cause or consequence? - hkgs

Inter-hospital Geriatric Meeting

Cause or Consequence ?

Presenter: Dr. King-Son LAI (TPH)

Chairperson: Dr. Catherine CHUI (TPH)

25 October 2013

Case History

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

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

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

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

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

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

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

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

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

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

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)

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

Working Diagnoses

1) Syncope

(micturition-related ± orthostatic hypotension)

2) Underlying Parkinson’s disease

3) ? Hypoglycaemia

Topic Discussion

A. Syncope

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’

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

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.

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

Pathogenesis – Neurally-mediated

• Vasovagal attacks – exaggerated

baroreceptor response

• Cough / swallowing / micturition

syncope – probably related

exaggerated Valsalva straining during

these situations

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

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

Presentation

Symptoms:

• Dizziness or light-headedness (70%)

• Nausea , epigastric discomfort

• Warmth

• Palpitations

• Blurred / faded vision

• Lower limb weakness

• Diaphoresis

• Pallor

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)

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

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

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

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

Tilt-table Test – Interpretation

Test considered to be +ve if :

• BP ↓ + HR – or ↑ → orthostatic hypotension

• BP ↓ + HR ↓ → vasovagal attack

• Significant symptom reproduction

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

Management

• Neurally-mediated – supportive

• Hypotension – remove aggravating factors

• Cardiac – treat the underlying causes

(e.g. permanent pacing in arrhythmia ,

drugs ± surgery for valvular diseases)

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

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

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)

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

Let’s continue Mr. Y ’s story …

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

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

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)

Further Workup Arrangements

• Holter booked on 15/4/2013

• EEG booked on 27/6/2013

Gradual improvement in the following week …

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

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

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

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

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

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

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

Final Diagnosis

Acute on chronic subdural haematoma, as a

consequence of syncope with fall

Topic Discussion

B. Subdural haematoma (SDH)

Contents

• Types , epidemiology

• Causes

• Presentation

• Diagnosis

• Management

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]

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%)

Epidemiology

• Acute SDH

– 40-70% among all comatose / transient loss of

consciousness patients presented to AED

– Nearly 80% had recent fall injury on presentation

Pathogenesis

• Tear of bridging

veins in subdural

space →

accumulation of

blood between dura

and arachnoid

• Usually slower

progression than

EDH and SAH

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

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)

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

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

Prognosis

Age-related mortality

• <40Y : < 20%

• 40-65Y : 50%

• >= 80Y : > 80%

• Overall mortality : 40–80%

• Favourable outcome: 10–40%

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)

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

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

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

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

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

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

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