Download - Cause or Consequence? - HKGS
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Inter-hospital Geriatric Meeting
Cause or Consequence ?
Presenter: Dr. King-Son LAI (TPH)
Chairperson: Dr. Catherine CHUI (TPH)
25 October 2013
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Case History
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M/88Y
• Ex-smoker and non-drinker
• Retired construction site worker
• Lived and cared by maid ; wife moved to OAH
in 4/2012 after fall injury
• Admitted for syncope and fall in 3/2013
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Past Medical History
A. Parkinson’s disease (diagnosed in 2005)
• Impaired mobility, in the form of small-stepped gait +
limb rigidity ; no mask face or hand tremors
• CT-Brain: ‘prominent ventricles and cerebral sulci ,
likely age-related cerebral atrophy ; no space-
occupying lesions or haematoma’
• Previously had rehabilitation at AHNH GDH
• Able to walk with stick under supervision
• No recent mobility deterioration
• No recent fall episodes
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Past Medical History
B. Vitamin B12 deficiency
• No sensory (proprioception) deficit
• OGD in 2008: No atrophic gastritis
• Vitamin B12 level 100 , anti-PA weakly +ve ; Hb
12.0 and MCV 96.0 ; folate / TSH normal
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Past Medical History
C. Hypertension
• Baseline BP 130/70 mmHg on drugs
• CXR: Heart size not enlarged
• ECG: SR , LVH by voltage
D. Diabetes mellitus
• HbA1c 7.2% , baseline H’stix 6-10
• Background retinopathy ; no nephropathy
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Medications
1. Sinemet 25/100 , tab 1 tds
2. Lisinopril 5mg daily
3. Amlodipine 5mg daily
4. Metformin 500mg BD
5. Vitamin B12 , 1mg IM injection 3-monthly
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Presenting Complaint
• Witnessed collapse at home at ~8am , 21/3/2013
• Some ‘cloudiness’ in thought at the time of fall ,
then regained full consciousness shortly
afterwards (within few minutes)
• According to maid , patient had the collapse just
after he went out from toilet
• No witnessed seizures , no incontinence
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Admission to AHNH
Assessment at AED
• BP 145/85 mmHg , pulse 90 bpm regular
• GCS 15/15 , PEARL (pupil size 2mm)
• Limb power 5/5 in 4 limbs ; bilateral upper
limb cogwheel rigidity ; reflexes not brisk ;
plantar down-going on both sides
• No heart murmurs
• No carotid bruits
• Chest clear , abdomen soft and non-tender
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Investigations
• ECG: NSR at 88 bpm
• CXR: Clear lung fields
• SXR , X-ray Pelvis: No fracture
• CT-Brain: Cerebral atrophy , thin rim (4mm) of
bilateral fronto-parietal subdural effusions
without acute haematoma , no mass effects
→ PWH-NS : likely chronic , for observation and
repeat CT-Brain 2 weeks later
• H’stix 6.6 ; CBC , R/LFT all unremarkable
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Transferral to TPH (21/3/2013 afternoon)
History clarification (the collapse)
• Attended toilet uneventfully , could urinate smoothly on
standing , denied excessive straining during voiding
• No fall / impact on objects in toilet
• ‘Felt a sense of dizziness and tendency to fall ; then only
found himself lying on the floor with many people
surrounding himself’
• The ‘dizziness’ was not spinning in nature
• No lower limb weakness or pain before the ‘dizziness’
• No chest pain , palpitations , sweating , hunger sensation
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Transferral to TPH
History clarification
•No history of syncope / severe dizziness / vertigo all
along
•Did not recall any fall episodes until this hospitalization
•Independent up to dressing ; supervision in toileting and
bathing
•Goes out to have short walk in nearby park in the
afternoon with maid , about 3-4 times weekly
•Had taken drugs in the morning as usual
•Not yet taken breakfast
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Transferral to TPH
History clarification
• Drugs prepared and given by maid , no side-effects /
complaints according to patient and maid
• HBPM at home : average ~135/75 mmHg , range
128-152/68-91 mmHg ; pulse ~85 bpm (readings
mostly taken in the morning)
• Infrequent HBSM monitoring , usually H’stix 5–7
(readings few times monthly)
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Postural BP and H’stix
(21/3) 140/72 mmHg → 132/65 mmHg ; H’stix 5.6
(22/3) 145/78 mmHg → 142/81 mmHg ; H’stix 5.4
(23/3) 139/70 mmHg → 121/61 mmHg ; H’stix 4.6
(24/3) 133/68 mmHg → 127/69 mmHg ; H’stix 5.9
(25/3) 138/81 mmHg → 130/74 mmHg ; H’stix 4.4
(26/3) 143/80 mmHg → 126/70 mmHg ; H’stix 6.1
(27/3) 135/75 mmHg → 139/72 mmHg ; H’stix 5.8
All taken in the morning ; patient denied any symptoms all along
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Working Diagnoses
1) Syncope
(micturition-related ± orthostatic hypotension)
2) Underlying Parkinson’s disease
3) ? Hypoglycaemia
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Topic Discussion
A. Syncope
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The ‘dizziness’ symptom
• Pre-syncope – sensation of impending faint ,
related to many underlying causes
• Vertigo – sensation of spinning / angular
motion , related to disturbance of vestibulo-
basiliar function
• Dysequilibrium – sensation of imbalance /
unsteadiness , mostly related to disturbance of
neuro-sensory structures
• ‘Non-specific dizziness’
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Syncope
• Faint and transient loss of consciousness
± fall / collapse , followed by spontaneous and
complete recovery , if no other complications
occur
• A result of transient cerebral hypoperfusion of
just a few seconds
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Epidemiology
The incidence rates of syncope per 1000 person-years of follow-up increased with age among both men and women. The increase
in the incidence rate was steeper starting at the age of 70 years. Syncope rates were similar among men and women.
Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347:878.
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Subtypes of Syncope
• Neurally-mediated (~25%)
– Vasovagal attacks (~20%)
– Situational (e.g. cough / swallowing / micturition) (~5%)
• Hypotension (~30%)
– Orthostatic (hypovolaemia / drugs / prolonged standing /
autonomic dysfunction)
– Post-prandial
• Cardiac diseases (~35%)
– Arrhythmia (e.g. sick sinus syndrome) / conduction defects
– Valvular problems – aortic stenosis , mitral stenosis
– Outlet obstruction – left atrial myxoma
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Pathogenesis – Neurally-mediated
• Vasovagal attacks – exaggerated
baroreceptor response
• Cough / swallowing / micturition
syncope – probably related
exaggerated Valsalva straining during
these situations
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Presentation
Vasovagal Attack:
Stage 1
•↑ BP and HR (sympathetic tone)
Stage 2
•Abrupt ↓ BP and HR (parasympathetic tone)
•Patient lies down / falls
Stage 3
•Increase in venous return ,
balanced sympathetic & parasympathetic tones
•Rapid recovery upon recumbence
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Pathogenesis – Other Causes
• Decreased plasma volume
(hypovolaemia)
• Vasodilatation (e.g. drugs)
• Reduced heart rate / impaired heart
beating
(brady-arrhythmia / heart blocks)
Reduced cardiac output
• Carotid stenosis
• Cerebrovascular steal syndrome
cerebral hypoperfusion → syncope
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Presentation
Symptoms:
• Dizziness or light-headedness (70%)
• Nausea , epigastric discomfort
• Warmth
• Palpitations
• Blurred / faded vision
• Lower limb weakness
• Diaphoresis
• Pallor
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Differential Diagnoses to ‘Dizziness’ /
Altered Consciousness
• Hypoglycaemia
• Electrolyte disturbance / other metabolic causes
(e.g. uraemia / hepatic failure)
• Epilepsy
• Cerebrovascular diseases (TIA , stroke , SAH , SDH ,
EDH)
• Other neurological diseases (e.g. meningoencephalitis ,
prion disease)
• Drug overdose (e.g. sedative-hypnotics , anti-psychotics)
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Workup
History
•The exact meaning of ‘dizziness / syncope’ symptom to the elderly
•The past history of such ‘dizziness / syncope’
•Fall history , whether or not related to the ‘dizziness / syncope’ , if
so , the mechanism of the fall episode(s)
•Any new neurological symptoms
•Any new cardiac symptoms (palpitations ± chest discomfort / SOB)
•Usual functional status (indoor / outdoor)
•Social background (home environment , caregiving practice)
•Medications (esp. anti-HT / anti-arrhythmic / vasodilators /
psychiatric drugs) ; ask for compliance , any recent changes
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Workup
P/E
• GCS / BP and pulse / SaO2
• Postural BP
– Keep patient in lying position for 5 minutes and measure BP ,
– Then ask the patient to stand up and measure BP
– +ve if SBP ↓ by 20 mmHg / DBP ↓ 10 mmHg / symptom reproduction
• ± Post-prandial BP (~2 hours after meal)
• Any superficial injuries / fractures / joint pathology
• Neurological examination (motor + sensation)
• Cardiovascular – ? irregular pulses / missed beats , heart murmurs
• ? Carotid bruits
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Workup
Investigations
•Basic blood tests (to exclude anaemia / electrolyte disturbance)
•H’stix (to exclude hypoglycaemia)
•ECG (to screen for any pathological arrhythmia)
•X-rays (to exclude any fractures / dislocations)
•CT-Brain (to screen for any significant intracranial pathology)
± Tilt-table test (to document vasovagal attacks)
± 24-hour ECG (Holter)
± EEG (to screen for epileptiform activities) / further neuro-imaging
± Trans-thoracic echocardiogram
± Carotid Doppler ultrasonography
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Tilt-table Test
• A bed that can be tilted to near-upright position , with safety belts
securing the patient undergoing test
• Attempt to reproduce vasovagal symptoms in a well-controlled
environment for documentation
• Patient kept in quiet environment (to reduce disturbance)
• Lying flat for 20 minutes
• Tilt patient to 60º for another 30-45 minutes (to allow venous
blood to pool in the lower extremities)
• If –ve , proceed to provocation test (by either SL TNG spray or
IV isoprenaline) for another 20-30 minutes , see the response then
• Recovery (lying) position for the last 20 minutes
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Tilt-table Test – Interpretation
Test considered to be +ve if :
• BP ↓ + HR – or ↑ → orthostatic hypotension
• BP ↓ + HR ↓ → vasovagal attack
• Significant symptom reproduction
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Syncope – Impacts in Elderly
As a consequence
• Many common causes predisposing to hypotension
(anti-HT drugs , post-prandial)
• Underlying cardiac → ? pacing as definitive treatment
• Underlying neurological causes with autonomic
dysfunction → ? prognosis
As a cause
• Symptoms → anxiety , not willing to walk again →
immobility
• Fall / collapse → subsequent morbidity / mortality
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Management
• Neurally-mediated – supportive
• Hypotension – remove aggravating factors
• Cardiac – treat the underlying causes
(e.g. permanent pacing in arrhythmia ,
drugs ± surgery for valvular diseases)
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Management – General Measures
A. Patient ± carer education
• Try to recognize the triggering factors and attempt to
remove them (e.g. drugs , pain)
• Exposure-based exercises under therapists’ supervision
for the situational syncope (cough / micturition etc.)
• Teach them how to respond if pre-syncope symptoms
occur (by lying down , crossing legs etc. , in order to
increase cerebral blood flow before syncope)
• In case syncope and fall occurs , lie in recovery
position with head turning to the side + loosen clothes
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Management – General Measures
B. Avoid orthostatic hypotension
• Review ± adjust medications
– Anti-HT drugs
– Diuretics
– Vasodilators (e.g. nitrates , drugs for PVD)
– Anti-parkinsonian drugs
– Psychiatric drugs
• Adequate fluid intake
• Adequate salt intake if not contraindicated
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Management – General Measures
B. Avoid orthostatic hypotension
•Change position slowly from lying to standing
•Tilt training
•Leg-crossing / muscle-tensing manoeuvres
•Dorsiflexion of feet before standing
•Graded pressure stockings
•Pharmacology
– Fludrocortisone (a mineralocorticoid that increases salt and
thus water retention)
– Midodrine (a vasopressor – avoid in PVD)
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Management – General Measures
C. Avoid post-prandial hypotension
• As those in preventing orthostatic hypotension
• Re-adjust diet carbohydrate composition
• Frequent small meals
• Pharmacology
– Caffeine
– Octreotide
– Acarbose
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Let’s continue Mr. Y ’s story …
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Postural BP and H’stix
(21/3) 140/72 mmHg → 132/65 mmHg ; H’stix 5.6
(22/3) 145/78 mmHg → 142/81 mmHg ; H’stix 5.4
(23/3) 139/70 mmHg → 121/61 mmHg ; H’stix 4.6
(24/3) 133/68 mmHg → 127/69 mmHg ; H’stix 5.9
(25/3) 138/81 mmHg → 130/74 mmHg ; H’stix 4.4
(26/3) 143/80 mmHg → 126/70 mmHg ; H’stix 6.1
(27/3) 135/75 mmHg → 139/72 mmHg ; H’stix 5.8
All taken in the morning ; patient denied any symptoms all along
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Drugs Titration
Hypertension
• Stopped amlodipine and kept lisinopril
• BP stayed at high-normal levels (130-145/80-90 mmHg)
Diabetes mellitus
• ↓ metformin to 250mg BD
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Rehabilitation
Physiotherapist –
• EMS 12/20 , MFAC Cat III with stick , Cat IV with
rollator
Occupational therapist –
• MMSE 22/30 , MBI 65/100 (independent up to UG
dressing , assistance in LG dressing / toileting /
bathing)
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Further Workup Arrangements
• Holter booked on 15/4/2013
• EEG booked on 27/6/2013
Gradual improvement in the following week …
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Progress
• Impaired cognition with occasional confusion
since early 4/2013 (after Ching Ming Festival)
• Subjectively ↑ bilateral lower limb weakness
• No ↑ parkinsonism feature
• No further fall or head injury
• No recurrent syncope / LOC
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Progress
• Also noted functional decline
–PT: EMS 15/20 → 7/20 only , barely walked few
steps with frame , mainly chairbound
–OT: MBI 68/100 → 22/100 , independent up to
feeding only
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Investigation
• BP 142/86 mmHg and pulse 90 bpm ,
no significant postural change
• H’stix stable at 5–8
• Basic blood tests remained unremarkable
• ECG: NSR , no ischaemia / arrhythmia
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Investigation
CT-Brain (10/4/2013):
• Bilateral chronic hypodense subdural effusion , now
more on left side with slight increase in width there
• Some hyperdense fluid in the left SDH component
not seen in previous CT-Brain , likely corresponding
to recent bleeding
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Further Management
• Consulted PWH Neurosurgery Department , and
agreed to take-over case to PWH for further
management that afternoon
• Relatives interviewed , initially decided for
conservative treatment → oral dexamethasone
• Noted further decline in functional status ,
relatives interviewed again , Burr hole operation
suggested and they finally agreed
→ performed in late 4/2013 uneventfully
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Further Management
• Transferred to NS rehabilitation ward at SH
• Functional status slowly improving but still
worse than premorbid status
– PT – EMS 3 → 8/20 , walked few steps with
rollator , transfer with 2 major assistance ,
endurance ~10m
– OT – MBI 16 → 30/100 , ADL independent up to
feeding , otherwise with assistance / dependent
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Discharge
• Relatives interviewed
– Children live far away and have their own family,
need to work and thus no time to take up the caring
task
– Wife already in OAH
– Maid alone cannot care patient in view of his
heavy built
• Arranged private OAH in Sha Tin District as
patient’s placement
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Final Diagnosis
Acute on chronic subdural haematoma, as a
consequence of syncope with fall
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Topic Discussion
B. Subdural haematoma (SDH)
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Contents
• Types , epidemiology
• Causes
• Presentation
• Diagnosis
• Management
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Types
SDH
• Acute – immediate (within 72 hours) after injury
• Sub-acute – ~3 days to 1 week after initial injury
• Chronic – 2–3 weeks or more after initial injury
[c.f. epidural haematoma (EDH) and
subarachnoid haemorrhage (SAH) must be acute]
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Epidemiology
• Overall incidence
– 1–60 per 100,000 population
– at least 10 per 100,000 in ≥ 65Y
• Sex
– Male : female about 2 : 1 (64% vs. 36%)
• Age
– Elderly much more common
– ≥ 65Y : < 65Y more than 2 : 1 (69% vs. 31%)
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Epidemiology
• Acute SDH
– 40-70% among all comatose / transient loss of
consciousness patients presented to AED
– Nearly 80% had recent fall injury on presentation
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Pathogenesis
• Tear of bridging
veins in subdural
space →
accumulation of
blood between dura
and arachnoid
• Usually slower
progression than
EDH and SAH
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Pathogenesis
• Head injury as the most important cause ,
usually of rapid acceleration / deceleration
mechanism
• Severe injuries often precede acute SDH
• Chronic SDH patients , however , may only
have minor / trivial injuries before , and may be
unnoticed
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Risk factors
Medical
• Coagulopathy (diseases , iatrogenic)
• Fall tendency
• Dementia
• Alcoholism
• Epilepsy
Surgical / structural
• Cerebral atrophy (↑ the length the bridging veins between the
two meningeal layers , thus ↑ shearing forces causing a tear)
• Arachnoid cysts
• Intracranial hypotension (e.g. post lumbar puncture)
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Presentation
• Dizziness
• Headache
• Focal neurological deficits
(weakness , dysarthria , choking)
• Seizures
• Amnesia
• Cognitive impairment
(ataxia , dysphasia , disorientation)
• Blurred vision / deviated gaze
• Loss of consciousness
• Malaise
• Weakness / lethargy
• Nausea / vomiting
• Anorexia
• Altered breathing pattern
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Investigation
CT-Brain (mostly good enough to make diagnosis)
Hyperdense lesion in a crescent appearance , usually with
a concave surface away from skull , that follows the
contour of brain and expands along the inside of the skull
and passes its sutures
[c.f. epidural haematomata do not cross sutures]
Subdural haematoma Epidural haematoma
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Prognosis
Age-related mortality
• <40Y : < 20%
• 40-65Y : 50%
• >= 80Y : > 80%
• Overall mortality : 40–80%
• Favourable outcome: 10–40%
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SDH – Implications in Elderly
As a consequence
• More common than younger adults
• A result of head injury , e.g. after fall → its risk factors
• Underlying cerebral atrophy
As a cause
• Declined mobility as a neurological deficit → fall
• A potential reversible cause of dementia
• Increased morbidity and mortality , whether or not
properly treated (time for rehabilitation)
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Prevention
• Fall prevention (MMAI * approach)
– Treatment of hypotension , other underlying diseases
– Nutrition optimization
– Gait training , exercises
– Assistive device use training
– Safety awareness education
– Environmental modification
• Early recognition – neuroimaging
* MMAI – Multi-disciplinary multi-factorial Risk Factor Assessment and Intervention
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Management – Conservative vs. Operative
Consideration factors
• Clinical status
– GCS change (≥ 2 points drop from injury)
– Evidence of ↑ ICP (e.g. dilated / unequal pupils)
– Focal neurological deficits
• SDH status
– Haematoma thickness >10mm
– Midline shift >5mm
– Evidence of ↑ ICP or brain herniation
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Conservative Treatment Options
For SDH thickness <10mm , midline shift <5mm
• Mannitol – reduction of cerebral oedema
• Dexamethasone – inhibition of inflammatory
reactions + anti-angiogenic effect
• Close observation needed
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Reversal of Anti-coagulation Status
• Equally important , especially before any possible
operative treatment
• Need to balance between indications and risks of anti-
coagulation status
• Stop all anti-platelet and anti-coagulants
• Drugs to hasten clotting function normalization
– Prothrombin complex concentrates (PCC)
– Recombinant human factor VIIa
– Fresh frozen plasma (FFP)
– Vitamin K
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Operative Treatment Options
For acute SDH , SDH thickness >10mm , midline
shift >5mm , anticipated favourable outcome and
no absolute contraindications to surgery
• Burr hole trephination
• Twist-drill craniostomy
• Decompressive craniectomy
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Operative Treatment Options
No strict consensus / ‘guidelines’ on their choice:
• Burr hole trephination is the commonest and
relatively safe procedure , but more recurrence
• Twist-drill craniotomy can be done as bedside
procedure
• Decompressive craniectomy usually reserved for
massive haematoma + cerebral oedema
• Operative + adjuvant medical treatment may be
necessary
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Take-home Messages
• Syncope fall SDH
• Accurate recognition of syncope can provide
prompt definitive treatment or preventive
measures to reduce complications , esp. fall
• Be vigilant in detecting altered conscious level
in elderly , especially those with recent fall
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