Category: Psychiatry

Polyuria

Urine output of >3 litres per day.  Note that it is usually accompanied by urinary frequency, but that frequency itself may not indicate polyuria (i.e. frequently passing small vs large volumes).

Pathophysiology

  • In general, polyuria can be a result of anything that causes
    • Increased water intake (polydipsia)
    • Decreased ADH (antidiuretic hormone) secretion (central diabetes insipidus)
    • Decreased peripheral ADH sensitivity (nephrogenic diabetes insipidus)
      • ADH promotes water reabsorption in the renal collecting ducts
    • Solute diuresis (most commonly seen in uncontrolled diabetes mellitus- where high glucose concentrations cause a passive diuresis)

Assessment

  • History
    • Define the extent of polyuria and distinguish between urinary frequency i.e. how much urine
    • If polyuria is present, explore this
      • Onset, Duration, Progression, Triggers, Exacerbating/Alleviating factors
      • Associated symptoms- specifically thirst/drinking (polydipsia); weight changes, (also night sweats)
    • Specific things to ask about include
      • Any recent IV fluids/tube feeds; recent catheterisation/urinary obstruction; recent head trauma/surgery or stroke
        • Note patients can be polyuric following urinary obstruction
    • PMHx
      • Diabetes mellitus
      • Psychiatric disorders – on lithium treatment
      • Sickle cell disease
      • Sarcoid/amyloidosis
      • Hyperparathyroidism
      • Hypertension – on diuretics
      • Alcohol and caffeine intake
      • Smoking history
  • Examination
    • General examination of
      • Blood pressure/pulse
      • Weight
      • Mucous membranes (dry?)
      • Skin (dry, pigmented lesions, ulcers/nodules)
    • Neurological/psychiatric exam (doesn’t have to be extensive but may be further explored if there is any suspicion or positive findings
      • e.g. papilloedema; visual fields etc

Red Flags

  • Abrupt onset or onset in children
  • Night sweats, weight loss (particularly where there is a smoking history too)
  • Psychiatric disorder

Investigations

  • Serum or fingerprick (BM) glucose measurement and urinalysis to rule out diabetes mellitus
  • Where hyperglycaemia is absent
    • U&Es including serum Calcium
      • Hypernatraemia suggests excess water loss due to diabetes insipidus
      • Hyponatraemia suggests excess free water intake (polydipsia)
    • Urine osmolarity
      • usually low with water diuresis and high with solute diuresis
  • If a diagnosis is not yet clear, a water deprivation test can be done
    • (NB only to be done as an inpatient under supervision)
      • Typically a baseline set of weight, bloods and observations are performed in the morning.  The patient is then deprived of water.  Where possible, hourly samples of urine are tested for osmolarity and sodium concentrations.  Once the patient shows signs of deprivation (i.e. orthostatic hypotension; postural tachycardia; >=5% weight loss OR if the urinary concentration does not increase by >30mOsm/kg), baseline measurements are repeated and a bolus of exogenous ADH administered.  One hour later, measurements are repeated again.
    • Interpretation
      • Normal
        • Maximal urine osmolarity after dehydration (>700mOsm/kg), and osmolarity does NOT increase >5% following ADH injection
      • Central diabetes insipidus
        • Urine osmolarity unchanged during water deprivation but concentrates following ADH administration
      • Nephrogenic/peripheral diabetes insipidus
        • Urine osmolarity shows no significant change after either water deprivation or ADH administration
      • Psychogenic polydipsia
        • Initial urine osmolarity is low (<100mOsm/kg), but urine concentration will normalise with water deprivation (essentially normal response)
    • Other tests which may be appropriate include
      • Pituitary function tests
      • Serum lithium concentration
      • Autoantibody screen

Causes

polyuria

  • Other causes include
    • Cushing’s syndrome/disease
    • CKD
    • Hypercalcaemia
    • Fanconi’s syndrome

Delusional Disorder

Delusion(s) that persist for at least one month- without any other features of Schizophrenia (or mood disorder), and do not impair psychosocial functioning except from the ramifications of the delusion(s).

Background

  • Less common than schizophrenia (around 0.02% prevalence) and tends to occur in middle to late adult life
  • There tends not to be a large impact on daily living as with schizophrenia

Presentation

  • May arise from a pre-existing personality disorder (paranoid or schizo-affective type)
  • Delusion(s) can, in theory, be anything, although several subtypes are more common
    • Erotomanic type- delusions that another person is in love with them
    • Grandiose type- delusions of inflated worth, power, knowledge, identity, or special relationships to a deity or famous person/people
    • Jealous type- delusions of unfaithfulness, jealousy
    • Persecutory type- delusions that they (or someone close to them) is being malevolently treated in some way
    • Somatic type- delusions that they have a physical defect or medical condition
  • Delusions can be mixed type or unspecified
  • In general, patients have poor insight into their delusions

Note: it is important to differentiate between a delusion (firmly held unreasonable belief) and an over-valued idea (can be unreasonable but is rarely so firmly held).  Cultural/religious beliefs must be carefully considered.

Management

  • If possible/suitable- psychotherapy (supportive therapy and/or cognitive therapy) is the most effective treatment
    • There is little evidence to support the use of pharmacological treatments, although atypical antipsychotic medications may be tried in some cases.

Depression

Background

  • Characterised by persistent low mood and/or loss of pleasure in most activities and a range of associated features.
  • Extremely common: about 1 in 20 adults experience an episode of depression every year (majority mild and reactive)

Risk Factors

  • Complex interaction of:
    • Biological factors e.g. family history; head injury; physical illness
    • Psychosocial factors e.g. abuse, unemployment, lack of social relationships, poverty
    • Personality
  • High risk factors include
    • History of depression, suicide or abuse
    • Significant physical illness
    • Other mental health condition (including learning disability)
    • Family history
    • Frequent GP/A&E visits

Assessment of a patient who is at risk or presents with low mood

  • To screen ask about whether the patient has one of the core symptoms of depression
    • Have you been feeling down, depressed or hopeless recently (low mood)?
    • Do you have little pleasure or interest in doing things?
    • (Have you felt like you have no energy recently? While this is a core feature according to ICD, it is less specific for depression than the others.  NICE no longer consider it a core feature but as a minor feature)
  • Other symptoms of depression include
    • Worthlessness/excessive or inappropriate guilt
    • Suicidal ideation; recurrent thoughts of death
    • Diminished concentration/indecisiveness
    • Psychomotor agitation or retardation
    • Poor sleep pattern (insomnia/hypersomnia)
    • Loss or gain of appetite +/- weight change
    • (Reduced self-confidence)
    • (Bleak and pessimistic views of the future)
  • Ask about other psychiatric features, commonly anxiety
    • IMPORTANT to ask about mania/hypomania (e.g. feeling abnormally happy/high, irrational behaviour, expenditure etc) to exclude bipolar
    • Also eating disorders
    • Alcohol/substance misuse
    • Features of psychosis
  • ALWAYS ask about thoughts of suicide and self harm and go into detail where possible
  • Ask about possible triggers (e.g. relationship problems; employment issues; family problems etc), onset, timing, progression etc (i.e. take a full HPC)
  • It is important to take an extensive history in patients with possible depression, including HPC; Past psychiatric history; PMHx and drugs; FHx; Social Hx (drugs and alcohol are extremely important; as are housing, employment history, acitivities/hobies, relationships); Personal Hx (including developmental hx; childhood/growing up/school; family relationships; personal relationships; etc)
    • In reality, this may not be possible due to time constraints, so screening questionnaires e.g. PHQ-9 and HAD scale, may be useful
  • On MSE
    • Appearance and behaviour can vary from normal to unkempt, poor communication and eye contact, weepy, frustrated
    • Speech can be slowed and in extreme cases words may be few (word poverty)
    • Mood is often subjectively and objectively low and affect can be flat
    • There is rarely any disorder of thought or perception although the patient may obsess over ideas of suicide or self harm; guilt or worthlessness
    • Insight can be preserved or the patient may be so depressed as to be pessimistic about treatments
    • Cognition is rarely impaired significantly by depression but may be impaired by co-existent dementia

Diagnosis

  • NB Different associations have different criteria
    • NICE
      • At least 5 out of 9 NICE features (at least one out of two core symptoms)
      • Mild depression is where all symptoms are relatively mild, with little impairment of daily living
      • Moderate depression is defined as ‘symptoms and functional impairment between mild and severe depression’ (some marked symptoms)
      • Severe depression would be 7-9 symptoms, some of which are severe and impair daily living
    • ICD-10
      • At least 2 core symptoms and at least two minor symptoms (mild)
        • 3-4 minor symptoms (moderate)
        • All three core symptoms plus 4 or more minor symptoms with impairment of daily activity (severe)

Management

  • For mild/subthreshold depression- provide information and wait, giving follow-up in 2 weeks to see if they are better
    • Consider psychological therapy if symptoms persist
  • For moderate/severe depression
    • offer pharmacological therapy and high intensity psychotherapy
  • Psychological
    • Low intensity for subthreshold/mild depression
      • e.g. individual guided self-help or computerised therapy based on CBT principles (e.g. MoodJuice website and phoneline); group based activity programmes e.g. Dundonald centre/group based peer support
    • High intensity for moderate-severe depression
      • Group or individual CBT; interpersonal therapy; behavioural activation; couples therapy
  • Pharmacological
    • NB Consider toxicity and suicide risk; explain symptoms of anxiety may worsen initially and that most take some time to work
    • Usually, start with generic SSRI for most individuals (citalopram is often used first line, but fluoxetine, paroxetine and sertraline are alternatives)
      • Sertraline is often used in patients with significant physical illness due to its side effect profile
    • Antidepressant treatment should be trialled for minimum of 6 weeks (unless there are side effects after week 1)
      • If successful should be continued for 6 months before being reviewed and at least 2 years if the patient is at risk of relapse
      • If unsuccessful, trial another SSRI*
        • subsequently, other groups of antidepressants may be trialed
        • in general, stop the SSRI over 4 weeks before trialing a second (with fluoxetine, wait 4-7 days before starting alternative)
          • Venlafaxine may be cross-tapered

sssri

Dysthymia/Persistent low mood

  • Defined as subthreshold features of depression lasting >2 years

Treatment refractory depression

  • There are multiple definitions of treatment refractory depression
    • Some quote a minimum trial of at least 2 antidepressants of different classes (i.e. if followed guidelines- at least 3)
    • Some say at least four
  • Chronic depression is defined as criteria for depression lasting >2 years
  • In any case, it is important to rule out pseudo-resistance i.e. patient not taking medications
  • Treatment options include pharmacological combination treatment (namely SSRI or venlafaxine with mirtazapine); augmentation therapy (usually with lithium, although the evidence for this is minimal); ECT which has been shown to be effective but does include side effects such as impaired cognition; Vagal nerve stimulation/DBS (rarely used due to highly specialist nature).

Psychotic depression

  • Usually, there is pervasive low mood and marked psychomotor disturbance with accompanying delusions and/or hallucinations.  Constipation may be a feature (patients can think that their bowels have been sewn up or have turned to dust.
  • Typically paranoid and mood-congruent, or hypochondriacal:
    • “People are out to get and kill me.”  “I’m being poisoned  to punish me for my sins.”  “I’ve got cancer because I deserve it.”
  • Cotard’s syndrome
    • More commonly found in the elderly, Cotard’s is characterised by classic nihilistic delusions:
      • I’m dead- the world around me isn’t real.
  • Treatment
    • For many of these patients, ECT will be an option for first line treatment (particularly effective).
    • Antipsychotic plus an antidepressent should be only used in combination with caution as both can enhance the side effect profile of the other. Careful monitoring is required.  Alternatively, drugs with dual-effects e.g. Amoxapine (TCA with D2 antagonism) or Olanzapine may be used, especially for episodic attacks.

Atypical Depression

  • Clinical features seem depressive but are atypical (funnily enough).
    • Mood is low but reactive (i.e. able to ‘enjoy’ activities- maybe not as much as usual)
  • PLUS 2 or more of
    • Hypersomnia (>10hrs/day at least 3 days/wk for 3 months)
    • Weight gain/ increase in appetite
    • Leaden paralysis (heavy arms and legs)- at least 1 hour/day, 3 days/week for 3 months
    • Over-sensitivity to perceived rejection- can result in significant social impairment/work problems.
  • It is often associated with anxiety and often responds well to treatment with phenelzine (MAOI- which are usually 3rd line in depression).

Somatiform Depression

  • This subtype of depression is often more described as ‘biological’ depression.  It can often be more severe that other forms but is also more amenable to pharmacological treatment.  ECT is also often effective in these patients
  • It can be diagnosed in the presence of 4 or more of the following clinical features:
    • Marked loss of enjoyment/pleasure/interest in activities that are normally enjoyable (anhydonia)
    • Lack of emotional reaction to events or activites that normally produce an emotional response (blunt affect)
    • Early morning waking (>2hours before normal)
    • Depression worse in morning
    • Objective evidence of marked psychomotor retardation or agitation (reports from others)
    • marked loss of appetite and weight loss (>5% of body mass in 1 month)
    • marked loss of libido

Foetal Alcohol Syndrome

Background

  • Spectrum of disorders due to alcohol consumption in pregnancy
  • Alcohol is a teratogen: it disrupts cellular differentiation and growth, disrupts DNA and protein synthesis and inhibits cell migration.
    • The foetus depends on maternal alcohol metabolism (foetal ADH <10%).  Also alcohol can collect and remain in the amniotic fluid.
    • Finally, alcohol can impair the transfer of important carbohydrate, protein and nutrients across the placenta and indirectly cause growth restriction of the unborn foetus
  • It is not recommended for any pregnant women to drink alcohol, although 1-2 units once a week is not thought to be harmful (from literature).
  • Alcoholism/alcohol consumption can be difficult to recognise in any individual.  This can be true of pregnant women also.
  • Epidemiology
    • In the UK, recent figures suggest an incidence of around 0.2 per 1000 live births

Features/Diagnosis of FAS

  • Confirmed maternal alcohol exposure (this may be hard to determine)
  • Evidence of characteristic minor facial abnormalities- including two of the following
    • short palpebral fissures (<10th percentile)
    • thin vermillion border of the upper lip
    • smooth philtrum (ridge under nose/above lip)
  • Evidence of prenatal and/or postnatal growth restriction
    • particularly if <10th percentile
  • Evidence of deficient brain growth or abnormal morphogenesis including one or more of
    • structural brain abnormalities
    • head circumference <10th percentile
  • Evidence of a complex pattern of behavioural/cognitive/developmental problems that cannot be explained genetically, by family history or environment alone
    • Global developmental delay as a young child and cognitive/behavioural problems later in childhood
  • Birth defects may also be found
    • Heart
      • ASDs, VSDs,
    • musculoskeletal
      • contractures, scoliosis,
    • Renal
      • dysplastic kidneys, horseshoe kidneys, duplex ureter/kidney,
    • Eyes
      • strabismus, ptosis, retinal vascular anomalies, optic nerve hypoplasia,
    • Ears
      • conductive hearing loss, neurosensory hearing loss,
    • Other
      • short fifth digits, clinodactyly of 5th finger, pectus carinatum/excavatum, camptodactyly,

Management/Prognosis

  • Most patients just require supportive management and specialist services (e.g. developmental services etc)
  • Maternal counselling for this and future pregnancies is important
  • Individuals with FAS will often have behavioural problems which may cause difficulties later in life and social support is important later in life.

Autism Spectrum Disorder

Autism spectrum disorder (ASD) covers several disorders that greatly vary in presentation.  It is more common in boys and is usually diagnosed in children >3 years old (children below this age are usually difficult to assess).  Autism and Asperger’s syndrome are the two most known in the spectrum.

It is a spectrum of problems involving:

  • Qualitative impairments in reciprocal social interaction
    • May find relationships difficult to establish
    • May not be motivated by the need for social approval
    • May find group work difficult
    • Seem to relate better to objects than people (except very familiar people e.g. family)
    • May show no interest/awareness in the needs/feelings of others
  • Qualitative impairments in communication
    • May have no speech (see childhood development)
    • May echo speech- immediate or delayed
    • Conversely, may be verbally fluent but have little understanding of language
    • Eye contact is commonly reduced/absent
    • May have difficulty using pronouns
    • Stress, pitch, rhythm and intonation of speech may be odd
    • May have difficulty interpreting non-verbal communication
    • May have difficulty with similies/metaphors
    • Speech may be monotonous and mechanical
    • May be unresponsive to non-verbal feedback
  • Restricted, repetitive and stereotyped patterns of behaviour, interests and activities- including rituals and resistance to change
    • Generally think in concrete and literal terms
    • May have preoccupation with sameness- may become distressed at change/may impose routine on others
    • Will often engage in stereotypical movements and resist new experiences e.g. new food.
    • Sally- anne test

ASD individuals are at a higher risk of depression, anxiety, OCD, ADHD and other mental problems.

Management

Mainstream education should be tried if suitable. Speech and language therapy and special education is often required to help.  Therapies based on reflection are NOT to be used.