with compliance with those duties
Hard copies of the Drug chart and patient information leaflet are available in GP Practices and with Community Nursing teams. The version attached below is provided as a last resort as these are not designed to be printed locally.
Steroids’ wide range of actions means they have multiple uses in the palliation of patients with advanced illnesses, but also multiple potential adverse effects. As with any treatment, careful consideration must be given to the individual benefit versus burden of steroids in each patient.
In some instances, such as malignant spinal cord compression, superior vena cava obstruction (SVCO) and raised intracranial pressure, there is a reasonable body of evidence to support their use and to guide optimal dosing regimens etc. However, for most other indications, such as the palliation of fatigue, poor appetite and pain, the evidence is less clear. Consequently, prescribing practices may vary considerably between centres / settings.
Dexamethasone is frequently the steroid ‘of choice’ in palliative care since compared with prednisolone, it causes less fluid retention and the typical tablet burden for a given dose is less, despite carrying a potentially increased risk of proximal myopathy.
Service commissioned by NHS England on behalf of NS CCG
Depression in the palliative care setting
Estimates of the prevalence of depression in patients vary greatly but it is probable that at least 25% may develop a significant mood disorder in advanced cancer. A spectrum ranging from sadness to adjustment disorder to depressive illness is recognised.
Barriers to diagnosis include patient factors such as diurnal variation in symptoms such that it may be missed, social ‘cover up’, or presentation with physical symptoms. Professional barriers include a reluctance to ask about depression due to a fear of what might emerge or not wanting to upset the patient. Other confounding factors may be presentation with overriding anxiety or slowly developing worsening of personality traits, such as attention seeking, which may go unnoticed. Biological features such as weight loss and lethargy are not reliable as features of depression in patients with terminal illness and greater emphasis must be placed on psychological and behavioural features.
Depressed mood, irritability, loss of interest in anything, feelings of worthlessness and lack of hope for the future are important causes of suffering. Depression may be successfully treated in a high proportion of patients.
Management includes ensuring that any reversible causative factors, such as distressing symptoms, are eliminated and that adequate emotional support and counselling is available so that fears and concerns can be explored and channelled appropriately.
Endicott (1984) has published useful ways of modifying the usual screening and diagnostic procedures for depressive disorders in cancer patients.
•fearful or depressed appearance
•social withdrawal or reduced talkativeness
•psychomotor agitation or retardation
•depressed and non-reactive mood
•diminished pleasure or interest
•worthlessness or excessive guilt
•suicidal thoughts/recurrent thoughts of death
Hospital Anxiety and depression Scale (HADS) and Brief Edinburgh Depression scale, in conjunction with clinical review, can also be used in order to assess depression.
Under-treatment of depression is common.
Psychological therapies can be effective but may need to be brief due to limited life expectancy.
There is evidence of CBT’s effectiveness in the physically-ill population but there are few studies in palliative care. Other therapies that may alleviate depressive symptoms include mindfulness-based therapies, problem-solving therapy, interpersonal therapy, and couple therapy although more research is needed.
Antidepressants should be considered for treating depression in palliative care, although the evidence is limited concerning which drug is preferable:
a trial of at least 2 weeks, and preferably 4 weeks or more, is needed to properly assess response to an antidepressant. Discontinuation symptoms (withdrawal) will not usually occur if stopped within 6 weeks of starting.
use an SSRI unless other treatment specifically indicated:
dose escalation is not usually needed, so more rapid control of symptoms may be possible
side effects of SSRIs are generally better tolerated than tricyclics in ill cancer patients
However – note that SSRIs can increase the risk of GI bleeding, reduce platelet aggregation and may increase the QT interval (especially citalopram)
Coincidental symptoms that may be helped by the antimuscarinic effect e.g.:
nocturnal urinary incontinence
sialorrhoea / drooling
Convulsions can occur in the palliative setting in patients with primary or secondary brain tumours as well as in the presence of metabolic and infective complications.
Examples of metabolic causes of convulsions include hyponatraemia, hypoglycaemia and hypercalcaemia.
They can present with generalised (grand mal) or focal epilepsy.
Relatives will need support since it is very FRIGHTENING to witness a convulsion especially in a loved one.
Generalised MYOCLONIC TWITCHING may occur during the terminal stages and in uraemia and is also treated with anticonvulsants. When a dying patient is unconscious and no longer able to take oral anti-convulsant medication, suitable alternatives should be given subcutaneously to prevent further cerebral irritability.
EMERGENCY MANAGEMENT OF ACUTE SEIZURES
Safe positioning: place patient in recovery position
Consider rapidly treatable causes e.g. hypoglycaemia
Administration of anticonvulsant if seizure does not resolve within 5 minutes, choice reflects drug availability, IV access and setting:
lorazepam 4mg IV by slow injection (less than 2mg/min) or
midazolam 10mg buccal formulation or 5mg SC or diazepam 10mg rectal preparation PR or 2mg IV emulsion in boluses up to 10mg
Repeat once after 15-20 mins if seizures persist
If seizures are prolonged consider transfer to acute hospital if appropriate / in line with agreed ceiling of care / patient’s preferred place of care. If not for transfer, treat refractory seizures with:
midazolam 20-30mg SC over 24 hours via syringe pump and titrate
if midazolam infusion fails, phenobarbital 100–200mg IM stat followed by 200-600mg SC over 24 hours via syringe pump
Once seizures are controlled consider whether the following are indicated:-
conventional oral anticonvulsants
stopping drugs which may lower convulsive threshold e.g. antipsychotics
starting steroids or increasing steroid dose
Midazolam 20-30mg SC over 24 hours via syringe driver pump is also suitable when patients at high risk of seizures are unable to take their oral anticonvulsants.
In a semiconscious, unconscious or dying patient, there may be concern about whether to replace oral steroids with SC steroids. As death approaches, the reason for their prescription should be reviewed. If they were thought to be the best way of conveying benefit for symptoms, to stop abruptly would risk withdrawal with the possibility of destabilising symptom control – an issue to be avoided. However, historical practice - to stop steroids abruptly in patients’ final days anecdotally has not been associated with detectable issues, despite the established risks.
Generalised MYOCLONIC TWITCHING may occur during the terminal stages and in uraemia and can also be treated with anticonvulsants e.g. midazolam.
For patients with intracranial tumours, consider starting, or review dose, of corticosteroids.
Remember to advise the patient about restrictions on driving
Parenteral thiamine if alcohol abuse suspected (see delirium)
Consider and treat hypoglycaemia in at-risk patients.
Consider drug interactions that alter anticonvulsant levels e.g. Corticosteroids
Initiating anticonvulsant therapy
It is usually appropriate to initiate anticonvulsant therapy after one seizure in patients with terminal illness.
Sodium valproate is an appropriate first line anticonvulsant for almost all types of convulsions or seizures, including focal and partial seizures, and those caused by intracranial tumours.
Aim to increase dose to lower end of quoted 'usual maintenance dose' unless side-effects occur, or frail elderly patient.
Carbamazepine and phenytoin are suitable alternatives.
Patients unable to take oral medication
Patients who are unable to take oral medication due to dysphagia, vomiting or in terminal care, may need anticonvulsants by another route.
The half-life of most anticonvulsants is quite long (> 24h), therefore no parenteral anticonvulsant is usually needed if
there is a low risk of seizures, and
only a single dose is missed, or
the prognosis is measured in days.
The risk of seizures is higher if:
patient has decreased or stopped steroids (intracranial tumours)
recent rise in headache or vomiting or other signs suggesting rising ICP (intracranial tumours)
myoclonus or other twitching is present
history of poor control of seizures or recent seizures
previously needing >1 anticonvulsant to achieve control
Because of the long half life of anticonvulsants, parenteral treatment can be started any time within 24h after the last oral dose.
Management of prolonged seizures
Most seizures are self-limiting and require only supportive care. For more prolonged seizures occurring at home, a number of measures can be arranged in anticipation which can avoid inappropriate emergency admission to hospital.
Diazepam rectal solution 10mg PR - administered by district nurse or carer.
Midazolam 5-10mg SC (or preferably IM) - administered by district nurse.
Buccal midazolam 10mg/2mL can be administered by a carer if the rectal route for diazepam is unacceptable, and appears to be as effective and may be quicker-acting than rectal diazepam 10mg. Oral solution is available as a 'special' or the injectable preparation can be used.
Malignant Spinal Cord Compression (MSCC) occurs in 5-10% of patients with cancer, 10% of patients with spinal metastases develop spinal cord compression, the frequency being highest in multiple myeloma and cancers of the prostate, breast and bronchus. Incidence of MSCC is increasing along with advances in cancer treatment which are improving survivals to mean that the late complications of metastatic cancer are being seen more often. Those looking after such patients should always be vigilant in checking for early signs and symptoms of spinal cord compression.
It is important for all health professionals to have a high index of suspicion for possible MSCC because of the catastrophic consequences of a delay in diagnosis.
•Back pain, a sensation of weakness in the legs and often vague sensory symptoms may be early manifestations.
•For those presenting with profound weakness, a ‘sensory level’ and bladder and anal sphincter disturbance, which are relatively late features, the outcome is poor and the compression is much less likely to be reversible.
The keys to diagnosing Spinal Cord Compression include:
•Having a high index of suspicion in patients with spinal metastases particularly those with Multiple Myeloma, Breast, Lung and Prostate Cancer
•Taking patients’ complaints about back pain, difficulty in walking and in passing urine, seriously
80% of cases are caused by extradural deposits due to direct extension from the vertebral body into the anterior epidural space.
Lesions above L1 (lower end of spinal cord) may produce upper motor neurone signs and a sensory level, whereas lesions below L1 may produce lower motor neurone signs and peri-anal numbness (cauda equina syndrome).
All health professionals need to have a high index of suspicion for possible MSCC. As >75% of MSCC are secondary to extradural compression from bone metastases in the vertebrae, many patients present initially with symptoms suggestive of spinal metastases. Distinguishing the symptoms of spinal metastases from neurological symptoms or signs suggestive of MSCC will dictate the urgency of seeking a whole spine MRI and subsequent management.
Site of compression
Symptoms suggestive of spinal metastases include:
· increasing pain in thoracic or cervical spine
· progressive lumbar spinal pain
· severe unremitting lumbar spinal pain
· spinal pain aggravated by straining
· localised spinal tenderness
· nocturnal spinal pain preventing sleep.
Signs / symptoms of MSCC:
· 75% have weakness - of legs (+ arms/hands if cervical)
· 90% have pain
· tenderness over affected vertebra
· may be radicular pain only
· 50% have sensory level on examination
· 40% have sphincter dysfunction - a late sign, except with cauda equina compression
Making an urgent appropriate management decision is the priority
MSCC is an EMERGENCY and two questions need to be answered urgently.
1. Does this patient have a reasonable likelihood of having spinal cord compression?
Even the most skilled clinician is unable to diagnose early spinal cord compression with absolute certainty. Often by the time clinical signs are “classical”, the damage is irreversible. Once the compression has fully developed treatment outcome is very poor. Thus if intervention to prevent paraplegia is to be meaningful, spinal cord compression needs to be diagnosed early.
2. Would this patient benefit from instituting emergency investigation and treatment?
Once the possibility of MSCC has been raised, the patient may now be committed to a course of management that will include urgent transfer to a specialised unit where an MRI scan can be carried out and radiotherapy or other compression-relieving procedures performed. NICE guidance recommends performing a whole spine MRI within one week for back pain suggestive of spinal metastases and within 24 hours if pain is accompanied by neurological symptoms and signs consistent with MSCC.
Deciding which course of treatment is appropriate for a particular patient involves an overall assessment. NICE cautions against the unnecessary investigation of patients who are too frail or unfit for specialist treatment.
Where suspicion of MSCC is high, it is quickest to involve the oncological team who have been managing the patient, who will be able to co-ordinate the necessary scan and appropriate treatment rapidly. Some regions have a MSCC coordinator to help the patient through investigations and either oncological or surgical treatment. (See local info)
If the patient is still walking, emergency treatment gives a 1 in 3 chance of regaining leg strength and treatment should be started immediately with dexamethasone 16mg daily orally while arrangements are made for urgent transfer to an oncology centre. The dose should be split, and administered sc or iv if unable to swallow or there is rapid progression. Gastro-protection with PPI should also be considered.
Overall, 30% of patients with MSCC spinal cord compression may survive for one year. Function will be retained in 70% of patients who were ambulant prior to treatment but will return in only 5% of those who were paraplegic at the outset. Return of motor function is better in those with an incomplete block and particularly with partial lesions of the cauda equina. Loss of sphincter function is a bad prognostic sign. In practice, most patients with an established diagnosis are relatively unwell and have multiple metastases, and will be referred for radiotherapy, achieving similar results to those of surgery.
Management of Patients with Spinal Cord Compression
Such patients provide great challenges to the multidisciplinary team.
These challenges include:
•Mobility management, within the limits considered safe for the compromised spinal cord
•Skin care in a patient confined to bed
•Urinary system management
Local administrative information
Malignant Spinal Cord Compression Coordinators
WAHT - have a spinal cord compression co-ordinator as part of the Acute oncology team
UHB - in hours UHBristol Acute Oncology service and out of hours the On-call Oncology Reg.
NBT - During working hours it’s the AOS team who can be contacted on 07860783116 Out of hours it’s the Hub team . Nurses in the clinical hub provide this service and can be contacted on 0117 4140700
1.Consider differential diagnoses e.g.
renal or hepatic failure
drowsiness or sedation from drugs, brain tumour, hypercalcaemia
recent chemotherapy or radiotherapy
localised muscle weakness e.g. steroid-induced proximal myopathy, spinal cord compression etc.
Lambert-Eaton myasthenic syndrome
2.Exclude or treat reversible causes, including:
Review drug therapy if drowsiness is thought to be related to medication
Cancer-related fatigue may respond to corticosteroids or progestagens:
dexamethasone 4mg o.d. See Palliative Care Guidelines for more information.
Diagnosis of terminal agitation assumes that reversible conditions are excluded or failing to respond to treatment.
Sedation is needed in many patients, but pain (especially from urinary retention or painful faecal loading in rectum) should be excluded or treated appropriately.
Most patients can be settled with midazolam by CSCI. Tolerance is sometimes seen, and the addition of a sedative phenothiazine or barbiturate may be needed.
Midazolam- sc injection (TLS Green). BNF advises for confusion and restlessness in palliative care 10mg-20mg/24 hours, adjusted according to response, usual dose 20-60mg/24 hours.
Haloperidol- sc injection (TLS Green). For restless and confusion, BNF advises: 2mg, then 2mg every 2 hours if required PO and 2.5mg then 2.5mg every 2 hours if required by s/c injection.
Levomepromazine (TLS Blue)- sc injection if midazolam and haloperidol not effective. See BNF.
Phenobarbital (TLS Blue)- on advice of palliative care team ONLY
Raised intracranial pressure (ICP) can arise as a consequence of intracranial mass lesions, disorders of cerebrospinal fluid (CSF) circulation and more diffuse intracranial pathological processes. Its development may be acute or chronic.
Headache: more worrying when nocturnal, starting when waking, worse on coughing or moving head and associated with altered mental state.
Early changes in mental state include lethargy, irritability, slow decision making and abnormal social behaviour. Untreated, this can deteriorate to stupor, coma and death.
Vomiting (in early stages without nausea), which can progress to projectile with rising ICP.
Pupillary changes, including irregularity or dilatation in one eye.
Fundoscopy shows blurring of the disc margins, loss of venous pulsations, disc hyperaemia and flame-shaped haemorrhages. In later stages, obscured disc margins and retinal haemorrhages may be seen.
Unilateral ptosis or third and sixth nerve palsies. In later stages, ophthalmoplegia and loss of vestibulo-ocular reflexes.
Late signs include motor changes (hemiparesis), raised blood pressure, widened pulse pressure and slow irregular pulse.
•Localised mass lesions: traumatic haematomas (extradural, subdural, intracerebral).
•Neoplasms: glioma, meningioma, metastasis.
•Focal oedema secondary to trauma, infarction, tumour.
•Disturbance of CSF circulation: obstructive hydrocephalus, communicating hydrocephalus.
•Obstruction to major venous sinuses: depressed fractures overlying major venous sinuses, cerebral venous thrombosis.
•Diffuse brain oedema or swelling: encephalitis, meningitis, diffuse head injury, subarachnoid haemorrhage, Reye's syndrome, lead encephalopathy, water intoxication, near drowning.
This increases intracranial pressure (ICP) and is an independent predictor of poor outcome after severe head injury.
•Head of bed elevation:
Elevating the head of the bed to 30° improves jugular venous outflow and lowers ICP. In patients who are hypovolaemic, this may be associated with a fall in blood pressure and an overall fall in cerebral perfusion pressure.
•Analgesia and sedation:
Midazolam for sedation and morphine or alfentanil for analgesia and antitussive effect.
up to 16mg per day
avoid doses after 2pm as may add to insomnia
gradually reduce dose to minimum effective, monitoring that symptoms remain controlled
withdraw dexamethasone if no improvement after 7 days on 16mgs daily (phenytoin and carbamazepine may reduce therapeutic effect by up to 50%, and vice versa, by enzyme induction)
consider gastro-protection with a PPI and regular glucose monitoring
should be considered in the presence of cerebral malignancy, but normally reserved for those who have had fits
Anxiety and depression are common in patients with advanced cancer or other life-limiting disease with a prevalence reported between 6 and 49%.
Whilst some anxiety may be considered a natural response to life-limiting illness, it is important to identify and treat the exaggerated response which is classified as pathological anxiety. It is also necessary to consider untreated physical symptoms, psychosocial concerns or an underlying anxiety disorder.
Patients may present with the somatic symptoms of anxiety such as dyspnoea, insomnia, tremor and palpitations and these should prompt an assessment of mood and psychological state.
Assessment of anxiety
As with all symptoms, thorough assessment is imperative and will help to guide management. Assessment of the severity, duration and nature of anxiety may be helpful. It is also useful to enquire about pre-morbid personality and previous psychiatric history.
Hospital Anxiety and Depression Score (HADS) may be a helpful way of assessing anxiety.
A review of concurrent medical problems, medication as well as nicotine and alcohol intake is necessary; a review of family and social history and concerns may also be helpful.
Management involves addressing any reversible factors such as pain, or other symptoms. Stimulant drugs, excessive alcohol or withdrawal of drugs or alcohol may exacerbate anxiety and should also be reviewed appropriately.
It is necessary to provide the time and opportunity for patients to express their concerns and for these to be addressed on an individual basis, honestly and clearly.
It is important for all members of the palliative care team to be aware of the “infectious” nature of anxiety and for the team to avoid being driven to management extremes because of the anxiety of the patient or their family.
There is a lack of robust evidence to support the use of any specific medications in the management of anxiety within the palliative care population
Palliative Care Guidelines advise that benzodiazepinesare widely regarded as the mainstay of treatment for anxiety but have addictive potential, although this is less of a barrier to prescribing in palliative care patients than it might otherwise be. They are traditionally divided between compounds which have more sedating effects and those which have more anxiolytic actions. However there is considerable overlap on the anxiety/sedating spectrum. They are useful to break the anxiety cycle, to restore sleep, and to reduce the suffering of the situation where a patient feels that he/she is “losing control”. They are not a substitute for taking the time to allow a patient to ventilate their fears.
Diazepam (TLS Green) 1 - 5mg PRN PO Diazepam has a long half life and may therefore accumulate and be sedative.It should be possible to give it once a day at night. See Palliative Care Guidelines for dose range information.
The BNF advises up to 30mg daily in divided doses in adults, but for debilitated patients use elderly dose of 1mg three times a day increased to 7.5mg- 15mg daily in divided doses.
Lorazepam (TLS Blue) 0.5 - 2mg PRN PO- see BNF. Lorazepam is short acting, rapidly anxiolytic and less sedating than diazepam. It may be more addictive on a longer term basis.
Cognitive Behavioural Therapy (CBT) has been described by the pioneer of this therapy as: “an active, directive, time-limited, structured approach”. It has been shown to be effective in improving anxiety symptoms in patients with advanced cancer and for the treatment of anxiety and depression in non-cancer patients.
Whilst emotional distress is common in palliative care patients, there is rarely time for a full course of CBT and access to skilled psychological therapists is variable. There are now an increasing number of palliative care clinicians who have developed a set of CBT-based skills and can help patients in a coherent, systematic and skilled manner. The skills utilised can enable patients to feel supported and understood, helping them to identify their own inner sources of resilience and coping and consequently better able to manage the emotional distress they encounter from their illness.
Insomnia is a subjective complaint of poor sleep. This can mean insufficient, interrupted or non-restorative sleep or sleep at the wrong time.
It is important to distinguish between an inability to get to sleep (eg anxiety, confusion) and a tendency to wake early or repeatedly (eg depression, urinary problems, pain).
Causes of Insomnia to consider
•steroids, especially if taken late in the day
•depression - with anxiety symptoms stopping patients getting sleep, or early morning waking
•bladder or bowel discomfort
•anxiety and fears
Minimise the causes – control symptoms as far as possible, keep interruptions to a minimum, reduce drug therapy or give stimulants early in the day, counsel about fears and anxieties
Establish a good sleep pattern – allow a siesta to prevent going to bed too early
Encourage a consistent bedtime ritual, a warm milky drink may help
1.Regular or PRN night sedation should not be prescribed routinely.
2.If a patient is taking a regular benzodiazepine hypnotic e.g. temazepam, consider whether they need to continue with night sedation:
tolerance to benzodiazepines usually develops within a few weeks
withdrawal nightmares and insomnia can occur
3.Insomnia due to depression should be treated with a sedative antidepressant e.g. amitriptyline or mirtazapine. Sleep improvement may occur within a few days.
4.Anxiety and fear may be most appropriately treated by sitting and talking to the patient, a hot drink etc. rather than medication.
5.If a night sedative is appropriate, temazepam 10mg nocte should be prescribed, increased to 20mg if needed. See BNF for more information.
6.If temazepam is effective but causes unacceptable 'hangover' effects, shorter acting zopiclone 7.5mg may be tried. See BNF for more information.
An acute confusional state (or delirium) can cause acute distress to relatives and to staff especially if the patient becomes suddenly mentally disturbed, agitated and sometimes aggressive.
Delirium is associated with mental clouding (drowsiness), leading to a disturbance of comprehension which is characterised by decreased attention, disorientation and cognitive impairment. More specifically, delirium has been defined as, “anaetiologically, non-specific, global, cerebral dysfunction characterised by concurrent disturbances of level of consciousness, attention, thinking, perception, memory, psychomotor behaviour, emotion and the sleep - wake cycle”
Reversible Causes of Confusion
•hypo / hyperglycaemia
Drug or Alcohol withdrawal
Transient Ischaemic Attack (TIA)
Breathlessness and/or Hypoxia
Anxiety or Depression
Poor Nutritional Status
Terminal Phase - multifactorial
It may be helpful to think DELIRIUM:
Level of pain
Impaction of faeces
Treat or minimise the possible causes, especially drugs and infections.
Minimise stimuli: nurse in a room with diffused lighting, little extraneous noise, and few staff changes.
Attempt to keep patient in touch with reality and environment – eye contact and touch are often helpful.
Allay fear and suspicion – explain all procedures, don’t change position of patient’s bed, if possible have a friend or relative of patient present.
Stress that patient is not going mad and that there may well be lucid intervals.
Review all medicines, especially if renal or hepatic failure has developed
Explain to family
There is limited evidence of efficacy to support the use of medication in the treatment of delirium.
Antipsychotics are used commonly to manage symptoms of delirium when patients are restless and agitated especially if reversing the causes of delirium is not successful.
It should be noted that these drugs are off-label in delirium, as they do not have a UK marketing licence for this indication.
Doses should be started at the lowest, clinically-appropriate dose and titrated cautiously according to symptoms.
Antipsychotic medication is best avoided in patients with Parkinson’s disease and dementia with Lewy bodies.
Haloperidol also prolongs the QT interval with the potential to precipitate a serious, possibly fatal arrhythmia in at risk patients and can also lower the seizure threshold.
Atypical antipsychotics such as olanzapine and risperidone should be used with caution in patients at risk of cerebrovascular accident.
When antipsychotic medication is used, close monitoring is essential especially for extrapyramidal side effects.
Patients who develop acute dystonic reactions should be treated with procyclidine 5-10mg IM/IV or if oral route still possible, 2.5- 5mg PO t.d.s.
Choice of medication:
Medication may be required if verbal and non-verbal de-escalation techniques are not appropriate, or have not resolved symptoms:
Mild – moderate patient distress consider short-term use (up to 1 week) starting at the lowest clinically appropriate dose and titrating cautiously;
For patients with Parkinson’s disease, prolonged QT interval, alcohol withdrawal or pre-existing seizures, benzodiazepines may be used first line –
For patients with dementia, antipsychotic drugs are not usually recommended. In Dementia with Lewy Bodies they are linked to worsening of extrapyramidal features or acute, severe physical deterioration. In Alzheimer’s disease, vascular dementia or mixed dementias, antipsychotic drugs are linked to cerebrovascular adverse events and death. However, following a robust risk-benefit analysis, cautious use of antipsychotics can be considered for severe psychosis and/or agitated behavior.