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PC

Zara Sheikh & Ruben Thumbadoo


Presentation
 67 female
 Admitted on Section 2 via community due to non compliance with medication
 The relationship with her husband seems to have deteriorated. He has recently moved out. There have been
some verbal arguments. But no evidence of any physical altercation between them.
 Last year her mother had passed away and she had reported feeling depressed.
 She was started on Venlafaxine which was stopped due to evidence of Hypomania
 In early 2018, she visited her son in Thailand and since her return had stopped her Quetiapine which she has
been taking for over 3 years.
 She is grandiose in her beliefs. She is highly & suspicious paranoid about staff from crisis team. She reported to
have collected evidence against the staff members. She reported to have contacted the police and reported
doctors to them. She appears to believe her husband is talking to the crisis team behind her back. She said that
her husband has been mentally abusing her since 1990s. She stated that her husband has a mental health
problem. She had recently gone to the Citizen’s Advice Bureau stating that she wanted to go in to a women’s
refuge to get away from the mental health team. Repeated visits to different A&Es reporting physical health
symptoms and attributing these to medication, including visit to Addenbrookes where she absconded and was
recovered by police.
Past Psychiatric History
 Known Bipolar Affective Disorder.
Treated in the community for depression in 2013 and mania 2014.
On Quetiapine since 2014 until January 2018 stopped by patient
 Current medications on admission:
Olanzapine 2.5mg ON (non-compliant)
Bezafibrate 400 mg M/R od
Omeprazole 20 mg od
Calceos chewable tablets T OM
PRN Diazepam
Physical health
 Multiple physical health ED attendances in run up to admission, attributing
medication to physical health symptoms, no definitive diagnosis, awaiting
cardiology follow up at Lister with “undiagnosed AF”.
 Very adamant she has physical health problems because of medications
HTN
GORD
High cholesterol
Personal, & Social History
 Personal and Family History
 PC was born in London. Family moved to Stevenage when she was just 4 years old. She left
school at the age of 18 yrs and proceeded to a teachers training college in Bishop Stortford. She
later continued her education and obtained a degree from Cambridge University. She worked as
a teacher after which she retired. She married in 1973. She has 2 children (2 boys) and 3
grandchildren.

 Social circumstances
 She lives with her husband in a house in Guilden Morden since 1976.
 Her hobbies include Yoga, reading and painting.
 There is no issue with ADLs

 Alcohol, smoking and drugs:


 Occasionally, non-smoker and denied
Mental State on Admission
 Caucasian lady in late 60’s dressed casually. Highly suspicious of team.
 She engaged well at times. There was some agitation especially when she was talking
about the crisis team. Lots of energy, poor sleep, poor concentration
 Her speech was pressured. There was flight of ideas. Normal in tone and volume.
 Subjectively and objectively elated, reactive affective, slightly labile
 There was no FTD.
 No evidence of any perceptual abnormalities. Paranoid delusions re husband has had 3
affairs, persecutory delusions, grandiose delusions,
 Lacks insight into her difficulties at present. She does not have capacity to make
decisions with regard to her treatment. Non-compliant of medication.
Differential Diagnoses
 Excluded organic causes
 Excluded drug induced hypomania
Initial period on the ward
 Disruptive to ward, physically aggressive interfering with other service users requiring 2:1 observations
and rapid tranquilised.
 She was disinhibited, gave her number to young male staff member, forbid staff from discussing care with
her husband & wanted to divorce husband. Paranoid writing all conversations down, list of side effects of
medications kept in filling. Carried notes with her at all times
 Wanting to check all ID of all staff members, felt Watford hospital A+E is corrupt, and members of staff
her corrupt as well.
 Delusions regarding smoke detectors as cameras, birds singing as communication from police, that her
husband colluded with community services to section her.
 Delusions that air conditioning was “poisoning” patients, water contaminated, causing her paper thin skin
& Liver spot darkening with lead and is changing her urine to green. kept saliva and produced container
at ward round so it could be tested for poison.
 Appealed against section, raising 10000 pounds for GOSH and calling contacts at Tesco/M+S,
 Depot started as refusing all oral medications
Treatment
 Depot regimen – improvement throughout this period
 Started on test dose dexpiol and increased to 50mg fortnightly as present
 Oral medications
 When tribunal date set became compliant with oral olanzapine
 Physical health
 Review by ward GP and awaiting OP 24 tape and echo
 Observations
 Initial 10mins before being escalated to 2:1 gradually reduced to currently general
 Section
 Initial on section 2 converted to section 3
 OT groups and progress
 Unable to take part initial as lacked focus and ability to sit still but improvement on depot.
Current situation
 Accepts her diagnosis of bipolar disorder, in the future would like to consider going
back on Quetiapine but is happy to continue taking Depixol. Discussion regarding
medication and mood stabiliser, Patricia is keen to remain on depot for the time
being.
 Feeling much better and relationship with husband much improved, husband feels
improvement in mood even in the last week.
 Patient tells of her leave, mostly relaxing and not forcing herself to do to much.
 Discussion regarding day leave and overnight leave for next weekend, husband and
PC happy with plan, aim for discharge following week
Definition of Bipolar Affective Disorder
 ICD-10 : A disorder characterized by two or
more episodes, one of which must be
hypomanic, manic or mixed, with a history ICD-10 Bipolar affective disorder
of depressive episodes. Recovery is usually Current episode: Hypomanic
complete in between. Current episode: Manic without psychotic symptoms
Current episode: Manic with psychotic symptoms
 Manic episode – hypomania or mania Current episode: Mild or moderate depression
without a history of depressive episodes
Current episode: Severe depression without psychotic
symptoms
 Mixed episodes: The occurrence of both Current episode: Severe depression with psychotic symptoms
manic/hypomanic and depressive symptoms
Current episode: Mixed
in a single episode, present everyday for 2
weeks Currently in remission
Mania vs Hypomania
 Mania: A distinct period of abnormally and persistently elevated, expansive, or
irritable mood, with 3 or more characteristic symptoms of mania. Symptoms
should last at least 1 week or less if hospital admission is required.

 Hypomania: 3 or more characteristic symptoms lasting at least 4 days and are


clearly different from ‘normal’ mood. Not severe enough to interfere with social or
occupational functioning, require admission to hospital, or include psychotic
features.
Epidemiology

 About 1 in every 100 adults has bipolar disorder at some point


in their life.
 It usually starts between the ages of 15 to 19 - and it
rarely starts after the age of 40.
 Men and women are affected equally.
Aetiology of BPAD
 Genetics – influences 60-80% of the risk. Strong hereditary component. 40% concordance
with identical twins compared to about 5% with fraternal twins. First degree relatives are 7x
more likely to develop the condition. 2 genes have been implicated: ANK3 and CACNA1C
 Environmental – 30-50% of diagnosed adults report traumatic/abusive experience in
childhood.
 Biochemical: Increasing evidence of importance of glutamate in bipolar and major depression.
Catecholamine hypothesis study suggests that an increase in epinephrine and norepinephrine can
cause mania, while a decrease causes depression. Drugs that can cause mania such as Cocaine, L-
Dopa, Amphetamines, Antidepressants) suggest a role for Dopamine and Serotonin overactivity
 Neurological – can be associated with stroke, traumatic brain injury, HIV, MS amongst others.
Pathophysiology (diagram)
 MRI has shown decreased volume in left
rostral anterior cingulate cortex, fronto-
insular cortex and claustrum. Increased
volume in lateral ventricles, globus
pallidus, subgenual anterior cingulate and
amygdala. This is thought to contribute
to emotional regulation and mood
symptoms.
Differential Diagnosis
 Schizophrenia, schizoaffective disorder, delusional disorder, other psychotic
disorders
 Major depressive disorder
 Anxiety disorders/PTSD
 ADHD
 Circadian rhythm disorders
 Alcohol or drug misuse
 Borderline personality disorder
 Antidepressant treatment
 Physical illness: SLE, MS, brain tumour, epilepsy, HIV
Clinical Features of Mania
Increased energy: Engagement with risk behaviour:
Overactivity Preoccupied with extravagant impracticable
Pressured speech (flight of ideas) themes
Racing thoughts Reckless spending
Reduced need for sleep Inappropriate sexual encounters

Increased self-esteem: Reduced attention/increased


Over-optimistic ideation distractibility
Grandiosity Marked disruption of work, social
Disinhibition activities and family life
Over-familiarity
Facetiousness
Depression and Psychotic features
Depressive symptoms: ICD-10 Psychotic symptoms
 Grandiose delusions, related to identity
Typical symptoms: depressed mood,
or role (special powers or religious
anhedonia, fatigue
content)
Core symptoms:  Suspicion may develop into persecutory
Disturbed sleep, loss of appetite, poor delusions
concentration, psychomotor agitation or
retardation

Mild: 2 typical + 2 core


Moderate: 2 typical +3 or more core
Severe: 2 typical + 4 or more core
Investigations
 Full physical examination and routine blood tests (FBC, U&E’s, ESR, glucose,
Ca2+, TFTs
 Urinary copper (Wilson’s), ANF (SLE), Infection screen (Syphilis, HIV)
 Psychiatric assessment
 Mood charting/mood disorder questionnaire
 Collateral history
 CT/MRI: Hyperintense subcortical structures, (temporal lobes in particular),
ventricular enlargement and sulcal promience
 ECG
Management of BPAD
Medications
Mood stabilisers (Depakote, Lithium, Lamotrigine)
Antipsychotics (Olanzapine, Quetiapine, Risperidone, Aripiprazole)
Antidepressants (Fluoxetine, Venlafaxine)
Anti-anxiety (Benzodiazepines)
Psychosocial
Psychotherapy
Cognitive behavioural therapy
Family focused therapy

Psychoeducation
ECT
Management of Mania/Hypomania: NICE
If not on any mood stabiliser…

• Start olanzapine, quetiapine, haloperidol or risperidone

• If poorly tolerated at any dose or ineffective - trial an alternative antipsychotic

• If an alternative antipsychotic is not sufficiently effective consider adding lithium

• If lithium is not suitable or ineffective (for example, because the person does not agree to
routine blood monitoring), consider adding valproate

• If a person develops mania or hypomania and is on an antidepressant in combination with a


mood stabiliser, consider stopping the antidepressant.
If already on a mood stabiliser…

If on lithium, check plasma lithium levels + consider adding haloperidol, olanzapine, quetiapine
or risperidone,

If they are already taking valproate or another mood stabiliser as prophylactic treatment,
consider increasing the dose, up to the maximum level depending on clinical response. If there is
no improvement - add haloperidol, olanzapine, quetiapine or risperidone

If the clinical presentation is of a mixed affective state, characterised by both manic and
depressive symptoms, follow recommendations above for the treatment of mania, and monitor
closely for the emergence of depression.

Electroconvulsive therapy - for severe mania that hasn’t responded to other treatment
Reviewing treatment for mania
 Within 4 weeks of resolution of symptoms, discuss with the person, and their
carers if appropriate, whether to continue treatment for mania or start long-term
treatment. Explain the potential benefits of long-term treatment and the risks,
including side effects of medication used for long-term treatment.

 If the person decides to continue treatment for mania, offer it for a further
3-6 months, and then review.
Managing Bipolar Depression
 Psychological interventions

 Cognitive behavioural therapy, interpersonal therapy or behavioural couples therapy

 Pharmacological interventions If on Lithium or Valproate:

 Check plasma lithium level. If at maximum


If not on any treatment : level, add fluoxetine combined with
olanzapine or add quetiapine
 Consider fluoxetine+olanzapine, or
quetiapine on its own  Or consider adding olanzapine (without
fluoxetine) or lamotrigine[15] to lithium.
 Or consider either olanzapine (without
fluoxetine) or lamotrigine alone  If there is no response, stop additional
treatment and consider adding lamotrigine
 If no response to fluoxetine + olanzapine or
to lithium.
quetiapine, consider lamotrigine
Longterm management of BPAD
Principles of management
 Following remission, ensure therapeutic dose of mood stabiliser

 Withdraw gradually any additional antipsychotic or BZD

 Following depressive episode, consider tapering antidepressant 8 weeks after patient


euthymic

 Manage with lowest dose of maintenance medication and aim for single agent if
possible, however need a mood stabiliser + low dose antipsychotic or mood stabiliser
+ low dose antidepressant
Long-term management of BPAD
 Pharmacological interventions

 Take into account drugs that have been effective during episodes of mania or bipolar
depression. Discuss with the person whether they prefer to continue this treatment or switch
to lithium, and explain that lithium is the most effective long-term treatment for bipolar
disorder.

 Offer lithium as a first-line and if lithium is ineffective, consider adding valproate

 If lithium is poorly tolerated, or is unsuitable, consider valproate or olanzapine instead or, if


it has been effective during an episode of mania or bipolar depression, quetiapine.
Lithium:
 Gold standard treatment in BPAD
 Mechanism of action: Uncertain MOA. Can substitute Na+, K+, Mg2+ and Ca2+ and may
affect cell membrane electrophysiology
 Interactions
ACE inhibitors
SSRIs
Anti-epileptic
 Prior to commencing: baseline physical exam & bloods – FBC, U&Es, TFTs, BMI, ECG
 Monitor lithium levels 7 days after commencing & 7days after dose changes, samples 12hr post
dose.
 Once therapeutic level established - check Lithium levels and renal function every 3 months and
TFTs every 6 months, monitor BMI and look for side effects
Lithium adverse effects
 Dose related
Polyuria/polydipsia
Weight gain
Cognitive problems
Tremor
Sedation or lethargy
 Cardiac conduction problems
 Long term effects
Renal function
Hypothyroidism
 Teratogencity
 Cognitive impairment
Lithium Toxicity
 Narrow therapeutic window - 0.4-1.2
 >1.5 = symptoms of toxicity >2 = Life threatening toxic effects
 Early signs & symptoms
Marked tremor, anorexia, nausea/vomiting. Diarrhoea with dehydration & lethargy
 As lithium levels rise
Severe neurological complications – restlessness, muscle fasciluations / myoclonic
jerks, choreoathetoid movements, marked hypertonicity
Progresses to ataxia, dysarthia, confusion/ delirium and seizures
Prognosis
Non-compliance is the greatest barrier to recovery – 75% of patients with bipolar are non compliant
50% achieve syndromal recovery within 6 weeks and 98% within 2 years
40-50% go on to experience a further episode of mania or depression within 2 years of syndromal recovery.
50-60% of patients on Lithium gain control of symptoms (7% no recurrence, 45% some future episodes,
40% recurrence)
1 out of 2 people with bipolar will attempt suicide at least once during their life.
Poor prognosis is associated with
Rapid cycling
Family history of bipolar
Early onset
Psychotic features
Alcohol abuse
Depressive features between episodes
Male
Late intervention/recognition