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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
Temporal arteritis(E OHAM4p. 682.)
SymptomsHeadache, jaw pain on eating, visual problems, aching muscles.
SignsTemporal artery, tender scalp, pulseless/ nodular temporal artery.
Investigations blds ii ESR (>50mm/ h), iCRP, iplts, dHb all suggestive; de-
nitive diagnosis requires biopsies (multiple sites) ≤wk of starting therapy.
Treatment Start 60mg/ 24h prednisolone PO and strong analgesia.
Discuss with on- call surgeon/ ENT to arrange urgent out- patient biopsy
and liaise with ophthalmology to exclude visual complications; Doppler
USS of the artery can be helpful. Out- patient rheumatology follow- up.
ComplicationsBlindness (0– 50%), TIA/ stroke.
Migraine(E OHCM1p. 454.)
$ Recurrent, pulsatile headaches with strong familial tendency. Suspect an
alternative pathology if sudden onset, or >55yr with no previous migraines.
Symptoms Throbbing headache, initially unilateral often with nausea
±vomiting, photophobia; 20% may experience a preceding aura (ashing
lights, zigzags, visualloss).
SignsMay mimic TIA (visual defects, focal neurology) but sloweronset.
InvestigationsNormal; perform blds, CT, LP as required to rule out alter-
native/ coexistent pathology.
Treatment Abortive Simple analgesia (E pp. 92–4), ±anti emetic, ±5HT
agonists (eg sumatriptan);
Preventative β- blocker (eg propranolol), or
anti epileptics (eg topiramate).
Sinusitis
$ Inammation of the mucosa of the paranasal sinuses due to bacteria,
viruses, or fungi; may become chronic.
SymptomsBlocked nose, nasal discharge, facial pain, unable tosmell.
Signs Tender over sinuses (above medial eyebrows, bridge of nose,
below eyes), purulent nasal discharge, temp usually normal.
TreatmentTry a mixture of beclometasone nasal spray 2 sprays to each
nostril/ 2h ±ephedrine nasal drops – 2 drops in each nostril/ 6h (7d
max) ±saline NEB 5mL/ 2– 4h. If severe (eg purulent mucus, systemically
unwell) prescribe amoxicillin 500mg/ 8hPO.
ComplicationsLocal spread of infection, chronic sinusitis, meningitis.
Cluster headaches
$ Recurrent, short- lived, severe, unilateral headaches occurring up to several times/ day (often in early morning). Patients become agitated during
attacks, and may experience rhinorrhoea, lacrimation, or facial sweating.
Treatment Abortive5HT
PreventativeCa
agonists (eg sumatriptan nasal spray), 5L/ minO2;
2+
channel blockers (eg verapamil), lithium.
Post- dural punctureUsually presents within 4– 5d of LP, epidural, or
spinal anaesthetic (rarely up to 7d); lie patient at, treat with analgesia
and iuid intake (especially caeinated drinks). Contact anaesthetist if
severe/ persistent to consider epidural bloodpatch.
3
Hypertensive crises Hypertension usually represents a response
to pain of headache and responds to headache treatment. However, BP
>200/ 20mmHg may represent the cause of a headache (Ep. 276).
373HEADACHE
374 CHAPTER2 Neurology
Dizziness
2Worrying features Hypoxia, iHR, irregular HR, dBP, dglucose,
chest pain, sudden onset, unable to stand, loss of consciousness.
Think about Vertigo Labyrinthitis, vestibular neuronitis, benign pos-
itional vertigo, trauma, ototoxic drugs, Ménière’s, CVA, multiple sclerosis, acoustic neuroma;
Wernicke’s encephalopathy, CVA, cerebellar space- occupying lesion,
intracranial infection, vitamin B
alus;
Syncope/ presyncope(Epp. 464–5).
Ask about See Box 2.2;PMH Previous dizziness, iBP, DM, MS,
IHD;
DH Antihypertensives, diuretics, aminoglycosides, insulin, oral
hypoglycaemics;
ObsTemp, HR, lying and standing BP, glucose,GCS.
Look for Ability to stand, gait; Romberg’s test (Box 2.3), change with
position, cerebellar signs (DANISH— dysdiadochokinesia, ataxia, nystagmus,
intention tremor and past pointing, slurred speech, hypotonia), focal neurology, examine ear using otoscope (eusion, perforation); irregularpulse.
InvestigationsThe type of dizziness (vertigo, ataxia, postural, syncope)
should be determined from history alone; if syncope is suspected, investigate for cardiogenic causes (E p. 274); for vertigo and ataxia, acute investigation is rarely required; consider a
suspected or there are cerebellar signs;
K Box 2.2 Key questions in‘dizziness’
The sensation of dizziness is dicult to describe (‘giddy’, ‘funny do’, ‘muzzy
headed’) and reects some critically dierent underlying pathologies; try to
map your patient’s symptoms onto a medical equivalent by askingabout:
•
Loss of consciousness Suggests seizures (E p. 361) or syncope (E p. 274).
An impending sense of loss of consciousness, often with a ‘greying out’ of
vision, is described as presyncope; management is similar to syncope
• Postural symptoms Worse on standing after a sedentary period; this suggests
postural hypotension and should prompt a review of medications
• Vertigo Is the sensation of the world moving or spinning about the patient
and is worse on sudden head movements; this suggests a problem with the
labyrinth, vestibular nerve, or brainstem (Ep. 375)
• Ataxia Is shown by the inability to stand or walk straight; patients may
have problems with ne limb movements; this suggests problems with
proprioception or cerebellar function (Ep. 375).
Always ask about onset, deterioration, hearing loss, tinnitus, nausea, vomiting.
Imbalance Hypoglycaemia, alcohol intoxication,
deciency, normal pressure hydroceph-
2
SHAlcohol.
CT head if a stroke or tumour is
Audiometry If vestibular features.
K Box 2.3 Romberg’stest
The cerebellum normally receives information needed to keep us upright
from two sensory systems:vision and proprioception (via the spinal dorsal
columns). Normally, one system can compensate for loss of the other. With
the eyes closed and the feet placed together, a patient who sways excessively
or falls is ‘Romberg +ve’, having lost proprioception. With a cerebellar lesion, the patient will struggle to maintain posture even with the eyes open.
6
Described by the pioneering C9th German neurologist Moritz Romberg, working among the
destitute of Berlin with tabes dorsalis (tertiar y neurosyphilis).
6
Vertigo(E OHCS1p. 404.)
2Worrying features Focal neurology, multidirectional or non- fatiguing
nystagmus.
Treat sensation of vertigo while determining underlying cause. Centrally acting
antihistamines (eg cyclizine 50mg/ 8h PO) and phenothiazines (eg prochlorperazine 5mg/ 8h PO) are eective; betahistine 6mg/ 8h PO is also used.
Benign positional vertigo Sudden- onset vertigo lasting seconds following
specic head movements. Treated with Epley manoeuvre (a series of
movements to dislodge the vestibular debris causing the symptoms; E
OHCS1 p. 405) and referral to physiotherapy for vestibular exercises.
Inner ear inammationThis causes sudden- onset vertigo, nystagmus, and
severe nausea without focal neurology. Reassure and treat asabove.
Vestibular neuronitis Viral infection of the vestibular nerve; improves
within – 2wk but can take 2– 3mth to fully resolve.
LabyrinthitisAs for vestibular neuronitis with hearing loss or tinnitus.
Ménière’sAttacks of severe vertigo lasting several hours, with tinnitus and
progressive low-frequency hearing loss. Treat as above, and refer to ENT.
Motion sicknessCinnarizine 30mg PO 2h before journey is eective.
Cerebellar infarction Acute vertigo without other neurological features.
Head impulse test negative.
NystagmusThis is found with many peripheral and central causes of ver-
tigo. Causes include:stroke, MS, space- occupying lesions, labyrinthitis,
vestibular neuronitis, benign positional vertigo, trauma, drugs of abuse
(alcohol, LSD, PCP, ketamine), medications (lithium, SSRIs, phenytoin),
Ménière’s, Wernicke’s encephalopathy; congenital (rare).
Imbalance/ ataxia
Ataxia can be dierentiated from vertigo on history; there are twotypes:
Cerebellar‘DANISH’ signs (see earlier in this topic); unstable with eyesopen.
Sensory Romberg’s +ve (Box 2.3), loss of proprioception, preserva-
tion of ne coordination; ‘stamping’ gait, spinal/ neuropathysigns.
Cerebellarataxia
CausesCVA, multiple sclerosis, alcohol toxicity, Wernicke’s encephalop-
athy, phenytoin, vitamin B
infection, space- occupying lesions, trauma, paraneoplastic.
ManagementMRI is the most useful diagnostic test (consider CT if acute
deciency, normal pressure hydrocephalus,
2
onset), neurology referral, some underlying causes are treatable:
• Wernicke’s encephalopathy Thiamine (vitamin B
of chronic alcohol excess results in confusion, ataxia, ophthalmoplegia, and
) deciency often as a result
nystagmus; treated with thiamine (PO/ IV, E p. 216), as for Korsako’s
syndrome, to which it may progress if left untreated.
Sensoryataxia
CausesCervical spondylosis, MS, peripheral neuropathy, syringomyelia, spinal
tumour, spinal infection, vitamin B
ManagementUrgent MRI if acute onset, otherwise consider tests for per-
deciency, Friedreich’s ataxia, syphilis.
2
ipheral neuropathy (E p. 357), spinal X- rays, routine MRI, nerve conduction studies, neurology referral; often treated with vitaminB
.
2
375DIZZINESS
Chapter3
Psychiatry
2Aggressive behaviour emergency 378
Mental Health Act (MHA) 379
Alcoholism 380
Aggression and violence 38
Acute confusion 382
Dementia 384
Mood disturbance/psychosis 386
Anxiety disorders 390
Insomnia 39
377
378 CHAPTER3 Psychiatry
2Aggressive behaviour emergency
2Safety
• Stay between the aggressor and theexit
• Get extra help from other sta and/ or security
• Consider phoning the police.
Aggression often stems from fear. Agitated patients are usually frightened, so try to remember this when approaching the situation.
Regardless, the safety of yourself and others is paramount at alltimes.
3Call for
•
Assess the safety— is anyone at acuterisk?
• Attempt to
senior help/ security early if the situation is deteriorating.
defuse the situation, maintain your own safety at alltimes
• Try to establish the precipitant from sta/ relatives (Box3.)
• Ask a
member of sta who knows the patient to accompanyyou
• Invite the patient to
•
Listen until they feel they have explained the problem
•
Assess the patient for signs of psychosis or acute confusion— are they
sit down with you and discuss the problem
physiologically unwell, psychologically disturbed, or angry?Why?
•
Apologize and/ or oer sympathy as appropriate
•
Address any concerns raised by the patient
•
Ask specically about pain orworry
• Consider oering
• Emergency sedation if they are a risk to themselves or others:
•
lorazepam – 2mg (mg elderly/ renal failure) PO/ IM/ IVSTAT
•
haloperidol 5– 0mg (2mg elderly) PO/ IM/ IVSTAT
•
can be used together or separately.
oral sedation or analgesia
2Box 3. Commoncauses of aggressive behaviour
• Acute confusion (delirium)Epp. 382–3
• Intoxication (drugs/ alcohol)
• Psychosis due to an underlying psychiatric disorderEpp. 386–9
• Anger/ frustration/ poor communicationEp. 23
• PainEpp. 92–5
• HypoxiaEp. 284
• Hypoglycaemia Ep. 337
If a patient poses a risk to themselves or others any doctor can give emergency sedation, without
the patient’s consent and with restraint, under the Mental Capacity Act (2005).
Mental Health Act(MHA)
In England and Wales, this Act allows the hospitalization of individuals
who are believed to be aected by a mental disorder (alcohol and drug
addiction alone are insucient)that:
• requires assessment (under section 2)or treatment (under section 2 or3)
and
• is suciently serious to pose a threat to self or othersand
• requires hospitalization to which they are unable/ unwilling to consent.
If you feel this applies to your patient, speak to your seniors and the
psychiatrist on call urgently. They may recommend an urgent MHA assessment to consider detention under section 2 (if further assessment required) or 3 (if patient well known and symptoms typical). See Table3..
2These powers cannot be used to detain for treatment of physical illness,
unless the direct consequence of the mental disorder (eg self- harm,
weight loss in anorexia nervosa). Patients under the MHA may have capacity to decide on treatment for physical health unrelated to their mental
illness. In this case, treatment decisions should be based upon an assessment of capacity which is decision specic (Ep. 30).
Table3. Key sections ofthe Mental Health Act,2007
Section 2 A period of assessment and treatment which lasts for up to
Section 3 Admission for treatment up to 6mth. Is renewable for a further
Section 4 Emergency admission for assessment. Lasts 72h. Requires
Section 5(2) Issued by a doctor. Allows detention of an informal patient
Section 5(4) Issued by a mental health nurse. Allows detention of an
Section 7a Supervised community treatment order
Section 36 Allows police to arrest a person in a public place and who is
28d. Not renewable. An approved mental health professional
(AMHP) makes the application on the recommendation
of two doctors. An AMHP may be a social worker, nurse,
occupational therapist, or psychologist
6mth and annually thereafter. AMPH makes the application on
the recommendation of two doctors
one medical practitioner and AMHP to enact. Can be used if
admission under section 2 would cause an undesirable delay
for up to 72h. Designed as an emergency order in order for a
Mental Health Act assessment to take place
informal patient for up to 6h until doctor assessment
believed to be suering from a mental disorder. Lasts up to 72h.
The person is taken to a place of safety (eg ED)
379MENTAL HEALTH ACT(MHA)
2Familiarize yourself with local legislation before you have to use it.
The Mental Health (Care and Treatment) (Scotland) Act 2003 and The
Mental Health (Northern Ireland) Order 986 provide similar frameworks for emergency hospitalization but precise powers do dier.
380 CHAPTER3 Psychiatry
Alcoholism
Alcoholism Many patients will drink over the recommended limits
(4units per week ♂ and ♀), but not all of these will be ‘alcoholics’.
Dening alcoholism is hard; if drinking, or its eects, repeatedly harms
work or social life it is clearly a problem. Answering ‘yes’ to three out of
four of the
down on your drinking? Have people Annoyed you by criticizing your
drinking? Ever felt Guilty about your drinking? Ever had an Eye- opener
in the morning?
Excessive drinking can be a psychiatric issue in its own right but can also
complicate many psychiatric diseases. Modifying drinking behaviour is
dicult and patients must want to change.
Abuse Excessive drinking despite mental or physicalharm.
DependenceAlcohol tolerance, withdrawal when not drinking.
Alcoholism management Have a low threshold for commencing
benzodiazepine therapy to avoid withdrawal (E Table5.2 or your local
protocol). Start vitamin B
oral thiamine and multi- vitamins.
Untreated, thiamine deciency can lead to Wernicke’s encephalopathy
(E p. 375). Characterized by a triad of nystagmus, ophthalmoplegia,
and ataxia, but can also present with confusion, altered consciousness, vomiting, and headache. Untreated it can progress to Korsako ’s
syndrome characterized by an irreversible anterograde memory loss and
confabulation. Both are treated with Pabrinex
memory loss in Korsako ’s is usually permanent.
Other management Alcohol diaries, reduced intake/ abstinence plans,
counselling, eg Alcoholics Anonymous, medication, eg disulram, address underlying social and psychiatric problems.
Alcohol withdrawal(OHAM4 Ep. 436.)
Symptoms 2– 36h post- alcohol: anxiety, shaking, sweating, vomiting, tonic–
clonic seizures; 3– 4d post- alcohol: delirium tremens may develop:coarse
tremor, confusion, delusions, hallucinations (untreated mortality5%).
SignsHTN, iHR, sweaty, tremor, dglucose; delirium tremens: pyrexia.
Investigations bldsMay have dMg
LFTs and consider investigation for chronic liver disease.
Treatment Prescribe reducing dose of chlordiazepoxide (E Table 5.2);
correct electrolyte abnormalities; give vitamin replacements PO (thiamine 25mg/ 24h and vitamin B (compound strong) one tablet/ 24h) or IV
(Pabrinex
drawal seizures are usually self- limiting, treat as E p. 359 if required.
ComplicationsSeizures, coma, encephalopathy, hypoglycaemia.
CAGE questions suggests alcoholism:Ever felt you should Cut
supplementation with either IV preparations or
®
or oral thiamine, but the
2+
3−
, dPO
, dCa2+, dK+, and durea. Check
4
®
2 pairs/ 8h IV for 5d). Monitor BP and blood glucose. With-
2
2
NICE guidelines available at M guidance.nice.org.uk/ CG5
Aggression and violence
The majority of patients have respect for NHS sta; however, under
certain circumstances anyone can become aggressive:
• Pain (Epp. 92–5)
• Reversible confusion or delirium, eg hypoglycaemia (Epp. 336–7)
• Dementia (Epp. 384–5)
• Inadequate communication/ fear/ frustration (Ep. 22–3)
• Intoxication (medications, alcohol, recreationaldrugs)
• Mental illness or personality disorder (E pp. 386–9).
The aggressive patient Ask a nurse to accompany you when
assessing aggressive patients. Position yourselves between the exit and the
patient and ensure that other sta know where you are. The majority of
patients can be calmed simply by talking; try to elicit why they are angry
and ask specically about pain and worry. Be calm but rm and do not
shout or make threats. If this does not help you may have to call hospital
security or the police in a GP setting. It may be appropriate to oer an
oral sedative or give emergency IM/ IV sedation (E p. 378). Mental health
nurses are trained in how to give both IM and IV sedation. In a GP setting,
add an alert to the patient’s records to detail the incident and inform the
practice manager.
The aggressive relative Relatives may be aggressive through fear,
frustration, and/ or intoxication. They usually respond to talking, though
make sure you obtain consent from the patient before discussing their
medical details. Consider oering to arrange a meeting with a senior
doctor. If the relative continues to be aggressive, remember that your
duty of care to patients does not extend to their relatives; you do not
have to tell them anything or listen to threats/ abuse. In extreme cases you
can ask security or police to remove the relative from the hospital.
Violence Assault (the attempt or threat of causing harm) and battery
(physical contact without consent) by a patient or relative is a criminal offence. If you witness an assault or are assaulted yourself, inform your seniors
and ll in an incident form including the name and contact details of any witnesses. If no action is taken on your behalf, inform the police yourself.
Abuse Abuse is a violation of an individual’s human and civil rights and
may consist of a single act or repeated actions. It may be physical, sexual,
nancial, psychological, or through neglect. Patients of any age can be
abused. Do not be afraid of asking patients how they sustained injuries or
asking directly if someone caused them. Inform a senior if you suspect a
patient has been abused (E Box 2.3). Have a low threshold for involving
adult/ child safeguarding teams where you have concerns.
381AGGRESSION AND VIOLENCE
382 CHAPTER3 Psychiatry
Acute confusion
$ Delirium or acute confusional state is a common but easily missed
diagnosis associated with increased morbidity and mortality. Delirium
can aect any patient but is especially common in the hospitalized
elderly, where it may be misdiagnosed or herald dementia (or it may
coexist in up to 50%). Unlike dementia, delirium is often uctuating
(Box 3.2), worse at certain times of day and may persist for months.
There are two subtypes:hypoactive (higher mortality) and hyperactive.
2Beware the quietest and loudest patients on theward.
Risk factors for delirium Age >65yr, cognitive impairment/de-
mentia, hip fracture, severe illness.
Think about 2Emergencies dO
meningitis, encephalitis, anticholinergic medications;
metabolic (dglucose, dNa
lithium, serotonin syndrome, neuroleptic malignant syndrome, post
GA), heart failure, head injury, alcohol withdrawal or intoxication, postictal, urinary retention, constipation,pain, and unfamiliar environment.
Ask about Use direct questions to assess eg for pain; further history
from the ward sta, relatives, notes, or residential/ nursing home: speed
of onset, chest pain, cough, sputum, dysuria, frequency, incontinence,
head injury, headache, photophobia, vomiting, dizziness;
heart, lung, liver, or kidney problems, epilepsy, dementia, psychiatric
illness;
DH Benzodiazepines, antidepressants, opioids, steroids, NSAIDs,
antiparkinsonian drugs; anticholinergics, antispasmodics, antiepileptics,
antipsychotics;
SHAlcohol, recreational drugs, baseline mobility andstate.
ObsGCS (E Table2.2), temp, HR, BP, RR, O
Look for Respiration Rate, depth, added sounds, cyanosis; Pulse Rate
and rhythm;
Neuro Signs of head injury, pupil responses, neck stiness, photophobia,
Abdomen Rigidity, palpable bladder; PR Faecal impaction;
focal neurology, plantar responses;
Investigations UrineDipstick,M,C+S; blds FBC, U+E, LFT, CRP, glucose,
2+
Ca
, consider cardiac markers, blood cultures, amylase, TFT, B2, folate;
ABG dO
±diCO2; ECG Arrhythmias; CXR Infection or aspiration; CT If
2
focal neurology, head injury, or non- resolving confusion;
Management
• Nurse in a quiet, appropriately lit environment with close, supportive
observation (relatives, ‘special’ nurse); avoid restraints. Optimize
hearing, vision, sleep, and nutrition.
• Investigate and reverse the underlying cause. Think
Infection, Constipation, Hydration, Medication, Environment.
• Sedate only if patient or sta safety threatened; use oral route where
possible (eg haloperidol 0.5– mg PO/ – 2mg IM every – 2h, max
5mg/ 24h; if PMH Lewy body dementia, alcohol excess, or Parkinson’s,
lorazepam 0.5– mg PO/ IM every – 2h, max 2– 4mg/ 24h).
3
NICE guidelines available at Mguidance.nice.org.uk/ CG03
4
Typically ‘out- of- hours’, when you may be asked to review while on call.
5
Inouye SK, etal. Ann Intern Med 990;3:94 (requires subscription).
3
, iCO2, MI, CVA, intracranial bleed,
2
+
), drug toxicity (opioids, benzodiazepines,
sats.
2
Common Sepsis,
AMT(Table3.2); Drug chart.
LPIf CT normal.
PInCH ME:Pain,
PMH DM,
3,4