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Psychiatric emergencies
https://t.me/med1917
Major Minor Medical
Suicidal patients (30%)
Agitated/violent patients
1. ASSESSMENT
History: need to rule out organic cause e.g. infection
Establish any diagnoses & medication
Any previous similar episodes & cause/Tx
Consider medication compliance or SEs
Use of alcohol / illicit drugs
Recent changes in social life e.g. employment/relationships
History of self-harm/suicide attempt/violence – risk assess
2. NON-PHARMACOLOGICAL MANAGEMENT
Encourage patient to move to area away from others
Speak confidently, slowly, clearly
Non-threatening body language, give space
Explore & acknowledge concerns with patient try to build rapport
Grief reaction
Rape
Panic attacks
Neuroleptic malignant syndrome
Serotonin syndrome
Delirium
Overdose/withdrawal
   
Chapter 6: Psychiatry 217
40% of psychiatric emergencies need admission to hospital
Factors to consider when deciding need for treatment/admission
Severity of illness
Level of insight
Risk of harm to self or others
Other support available
3. PHARMACOLOGICAL MANAGEMENT / PHYSICAL RESTRAINT
Rapid tranquilisation calm the patient without full sedation
BZDs, antipsychotics, promethazine minimum dose, PO if possible
AETIOLOGY: RARE (<1%), adverse
reaction to antipsychotics (DA blockade
causes hyperactivity of SNS)
Hard to predict
SYMPTOMS:
Fever, diaphoresis (sweating)
Rigidity
Confusion, fluctuating consciousness
Autonomic instability (fluctuating BP,
HR, salivation, incontinence)
INVESTIGATIONS
Raised CK may be >1000
Raised leucocytes
Deranged LFTs
MANAGEMENT: withdraw
antipsychotic medication
Rehydration
Monitor temperature, BP, pulse
Consider BZDs to muscle activity &
temperature (lorazepam, diazepam)
 LINE!
AETIOLOGY: increased serotonin due to synthesis, uptake/metabolism or
direct receptor activation more predictable
SYMPTOMS
Psychiatric: restlessness, confusion, agitation Autonomic: hyperthermia, diarrhoea, HR, hypo-/hypertension, mydriasis Neuromuscular: myoclonus, rigidity, tremors, hyperreflexia, ataxia, convulsions
MANAGEMENT: stop precipitating medicine restart cautiously after 48h
Rehydration
May need cyproheptadine (anti-serotonergic)
BZDs if agitated (lorazepam, diazepam)
Will need close medical monitoring afterwards
Risk factors for NMS:
Hx: previous NMS, brain damage, alcoholism Mental state: agitation, hyperactivity, catatonia Physical: dehydration Treatment: recent or dose, high dose,
IM injections
more likely with 1st generation APs
If severe:
Bromocriptine
Dantrolene ( rigidity)
ICU, intubation + ventilation
Common causes of serotonin syndrome:
Switching antidepressant
Combining antidepressants
(with other ADs or supplements)
May need ICU, intubation + ventilation if severe
218 Chapter 6: Psychiatry
https://t.me/med1917
Risk of suicide is 66× greater if self-harmed
Factors predicting repetition of self-harm
Number of previous episodes
Personality disorder
History of violence
Alcohol misuse
Unmarried
Factors indicating suicidal intent
Trying to avoid intervention
Feelings of hopelessness about the future
Planning suicide
Leaving a note
Anticipatory acts (leaving a will, settling
debts)
Use of violent methods
Risk assessment
Impulsive or planned?
Ongoing or resolved trigger?
Precautions to avoid discovery
Preparations (note/ will written)
Do they regret it? want to try again?
Use of alcohol/ drugs?
Any protective factors?
Social support network?
Willing to engage in Tx?
Neuroleptic malignant syndrome
Associated treatment
Onset Slow (days–weeks) Rapid Progression Slow (24–72h) Rapid Muscle rigidity Severe (lead pipe) Less severe rigidity, clonus present
Activity Bradykinesia Hyperkinesia
Blood results
Antipsychotics
Idiosyncratic/normal dose
CK & WCC or normal CK
EPIDEMIOLOGY: F>M, are aged <35y
RISK FACTORS
Biological Psychological Social
Genetics
Age (teens/young adults)
Personality disorder
(particularly EUPD)
Abuse: sexual, physical,
emotional
Bullying
Bereavement
Relationship breakdown
Endings/changes
MANAGEMENT:
1. Assessment
Physical & mental health
Safeguarding concerns
Further self-harm and suicide risk
2. Treatment
Of physical injuries
Specialist psychosocial assessment
Monitor in a healthcare setting to reduce risk of recurrence
Consider need for admission to mental health ward
Serotonin syndrome
Serotonergic medications
Overdose/combinations
(involuntary rhythmic muscle contractions)
Overdose & cutting are the most common forms
Substance misuse
Friends who self-harm
Financial/living concerns
Work/school pressures
Isolation/loneliness
Divorced > Single > Widowed > Married
EPIDEMIOLOGY: second leading cause of death in those aged 15–29y
RISK FACTORS
History of self-harm or suicide attempt
Severe depression
Occupation (farmers, doctors)
Social isolation
Anorexia
Unemployed
Alcohol
Male
Safety plan: identify support, recognise early warning signs, avoid alcohol/drugs, identify emergency contacts
Hanging/strangulation is most common method
Chapter 6: Psychiatry 219
https://t.me/med1917
Child & adolescent psychiatry
Mental illness affects 10% children50% present to GPs
Children: neurodevelopmental disorders Adolescents: mood/anxiety disorders*, eating disorders, substance misuse
*self-harm is common
History, MSE, risk assessment SAFEGUARDING ISSUES?
Consider impact on family/carers
Legally presumed that those ≥16y have capacity to make decisions regarding their care BUT encourage discussion with family.
However, must assess capacity on an INDIVIDUAL BASIS (some <16y may
have competence)
If deemed to have competence, a child can consent to treatment BUT parents can still override refusal of treatment if it is in child’s best interests (avoid if
possible)
If a child lacks competence, a parent can consent to treatment on their behalf if it is within scope of parental responsibility
If a parent refuses treatment that is in child’s best interests, further advice should be sought from courts.
There is no age restriction for Mental Health Act.
Summary of consent
Capacity/competence No capacity /competence
16–17y Can consent/refuse admission or
treatment
<16y Can consent, but if refuse can use
MHA
Impacts development, education,
relationships

Parental consent may be adequate, may need MHA
Parental consent may be adequate, may need MHA
Child <16y Young person 16–17y Adult ≥18y
If ≥16y, capacity is presumed. If concerns regarding capacity to make a decision, this can be assessed under the MCA.
If <16y, capacity is not presumed & MCA does not apply. Instead ‘Gillick competence’
must be assessed to decide whether child understands enough to make the decision.
Capacity depends on the decision – a child may be competent to consent/refuse a simple, low risk procedure, but not more complex, riskier ones
May lack competence/capacity due to age or a mental health disorder
If child has competence, should respect their decisions regarding
confidentiality/disclosure of information unless:
There is overriding public interest in the disclosure
Disclosure is required by law
If child lacks competence and refuses disclosure of information to parents you should:
Firstly try to persuade them to involve parents/carers
Disclose information to parents/authorities if you deem it necessary in child’s
best interests
Biological: usually less common/limited evidence as 1st-line treatment
consider in ADHD and depression
Psychological: most commonly used are CBT and family therapy
Social: very important – especially regarding education and social services
need good intra-agency working
Should encourage child to involve family/carers in their care if possible
Use of antidepressants in children/ adolescents
Concerns of suicidal behaviour in teens taking SSRI
Only prescribed by specialist (child psychiatrist)
FLUOXETINE = ONLY ANTIDEPRESSANT LICENSED FOR PAEDIATRIC USE (although
others sometimes used)
220 Chapter 6: Psychiatry
https://t.me/med1917
Eating disorders
Prevalence = 0.6% most common in adolescent girls.
General risk factors
Perfectionism
Body image disturbances
Weight stigma / teasing / bullying
Low self-esteem
Early sexual development
History of abuse
Personality disorder
FHx of eating disorders
Exposure to ‘diet culture’
Higher socioeconomic status
Comorbid mental illness
(e.g. anxiety disorders)
Peak onset = adolescence. F:M = 10.1
FEATURES
BMI <17.5
Persistent restriction of energy intake
Fear of gaining weight / becoming fat
Often excessive exercise (to compensate for food)
Lack of insight into seriousness of low BMI
Menstrual abnormalities
SYMPTOMS
DDx anorexia nervosa
Hyperthyroidism
Depression, anxiety, OCD
Psychosis, substance misuse
Body dysmorphic disorder
Poor prognostic factors
Low body weight
Late onset
Bulimic features
Family difficulties
Personality disorder
Longer illness duration
Poor support/relationships
Comorbid mental illness
10-year prognosis
50% recovered 40% chronic problem 10% mortality (1/3 suicide)
Indications for hospitalisation
Psychiatric: brain atrophy
Inflexible thinking
Obsessions/habits
Poor concentration
Irritable / flattened mood
Interests centre around
food
Heart
Low BP & pulse
Risk of arrhythmias &
heart failure
Metabolic disturbances: hypokalaemia, cortisol, GH & cholesterol, hormone levels
MANAGEMENT
Biological
Weight restoration risk refeeding syndrome
Regular monitoring weight, FBC, U&Es, LFT, glucose, bone profile, Mg2+,
CK, B12
± DEXA scan
± ECG prolonged QTc, HR <50, arrhythmias
Psychological*
Psychotherapies: CBT, motivational interviewing, compassion-focused,
interpersonal, family therapy
Family therapy if <18y
Social
Education: dietar y advice / multivitamins
Involve family/friends for support
Carer support
12
Reproductive:
hypothalamic changes
Reduced libido
Amenorrhoea (females)
Low testosterone (males)
Reproductive dysfunction
Muscles
Wasting/cramp
Bones: irreversible
Osteopenia/osteoporosis

Hair/skin
Broken skin, dry & brittle hair
Hair over face/body (lanugo)
Other
Cold extremities / hypothermia
Infections
Iron-deficiency anaemia
Leucopenia,
thrombocytopenia
Metabolic disturbances
BIOPSYCHOSOCIAL APPROACH
Treat coexisting mental health illness
e.g. SSRI for depression
*Psychological Tx has limited effect if BMI <13, so restore
weight first
BMI <13.5
Very deranged bloods
Syncope/arrhythmias
12
NICE (2017, updated 2020) Eating disorders [NG69]
FEATURES
https://t.me/med1917
Recurrent binge eating (no prominent weight changes)
Recurrent compensatory behaviour (vomiting, laxatives,
diuretics, fasting, exercise)
SYMPTOMS
Chapter 6: Psychiatry 221
Prevalence = 1% often a history / coexisting anorexia nervosa
 for 3m
Psychiatric
Poor concentration
Irritable
Mouth
Tooth decay/erosion
Hoarse voice
Bleeding
Swollen parotid glands
(‘chipmunk face’)
Hands
Russell sign: calluses, scars, abrasions on backs of fingers due to self­induced vomiting
Electrolyte imbalance:
can be life-threatening
Seizures
Muscle paralysis
Abdomen
Swollen/painful stomach
Constipation
Delayed gastric emptying
Reflux/oesophagitis
Rectal prolapse
Renal failure
Arrhythmias

MANAGEMENT13
Biological
Antidepressant SSRI (usually fluoxetine)
Advise laxative and alcohol cessation
Regular monitoring weight, FBC, U&Es, LFT, glucose and electrolytes
Psychological
Psychoeducation: regarding coping mechanisms
Psychotherapies: CBT, compassion-focused, interpersonal, family therapy
Social
Involve family/friends for support
Carer support
BIOPSYCHOSOCIAL APPROACH
10-year prognosis
70% recovered 1% mortality
Poor prognostic factors
Low body weight
Comorbid depression
13
NICE (2017, updated 2020) Eating disorders [NG69] & NICE BNF Fluoxetine
222 Chapter 6: Psychiatry
https://t.me/med1917
Intellectual disability
Significantly sub-average intellectual
functioning (IQ <70)
Impaired adaptive behaviour Onset of intellectual impairment
before 18y
Mild (85% cases) Moderate Severe Profound
IQ 50–69 35–49 20–34 <20 Prevalence 1.5–3% 0.5% 0.5% 0.05%
Functioning Only need help if
problems arise
Often not recognised as ID
prevalence in lower socioeconomic groups M>F
Association with overcrowding, poverty, irregular/unskilled employment
IQ tests are subjective – performed by clinical psychologists
May need supervision in some elements of daily living / work
Need help with many ADLs
Often physical disability
Limited communication
Extensive/total help with ADLs
Minimal communication
30% have no identifiable cause
GENETIC/CHROMOSOMAL CAUSES
Down syndrome
= trisomy 21
Most common chromosomal cause
Characteristic physical abnormalities
risk of deafness, cataracts,
hyperthyroidism, Alzheimer’s
Phenylketonuria
= autosomal recessive: 1 in 10,000 births
High serum phenylalanine
Epilepsy, hyperactivity, irritability
Short stature, hypopigmented, eczema
NB Intellectual disability (ID) is not same as autism spectrum disorders (ASD)
but often exist as comorbid conditions, along with epilepsy
Cri du chat syndrome
= deletion of short arm of chromosome 5
Fragile X syndrome
= abnormality on long arm of X chromosome
Most common genetic cause
More common in males
Elongated face / protruding
ears / microcephaly
Delayed development of speech & language by age 2y
Neurofibromatosis
= mutation on chromosome 7
Usually mild ID
Café au lait spots
Skin, bone, soft tissue, nervous system
abnormalities
Tuberous sclerosis
= mutated tumour suppressor gene chr 9 or 16
Results in autism & epilepsy with ID
Skin changes, brain/other tumours
PRENATAL, PERINATAL, POSTNATAL FACTORS
Prenatal Perinatal Postnatal
Fetal alcohol syndrome (most prevalent)
Congenital hypothyroidism
Pre-eclampsia
Placental insufficiency
TORCH infections
Birth trauma /
hypoxia
Intraventricular haemorrhage
Hyperbilirubinaemia
Brain infection/tumour
Head injury
Chronic lead poisoning
Malnutrition
Neglect/abuse
>50% of patients with ID have coexisting mental health problems
may present differently / patient has difficulty describing symptoms
Psychological therapies may need to be adapted/simplified
DIFFERENCES IN PRESENTATION:
Mania/bipolar
Challenging behaviour
Giggling
Delusions less elaborate
Depression
Exaggerated need for routine
Suicidal ideas rare & poorly planned
Less likely to complain of low
mood
Schizophrenia:
Delusions/hallucinations less elaborate
Persecutory delusions / thought disorder rare
Earlier onset
Presents as fear/withdrawal,
challenging behaviour, sleep disturbance
Perinatal psychiatry
https://t.me/med1917
Chapter 6: Psychiatry 223
All women should be screened at antenatal clinic for previous/current/FHx
of psychiatric disorder
Refer necessary cases for psychiatric assessment & referral
Regularly monitor mental state of all peri-/postnatal women, regardless
of whether they’ve been referred
WHO TO REFER?
1. PHx ± FHx of:
Schizophrenia/psychosis
Bipolar disorder
Puerperal psychosis
Severe depression i.e. required secondary care input (depression treated by
GP doesn’t need referral)
2. On mood stabilisers
Pregnant/postpartum women should have priority in psychiatric service pathways
NORMAL PSYCHIATRIC SYMPTOMS Due to hormonal changes ± physical & emotional exhaustion
‘The Pinks’: within 48h postpartum
Excitement, euphoria, overtalkative, overactive, insomnia
spontaneous resolution
‘The Blues’: day 3–10 postpartum
Emotional lability, tearful, anxious, irritable Does not affect functioning (most do not
develop PPD)
spontaneous resolution after 48h
POSTPARTUM DEPRESSION (PPD) bipeak onset at 2–4w & 3m postpartum
Symptoms:
Similar to normal depressive illness with more prominent anxiety
guilt & concerns over parental ability = common anxious preoccupation with baby’s health
reduced affection for baby / impaired bonding
obsessional phenomena (ego-dystonic in nature e.g. harming baby)
Edinburgh Postnatal Depression Scale: used to assess Sx during & after pregnancy
Puerperium: period of about 6w after childbirth

Important to identify at-risk women antenatally so we can effectively manage risks
Assess risk to baby
Obsessional/delusional Sx
Determine baby’s location & carer
Prevalence of PPD: 10%
  

Risk factors for postpartum depression
Previous episode of PPD / FHx of PPD
Depression during pregnancy
Hx of major depressive disorder
Management
Psychotherapy: CBT
SSRIs = 1st line (sertraline/paroxetine) may give prophylactically after birth
if high risk
Prognosis With Tx: 2/3 resolve within 2–3m No Tx: can take >6m to recover
children of treated mother experience fewer psychiatric symptoms/disordersif untreated, can result in insecure attachments, psychiatric problems in child, child less
compliant with their own health visits
POSTPARTUM BIPOLAR DISORDER highest risk 9–14d postpartum
Often affects those with Hx of bipolar disorder
high risk of relapse in pregnancy due to discontinuation of teratogenic mood stabilisers should consider continuing mood stabilisers that are safer to use in pregnancy
14
NICE (2014, updated 2020) Antenatal and postnatal mental health [CG192]
RISK ASSESS
Predictors of PPD
Anxiety in pregnancy
Stressful life events
Marital discord
Povert y
Small amounts transferred in breast milk but can still breastfeed
e.g. lamotrigine
224 Chapter 6: Psychiatry
https://t.me/med1917
Prevalence: 0.2%
 


Risk factors for postpartum psychosis
Previous PPP
Hx of bipolar disorder
Other RFs: primiparity, unmarried, obstetric complications
PUERPERAL/POSTPARTUM PSYCHOSIS (PPP) onset normally within 2–3w postpartum
Symptoms:
sudden onset behavioural disturbances
hallucinations/delusions – often a religious context
Management15: treat as EMERGENCY
Admission to mother & baby unit may need MHA
High intensity physical & psychological care including:
mood stabiliser ± antipsychotic treatment of anxiety & insomnia
Support services: support groups, help with childcare/housework etc.
Prevention of PPP and BPAD
If treatment for ongoing BPAD/psychosis stopped during pregnancy, restart immediately after delivery
If history of BPAD, continue treatment during pregnancy and postpartum
If history of PPP/BPAD in postpartum only, start treatment immediately after delivery
prophylactically

RISK ASSESS
Prognosis Good short-term progress if treated early: most severe symptoms last 2–12w, most make
full recovery within 12m
BUT associated with significant morbidity & mortality
Valproic acid Avoid in pregnancy & breastfeeding
Lithium Avoid in breastfeeding Lamotrigine Safe in pregnancy & breastfeeding
Atypical antipsychotics Safe in pregnancy & breastfeeding Sertraline/paroxetine Safe in pregnancy & breastfeeding (low levels in breast milk) Fluoxetine Safe in pregnancy & breastfeeding (higher levels in breast milk)
15
NICE (2014, updated 2020) Antenatal and postnatal mental health [CG192]
225
https://t.me/med1917
DERMATOLOGY
Psoriasis ...................................................................................... 226
Acne vulgaris
Eczema.........................................................................................228
Skin infestations Bacterial skin infections Viral skin infections
ABBREVIATIONS
ABPI – Ankle brachial pressure index ACEi – Angiotensin-converting enzyme
inhibitor
BCC – Basal cell carcinoma DLQI – Dermatology Life Quality Index EASI – Eczema Area & Severity Index HHV – Human herpes virus HPV – Human papillomavirus HSV – Herpes simplex virus IBD – Inflammatory bowel disease
.......................................................................... 227
..................................................................229
................................................. 230
...........................................................232
ICU – Intensive care unit LN – Lymph node OCP – Oral contraceptive pill PASI – Psoriasis Area & Severity Index PCOS – Polycystic ovary syndrome PDT – Photodynamic therapy SA – Surface area SCC – Squamous cell carcinoma SJS – Stevens–Johnson syndrome
07
Fungal skin infections Melanocytic (pigmented) lesions Non-melanocytic lesions Dermatological manifestations ofsystemic
disease
Drug eruptions
.................................................................................. 238
...................................................................... 240
...................................................... 234
............................236
................................................ 237
SSMDT – Specialised Skin Multidisciplinary
Team
TEN – Toxic epidermal necrolysis TNF – Tumour necrosis factor UC – Ulcerative colitis URTI – Upper respiratory tract infection UVA – Ultraviolet A UVB – Ultraviolet B VZV – Varicella zoster virus
Definitions of terms
Term Description
Eruption Rash Lesion Any small area of skin disease Macule Flat (non-palpable) area of colour change <0.5cm Patch Flat (non-palpable) area of colour change >0.5cm Papule Raised (palpable) lesion <0.5cm – usually dome-shaped Nodule Raised (palpable) lesion >0.5cm – usually dome-shaped Cyst Fluctuant papule/nodule containing fluid/pus/keratin Plaque Palpable, flat-topped lesion Vesicle Fluid-filled lesion/papule <0.5cm Bulla Fluid-filled lesion/papule >0.5cm Pustule Pus-filled lesion Wheal/weal Smooth, skin-coloured superficial swelling lasting <24h (often surrounded by erythema) Erosion Partial break in skin: loss of epidermis only Ulcer Complete break in skin: dermis included Fissure Small, slit-like break in skin Excoriation Erosion or ulcer due to scratching Lichenification Thickening of skin and increased markings due to chronic scratching/rubbing Scale Visible white loosening of outermost skin layer Crust Golden deposit on skin due to dried plasma
226 Chapter 7: Dermatology
https://t.me/med1917
Psoriasis
Bi-peak onset: early 20s & 50s 2% population (M=F)
Things that impact the patient:
Chronic, relapsing inflammatory skin disorder ( skin turnover & epidermal thickening)
Presentation
Red, scaly plaques with sharp demarcation – extensor surfaces + scalp
Psoriatic arthritis – in around 30%
Symptoms: pain, itching, bleeding
Psychological: self-esteem
Treatment: time-consuming & messy
Complications:
risk CVD, metabolic syndrome, lymphoma
Linked with other inflammatory conditions:
cardiovascular disease, metabolic syndrome, NASH (non-alcoholic steatohepatitis)
Other diseases associated with HLA gene:
lymphoma, asymmetric anterior uveitis, IBD
Fig. 7.1
Risk factors
1. Genetics: FHx, HLA-CW6, HLA-B27, HLA-B13, HLA-B17 genes
2. Environmental:
Strep throat infection, HIV
Medications – BBs, antimalarials, lithium, TNF-α inhibitors
Stress, alcohol, smoking, trauma (Koebner phenomenon)
Management
depends on severity & impact on patient*
1. EDUCATION: avoid lifestyle triggers e.g. smoking/alcohol/stress
2. TOPICAL TREATMENTS
Emollients e.g. E45
Corticosteroids + vit D analogues (mild/moderate ifsensitive area)
Keratolytics e.g. 5% salicylic acid for thick plaques
Coal tar products (used on scalp)
3. PHOTOTHERAPY = needs 2° care referral
Narrow band UVB = superficial (good if pregnant)
PUVA (psoralen tablets + UVA) = deeper (not if pregnant)
4. SYSTEMIC TREATMENTS
Therapy Side-effects Monitoring
Methotrexate Teratogenic, hepatotoxic, bone marrow suppression,
Acitretin Ciclosporin
1
GI upset/nausea
Teratogenic, hepatotoxic, lipids
Nephrotoxic, BP, tingling peripheries
*PASI/DLQI scores assess severity & impact
Avoid vit D analogues in pregnancy or breastfeeding!
LFTs, FBC
LFTs & fasting lipids BP, U&Es
5. BIOLOGICS (monoclonal antibodies) for severe or recalcitrant disease
Topical steroid use
Mild 1% hydrocortisone Any Moderate Eumovate (clobetasone) Caution on face Potent Betnovate (betamethasone) Adults V. potent Dermovate (clobetasol)
age
only
Anywhere
Not face/ genitals
Phototherapy
UV light exposure causes immunosuppression & skin inflammation UVB
or PUVA
2–3 × a week for 15–30 episodes
Base starting dose on skin type & gradually
time of exposure
Indications: acne, vitiligo, psoriasis, lichen planus Side-effects
Of UV: erythema/pruritus, cold sores, skincancer Of tablets: nausea & headaches
1
NICE (2012, updated 2017) Psoriasis [CG153]
Side-effects
Skin thinning
Can trigger acne/rosacea
Withdrawal can cause erythroderma
Reassure
Only very short exposure (secs–minutes) Dose is carefully calculated for skin type Goggles protect eyes & genitalia covered