Table of Contents

Neuro 1
Multiple sclerosis 1
Stroke 2
Peripheral neuropathy 3
Headache 4
CNS infections 6
Neurological emergencies 8
Epilepsy 9
MSK 11
Bone biology for medical students 11
Clinical assessment of back pain 12
Clinical approaches to patients with joint pain 14
Fundamentals of fractures, dislocation, lacerations 14
Upper limb injuries 16
Common lower limb injuries – diagnosis and treatment 17
Osteomyelitis 18
Clinical reasoning 19
Intro to clinical reasoning 19
Pain 20
Introduction to anaesthesia and anaesthetics 22
Trauma symposium 25
Eyes 28
Ears 31
Introduction to antibiotics 31

Neuro
Multiple sclerosis
- Demyelinating disease that can be affected by any causes of inflammation
- Symptoms present over days, prolapses/ remission
- Many factors causes MS, the real aetiology is unknown
Common symptoms?
- Optic neuritis
- Blurring of vision
- Sensory and motor deficits
- Urinary difficulties
- Uthoff’s phenomenon
Diagnosis of MS
- Need to have multiple lesions at different places and different times (eg, multiple attacks)
- MRI should show white flairs in the brain or spinal cord
- Oligoclonal bands – should found in CSF and not blood.
o They are IgG antibodies in the CSF
Prognosis
- Good if treated
o Tx: acute: IVMP, oral steroids. Long term: beta-interferons, orals, infusions
- Treatment before 40 = better outcomes
Drugs for MS
- injectable DMT
- Alemtuzumab
o Can cause autoimmune thyroid disease
- Amitriptyline has tentative evidence for use in MS to treat depression, pain, nocturia, fatigue
Anti-MOG antibody disease
- Antibodies to myelin oligodendrocyte glycoprotein
- Pattern
o Acute disseminated encephalomyelitis
o Monophasic optic neuritis +/- spinal cord disease
o Encephalitis

Stroke
- Neurological history is very important!
- Definition: neurological deficit due to acute focal injury of the CNS by a vascular cause, lasting
more than 24 hours
- Risk factors: AF, age, Female, family history, African Americans
- Types of stroke
o Ischaemic (thromboembolic, hypoperfusion, venous sinus thrombosis)
o Haemorrhagic (cerebral/intraparenchymal, subarachnoid)
- Transient ischaemic attack: brief episode of neurological dysfunction without evidence of acute
infarction
- Management:
o Acute: thrombolysis (rt-PA), this will break down clot
o Risk reduction: antiplatelets, ACEi if coexistent with hypertension, anticoagulation is
appropriate if the stroke is associated with atrial fibrillation
- Other intervention:
o intra-arterial thrombolysis (take the clot out)
o patent foramen ovale closure
- management for haemorrhagic stroke
o control blood pressure, stop antiplatelets, anticoagulation
- treatment + management differ with each patient, need to take into account other factors in
their life
- hereditary + genetic conditions associated with stroke
o Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and
Leukoencephalopathy (CADASIL)
o Cerebral amyloid angiopathy
 Accumulation of cerebral amyloid in the tunica media and adventitia of
leptomeningeal and cortical vessels
  Associated with Alzheimer’s
o Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes (MELAS)

Peripheral neuropathy
Classification
- Fiber type (motor, sensory, autonomic)
- Pattern of distribution (distal/proximal, symmetric/ asymmetric)
- Temporal course (acute, chronic, progressive)
- Key features (toxic, nutritional, malignancy)
- Pathology (axonal or demyelination)

Clinical features
- Sensory symptoms
o Numbness, paraesthesia, allodynia, hyperalgesia, neuropathic pain
- Motor symptoms
o Muscle weakness, fasciculation, muscle cramps, reduced reflexes
Diagnostic tests
- Blood tests
o Evidence of systemic disorder
o HbA1c, serum protein electrophoresis
o Vitamin B12
- CSF analysis
o Inflammation/ immune mediated neuropathy
o Albuminocytological dissociation
- Neurodiagnostics
o Nerve conduction study
o electromyography
- Imaging
o MRI spine: Nerve root enhancement
o Ultrasound
- Tissue biopsy
- Genetic test
- History and examination

Diabetic neuropathy
- Distal symmetrical polyneuropathy
o Sensory and motor symptoms
o Treatment focused on sugar control and symptoms
- Autonomic neuropathy of diabetes
o PSNS and SNS involvement
o Higher resting HR
o Impaired HR variability
o Orthostatic hypotension
o QT interval prolongation
o Erectile dysfunction
- Diabetic amyotrophy
o Asymmetrical
o Proximal weakness
o Acute to subacute onset
- Diabetic treatment-induced neuropathy
 o Triggered by rapid improvement in glycaemic control after prolonged hyperglycaemia
Guillain barre syndrome
- Neurological emergency
- Triggered by infection, trauma or surgery
- Features: progressive weakness of more than one limb, areflexia or hypoteflexia
Acute inflammatory demyelinating neuropathy
- GBS variants
- Miller fisher syndrome
Chronic immune demyelinating neuropathy
- Progressive decline over months
- Proximal muscle weakness, areflexia
- Can be associated with malignancy or paraproteinemia
Motor neurone disease
- Lots of different times (ALS most common)
- No sensory involvement
- Rapidly progressive
Nutritional neuropathy
- Vitamine B1,3,6,9,12 definicy can cause pain
- B12 definicey can also present with spinal cord issues
- Special consideration:
o Vitamine B6 toxicity can cause neuropathy
o Excess Zinc lead to copper deficiency
o Alcohol can cause wernicke’s encephalopathy
Paraproteinemic neuropathy
- Abnormal clonal proliferation of plasma cells or B cells
- Different types, all with different treatments
Toxic neuropathy
- Caused by toxins such as chemo, immunosuppressant drugs
- Coasting phenomenon – symptoms continues to get worse despite ceasing of medication – due
to Wallerian degeneration of nerves
Infectious neuropathy
- HIV, hepatitis, herpes etc
Hereditary neuropathy
- CMT1 – demyelinating
- CMT2 – axonal

Headache
Primary headache disorders
Condition Aetiology Examination Investigation Management
Tension  Most prevalent Unremarkable Normal  NSAID
Headache  Bifrontal, non-  Prevention with
throbbing amitriptyline,
mild/moderate venlafaxine or
intensity mirtazapine
 Band like  Exercise, biofeedback,
sensation acupuncture
Migraine  Brought upon by ICHD-3 diagnostic criteria  History Acute management
specific triggers - At least 5 attacks  CT or MRI  paracetamol, NSAIDS,
 Episodic migraine - Lasting 4-72 hours  EEG antiemetics
(less than 15 per - Unilateral location,  CSF  triptans or CGRP
 months) pulsating quality, analysis antagonists
 Chronic migraines moderate intensity,  CRP/ESR  IV injections, peripheral
(more than 15 per aggravation by or  FBC nerve blocks
month) causing avoidance of  neuromodulation
 Complicated routine physical Preventative management
pathophysiology activity  non-pharmacological
Phases - Nausea/vomiting  trigger avoidance
 Prodromal -> aura - Photophobia  moderate-heavy
-> headache -> WITH aura exercise
postdromal -> - Criteria above +  ketogenic diet
interictal symptoms of aura  riboflavin, magnesium
 antihypertensive,
antiepileptic, CGRP
inhibitors
antidepressant,
serotonin blockers
 injectables or infusions
can both be used
Cluster  localised to one Unremarkable  history Steroid injection, oral
headache side, comes on predinosone, lithium
and goes
 sinus, tension,
migraines, cluster
Cranial  pain caused by Lasting up to 2 minutes  MRI? Carbamazepine,
neuralgias nerve Severe intensiry lamotrigine, pregabalin,
compression Electric shock like pain nerve decompression etc

Secondary headaches
- Red flags
o Systemic symptoms
o Neurologic symptoms
o Onset
o Older patient
o Positional
o Prior history
o Pregnancy/ postpartum
o Precipitate by Valsalva
Subarachnoid haemorrhage
- Thunderclap headache
- Aneurysmal rupture, head trauma, hypertension

Spontaneous intracranial hypotension

- CSF leak
- Orthostatic headache
- Lumbar puncture
- Conservative management

Idiopathic intracranial hypertension

- CSF production ? CSF reabsorption
- Most common cause from sudden weight gain or weight loss
- Radiological features – optic nerve tortuosity,, empty sella, venous sinus stenosis
- Carbonic anhydrase inhibitors, venous sinus stent, ventricular-parietal shunt

Reversible cerebral vasoconstriction syndrome

- Thunderclap headache
- Ischemic or haemorrhiagic stroke
- Beading pattern in angiography
- Calcium channel blocker management

Neoplasms
- GBM, glioma, astrocytoma, melanoma, lung, breast, colon, renal cancers

Giant cell arteritis

- Headahces
- Jae claudication
- Unilateral scalp tenderness
- Vision loss
- Age > 50
- Raised inflammatory markers
- Temporal artery biopsy

Medication overuse headache

- Regular overuse for >3 months of one or more drugs
- Need to assess risk of withdrawal
o Low risk – stop the medication
o High risk – bridge therapy (headache prophylaxis, wean down medication)

CNS infections
Major CNS infections
- Community acquired meningitis
- Acute viral encephalitis
- Brain abscess
- Meningitis (inflammation of the meninges)
o acute onset of meningeal symptoms and fever, pleocytosis of the cerebrospinal fluid
- Encephalitis (inflammation of the brain matter)
o Causes altered mental status and focal or diffuse neurological signs
Meningitis
- Symptoms
o Triad: neck stiffness, fever, altered mental status
o Differentials: malaria, CNS infection, subarachnoid haemorrhage
- Signs
o Kernig sign – knee extension is painful
o Brudzinski sign – neck flexion leads to knee flection
o Jolt accentuation – turning head horizontally 2-3 times will worsen headache
o Nuchal rigidity – resistance to flexion
o Petechiae and palpable purpura in meningococcal meningitis
o The signs are very specific but not very sensitive

Encephalitis
- In addition to meningitis..
o Acute or subacute onset of altered level of consciousness
 o Lethargy
o Personality change
o Short term memory deficits
Causative organisms
- Arboviruses and enteroviruses – causes both
- HSV 1 – encephalitis
- HSV 2 – meningitis only

Community acquired bacterial meningitis

- Streptococcus pneumoniae – most prevalent cause of meningitis
- Neisseria meningitidis – A, W, X, B, Y strains
- Haemophilus influenza type B – used to be leading cause of meningitis – but has been eliminated
- Listeria monocytogenes – food-borne meningitis

Viral meningitis Pathophysiology

- Entry and replication of the viruses
- Enters the CNS hematogenously
- Virus can invade through choroid plexus or by direct penetration of the endothelium of the blood
vessels
- Retrograde travel along axons
- Viral replication in neural cells

Bacterial meningitis
- Colonisation, invasion, survival, entry into subarachnoid space

Diagnosis
- CSF examination
- Lumbar puncture (L3-L4 area)
o Contraindication
 Increase ICP, use of anticoagulants, evidence of cellulitis or abscess over the LP area,
significant degenerative joint disease
- Xanthochromia
- Cells – more than 5WBC/RBC is normal
- Chemical composition
o Protein, glucose, lactate
- CSF gram staining
o Gram positive or negative
o Rods or cocci
- CSF culture is gold standard in diagnosis bacterial meningitis
- CSF PCR
- MRI more helpful in diagnosing encephalitis rather than meningitis

Management
- Viral
o Supportive treatment
o HSV – IV Aciclovir +/- oral valaciclovir
- Bacterial
o Blood culture, lumbar puncture
o Start on empirical therapy for meningitis before getting the result back
o Ceftriazone, cefotaxime, dexamethasone
o If older or immunocompromised
  Benzylpenicillin, trimethoprime + sulfamethoxazole, vancomycin
Complication – bacterial
- Impaired mental status
- Increase ICP
- Focal neurologic deficits
- Sensorineural heating loss

Complication – viral
- Learning problems,
- Developmental delay
- Motor deficit
- Behavior problems

Prevention – vaccination

Brain abscess
- Results from predisposing factors
o HIV, immunocompromised drugs etc
- Features
o Headache
o No fever
o Neurologic signs depend on the site of the abscess
o Seizures
- Diagnosis
o CT with contrast, MR brain
- Management
o Neurosurgery
o Continuous drainage
- Complication
o Hydrocephalus
o Brain herniation
o Seizures
o Focal neurological deficits

Neurological emergencies
Acute stroke
- Ischemic vs haemorrhagic
- CT scan
- Ischemic – hyperacute management, thrombolysis, endovascular clot retrieval
- Thrombectomy – for large vessel occlusion
- Acute management – hydration and nutrition, blood pressure management, glycaemic
management, pyrexia, stroke unit care, decompressive craniotomy
- Secondary prevention – atrial fibrillation, antiplatelet therapy, long term blood pressure
management, dyslipidaemia, carotid stenosis, patent foramen ovale, smoking cessation, alcohol
consuption

Status epilepticus
- Seizure lasting more than 5 minutes
- 2 seizures between where this is incomplete recovery of consciousness
- Often caused by brain injury, withdrawl, metabolic, autoimmune encephalitis
- EEG investigation
- Bloods – serum glucose and a rapid finger stick or point of care glucose
- Management:
o Maintain open airway
o Nasopharyngeal device
o Hemodynamic support
- first line medication: benzodiazepines
- antiseizure medications
- magnesium sulphate for pre-eclampsia/ eclampsia
- refractory status epilepticus
o ongoing sieizures despite medications
o need to consider intubate them because the medication used will cause sedation ad
airway closure (midazolam, propofol etc)

Guillain barre syndrome

- acute demyelinating neuronal disease that is often caused by a trigger (infection)
- there are different variants that affects different parts of body
- sensory and motor deficit over hours to days
- absent deep tendon reflexes
- MRI spine shows nerve root enhancement
- Management- immunomodulatory therapy

Myasthenia gravis crisis

- Positive antibody in acetylcholine receptors
- Autoimmune neuromuscular junction disorder
- Presentation: bulbar weakness, respiratory failure, generalised muscle weakness
- Myasthenic crisis
o Precipitants – acute infection, surgery
o Management – admit to ICU, frequently monitor respiratory muscle strength
o Plasma exchange or IVIg

Movement disorder emergencies

Epilepsy
what is epilepsy?
- More than 2 seizures that are more than 24 hours apart
- 1 unprovoked seizures have a high risk of recurrence within 10 years
- Categorized by- seizure type, epilepsy type, aetiology, syndrome
Types of epilepsy
- Focal – conscious, one region
- Generalised – everywhere, usually symmetrical, no real target

Generalised epilepsy
- Childhood or early adulthood
- Generalised tonic-clonic seizures
- Absence seizures
- Myoclonic seizures

Generalised syndromes
- Juvenile myoclonic epilepsy
- Juvenile absence epilepsy
- Childhood absence epilepsy
- Generalised tonic clonic seizures only

Juvenile myoclonic epilepsy

- Most common
- 6-25 years old
- Morning myoclonus seizures
- GTCs (generlaised, symmetrical, fast amplitude  slow amplitude)
- Triggers – sleep, alcohol, missed meds

Juvenile absence epilepsy

- Is longer than JME
- 8-20 age onset
- EEG will show a longer burst

Childhood absence epilepsy

- Seizures multiple times a day but patient are not aware of it
- 2-12 age onset, usually gets better once they’re older

Generalised tonic-clonic seizures only

- 5-40 age onset
- Common in the first 1-2 hours of waking up

Focal epilepsy
- Most common adult epilepsy
- Classification: consciousness, initial dominant features

Tempooral lobe epilepsy

- Aura features – dehjavu, jamai vu, olfactory, dreaming sensation, autonomic features, fear
Dravet syndrome
- Severe myoclonic epilepsy of infancy
- Due to mutation in the sodium channel gene
- Remit by puberty
Lennox gastaut syndrome
- 1-7 age onset
- No cure, they will just continue to have seizures
- EEG – slow spike and wave, abnormal background

Seizure investigation
 - Is it provoked? Underlying predisposition? Natural history?
- After first stroke, increase risk of stroke
- EEG, MRI, basic metabolic screen

Epilepsy treatment
Meds Mechanism Pharmacokinetics Problems Good for Bad for Dosing
Phenytoin Na+ Enzymes inducer Hirsutism Focal Myoclonus 20mg/kg
channel Albumn binding Gum seizures
blockage hypertrophy
Sodium Generalised
channel SE seizures
Valproate Unknown Hepatic Weight gain, Generalised Pregnancy Use with
metabolism tremor, epilepsy lamotrigine
Enzyme parkinsonism 100mg BD
inhibition
Carbamazepine Sodium Enzyme inducer, Sedation, Focal Myoclonus 100mg BD
channel hepative cleance rash, drug epilepsy,
blocker interactions trigeminal
neuralgia,
neuropathic
pain
Levetiracetam SV2A Renal excretion, Mood (peak Everything Psychiatrist, 250mg BD
(first line) linear kinetics, at 6 months) PBS
safe in
overdosage
Lamotrigine Sodium Very long half life OCP, All seizures Myoclonus 25mg daily
channel (that’s why its pregnancy, Esp w/
blocker – good) can caused valporate
very well SJS
tolerated
Lacosamide Sodium Same as CBZ Focal Myoclonus
channel but milder, seizures
blockage headache

Epilepsy surgery

MSK
Bone biology for medical students
- Bone mass is replaced every 10 years
- Osteoblast – build bones
- Osteoclast – break down bones
- Osteocytes – central orchestrator of bone mass, have an effect on bone mass
- Chondrocytes – frictionless, makes cartilage
- Bone remodelling needs both osteoblast and osteoclast – both needs to be involved
o RANKL binds to RANK receptor to mature osteoclast – cut bones
o Osteoblast comes to restore and make new bones
- Bisphosphonate and denosumab decouple bone remodelling and inhibit osteoclasts
- Denosumab will cause rebound fracture – once you start taking it, can’t stop
- Bone-brain-gut axis – gut microbiota affects bone mass
- Vitamin D is also important in bone density – can cause osteomalacia
- PTH disease = increase PTH = increase break down of bone to release Ca
- Treatment for bone disease
o Treat causes – lifestyle changes
o Antiresorptive medications
 Bisphosphonate – integrate in bone and kill osteoclase
 Denosuman – inhibit RNAKL binding to RANK – inhibit Osteoclast differentiation and
activation
 Teriparatide– pulsed recomb-PTH anabolic

Clinical assessment of back pain

- Nerve supply only to the outer third of annulus fibrosis
- Types of referred pain
o Visceral referred pain
o Radicular pain
 Due to nerve compression
 Sharp and shooting pain
 Follows path of nerve to its dermatomal and myotomal distribution
o Somatic or spongylogenic referred pain
 Pain from muscle, joints, ligaments to any somatic structure innervated by the same
spinal level
 Deep and aching pain
 Myotomal in distribution, no neurological symptoms
 Caused by convergence of connections in spinal cord and brain
- Convergence theory – the neurons of the trigger points and other somatic structure (referred
pain) are connected by the same neuron to the brain, so the brain will signal pain to the other
site
o Intensity and distribution of referred pain is proportional to the intensity of source of pain
- Referral pain pattern:
o thoracolumbar junction  pain over lateral iliac crest
o mid lumbar spine  pain in low lumbar region and anterior thigh
o low lumbar spine  superior/lateral buttocks + posterior thigh/calf
o sacroiliac joints  inferior/medial buttocks + posterior thigh/calf
- pathoanatomical/structure model
o pain to anatomical or pathological structures
o limited by high frequency of abnormal findings in pain-free controls
o eg, pain in the facet joints
- intervertebral or segmental dysfunction model
o disturbance of the function of intervertebral segments, no individual structure
o recognises the limitation of history, examination and investigation to label a particular
structure as the source of pain
o right L5-S1 intervertebral dysfunction with referred pain to right gluteal region
- evidence based model
o limits the diagnostic options to those for which you have firm evidence and recognises the
firm evidence is often lacking
o right L5-S1 facet joint pain confirmed by medial branch blocks
o non-specific low back pain
- biopsychosocial model
 o explains pain and disability as a multidimensional, dynamic integration among multiple
factors
o chronic lumbar facet joint with some central sensitisation in the setting of anxiety and
financial stressors
o most appropriate for chronic pain
- Radicular pain and radiculopathy
o Radicular pain – sharp and showing pain
o Radiculopathy – neurological symptoms and signs arising from the nerve roots (numbness
etc..)
o Theories about radicular pain and radiculopathy
 Pressure on nerve roots give paraesthesia
 Pain results from ischemia
 Nucleus pulposus is irritant to nerve roots
 Immune reaction to displace nuclear material
- Spondylolisthesis
o Anterior translation of one vertebra on the vertebra below
o Can be caused by fracture, degenerative disease
o Increase risk of radicular pain with anrrowed apinal canal
- Spinal stenosis
o Narrowing of spinal canal caused by
 Congenitally narrow spinal canal
 Disc bulging
 Facet joint hypertrophy
 Hypertrophy of ligamentum flavum
- Cauda equina compression
o Caused by
 Large disc protrusion
 Spinal stenosis
 Spinal fractures
 Tumours
 Abscesses
 Haemorrhage
o Surgical emergency
- Functional model
o Intervertebral dysfunction
o Disturbance in function of a spinal segments manifested by
 Restriction with/out pain with global spinal segments
 Restriction at a segmental level
 Pain should be consistent with the segmental level
- Risk factors for chronicity for acute low back pain
o Physical, duration of back pain, past history, leg pain, BMI, work capacity, disability, job,
education, sickness impact score, depression, coping level, distress level, rating of loads,
fear
- Red flag causes
o Age <20 = structural, >50: osteoporosis, cancer
o Trauma – fracture
o Non-mechanical pain
o Past history of cancer
o Prolonged steroid use
o IV drug use or HIV infection
o Constitutional symptoms
o Neurological abnormality
o Structural abnormality
- Imaging guidelines for backpain
o Clinical suspicion of fracture, infection, malignancy or cauda equina syndrome
o Progressive pain or neurological signs
o Failure to settle or resolve after 12 weeks
o Xray have limited accuracy
o CT only indicated in trauma
o MRI superior for other conditions

Clinical approaches to patients with joint pain

- 3 joint symptom, 4 S of pattern, 5 point assessment
5 point assessments
- Is it articular or non articular?
o Non-articular means its not the joint itself, can be muscle tendon ach
- Inflammatory vs non-inflammatory
o CPR?
- Acute or chronic?
- Pattern of involvement
o Symmetry, size, sum, spine
- Associated hx/symptoms/signs
o Occupation, obesity, family history, other systems, impact on patient
3 joint symptoms
- Pain
- Stiffness
- Swelling

Fundamentals of fractures, dislocation, lacerations

Bone healing phase
- Inflammatory
o Neutrophils, macrophages, blood clots, cytokines comes
o Prevent further infection
- Reparative/ granulation
o Proliferation of osteoblast, fibroblast and chondroblast to make new bones
o Angiogenesis
o Formation of callus (soft callus first  hard callus)
- Maturation/ remodelling
o Volume of callus decrease
o Reconstitution of medullary canal and fat
o Remodelling is easier and faster in younger patients
Non-union healing
- When the bones do not line up properly
- Can be caused by movement, or poor circulation
- Need surgery to help heal
Bone graft
- If there is bone missing, bone graft is useful to help grow the bones
- Autograft – self bone
- Allograft – from different person – but its cleaned first
- Xenograft – from animals
- Synthetic bone substitute
Fracture management
- Reduce
o Close or open reduction
- Hold
o 1 fracture – non operative (cast, splint, orthoses)
o Multiple fractures – operative (nailing, external fixation, bridge plating)
- Rehabilitate
Which fracutres should be fixed with surgery
- Open reduction is required
- Articular fracture to prevent secondary osteoarthrist
- Artery and nerve damage
- Multiple fractures
- Risk of delayed healing
- Patient requirements (athletes or elderly)
Gustilo Anderson classification
- Open fractures
- Grade 1 to grade 3
Salter Harris classification
- When the physis are involved
Dislocation
- Loss of contact between articulating surfaces of joints
- Subluxation – partial loss of contract/ alignment
Management of dislocation
- Neurovascular assessment
- Urgent reduction under anaesthesia
- Surgery for fixation
- Immobilisation for ligament healing
- Rehabilitation
- Planned reconstructive surgery for instability

Skin healing
- Inflammation phase
- Proliferative phase
- Maturation and remodelling
- Healing by first intention – sutured, being looked after
- Healing by secondary intention – heal itself – heals badly
Tendon healing
- Inflammation
- Repair
o Fibroblast and collagen proliferation
- Remodelling
o Collagen
Nerve injury
- Wallerian degeneration (distal end of nerve dies off, proximal heals and grows)
- Repair by joining the epineural layer
- Nerve regenerate very slowly

Upper limb injuries

Clinical assessment of upper limb injuries
- Nature of wound
- Mechanism
- Vascular injury
- Repeated clinical examination
- Neurophysiological evaluation
- Surgical exploration
Open wound
- Sensory examination
- Motor examination
- Children: view if there is sweating
- Neurophysiology if unclear
- Be ware of any potential underlying osteoporosis

General principles
- History
- Physical examination
- X-ray and other imaging
- Non-operative treatment
- Operative treatment
- Rehabilitation

Clavicle fracture
- Usually middle 1/3 of the bone
- Close to plexus, subclavian vessels, and chest walls (compare pulse, big bruise)
- Careful NV exam, chest exam
- Non operative
o Minimally displaced, <2 cm shortening, closed injuries, children
- Indications to operate
o Open fracture, displaced fracture, multiple injuries, floating shoulder, deformity, non-
union after sling
Shoulder dislocation
- Posterior dislocation – always due to seizures
- Beighton score (9 points)
- Axillary nerve is most likely damaged
- Management: crews, plates or reverse shoulder replacement for older patients
Rotator cuff tears
- Lots of pain, loss of function
- MRI management
- Non-operative, physio and steroid injection
Humeral shaft fractures
- Sling, brace, surgery
- Can be closed or open dislocation
- Gartland classification
- Supracondylar fracture – most common in children, can lead to compartment syndrome
Colles fracture, smiths fracture, greenstick fracture, scaphoid fracture

Common lower limb injuries – diagnosis and treatment

- Lower limb injuries are more serious than upper limbs (affects mobility, increase risk of DVT/PE)
Principles of trauma management
- Systemic approach to detect and treat injuries
- ATLS (advanced trauma life support)
- EMST (early management of severe trauma)
- Primary survey
o A - airway
o B - breathing
o C - circulation
o D – disability
 o E – exposure
Pelvic trauma
- Caused by high energy blunt force
- High mortality rates due to bleeding
- intimate relationship between the blood vessels and pelvic organs
- young-burgess classification

bleeding control
- pelvic fixation  angioembolisation  pelvic packing

neck of femur fracture

- subcapital
- transcervical
- interochanteric
- subtrochanteric
- presentation: shortening, externally rotated, need to operated within 48 hours to reduce risk of
avascular necrosis

total joint or hemiarthroplasty?

- Total joint: young and active, independent living
- Hemiarthroplasty: elderly, medically unwell, discloation risk, nursing home

Hip dislocation
- High energy
- Risk of AVN
- Usually posterior (shortened, internally rotation, adducted, flexed)
- Sciatic nerve at risk
- Anterior dislocation – lengthened, externally rotated

Femur shaft fracture

- High energy injury
- Fix fracture when stable
- Discloation is also named in relation to the distal bone
o Posterior knee dislocation is worse – can affect the popliteal artery

Compartment syndrome
- Increase pressure  compressing of vessels  increase tissue death
- Pain, pallor, paraesthesia, paralysis, pulselessness
- Clinical diagnosis
o Interstitial pressure > capillary perfusion pressure
o Swollen limb
- Sometimes compartment syndrome is caused by the compression of the external bandages – so
need to remove all cast down to skin
- Management: fasciotomy – then close up the area slowly over few days

Vascular injuries
- Stabilise skeleton, repair artery, release fascial compartments

Tibial plateau fracture

- Common peroneal nerve injury
- Post traumatic arthritis
Ankle fractures
- Risk factors: obesity, alcohol consumption
- Ottawa ankle rules (to determine whether or not an x-ray is needed)
o If there is pain at medial or lateral malleolus
o Inability to bear weight both immediately and in emergency department
- Weber classification
- Management: stabilisation, surgery if its multiple fracture, surgery is ankle is dislocated

If patient is at risk of pulmonary embolism, give them DVT prophylaxis – should be considered in
all lower limb injuries

Osteomyelitis
- Different types:
o Timing – acute, sub-acute, chronic
o Organism – bacteria, fungal (takes 6 weeks to culture)
o Age –
- Causes: hematogenous, direct, contributing factors such as diabetes or immunocompromised
- Pathogenesis
o Site of infection 
o Blocked blood supply, forming callus
o Callus becomes new bone (involucrum), dead bone is known as sequestrum
- In 0-18 months baby, their epiphysis and diaphysis is not connected, but blood supply is
- 18m to 16 years – blood supply not connected either – so the infection will not spread

Septic arthritis
- Infection of joints
- Very bad if a child gets it – increase joint pressure causing cartilage damage and inhibits growth –
need a joint replacement when they’re older – will also be constantly in pain
Kocher criteria
- Child with painful hip
- Fever > 38.5
- Non weight bearing
- Increase leucocytes
- Increase ESR or CRP

Morrey’s diagnostic criteria

- Major (any 2)
o Pus aspirated
o ESR very high
o Xray changes
- Minor (any 5)
o Fever
o Pain made worse by passive ROM
o Joint swelling
o Systemic symptoms
o Good response to antibiotics
Bone scans
- Xray is the worse, but readily available
- Ultrasound can help guide aspiration, very helpful in child
- MRI is very good at recognising the spread of infection, diagnostic of osteomyelitis

Clinical reasoning
Intro to clinical reasoning
type 1 vs type 2 thinking
- Type 1
o Pattern recognition
o Subconscious
o Fast
- Type 2
o Hyoptheses driven deduction
o Analytical
o Slower
problem representation
- Who, when, what
Cognitive biases
- Decision making and judgement biases
- Social and attributional biases
- Memory and perception biases
- Motivational and emotional biases
- Anchoring bias - influenced by a reference point
- Premature closure bias - clinicians make a quick diagnosis (often based on pattern recognition),
fail to consider other possible diagnoses,
- Confirmation bias - tendency to interpret new evidence as confirmation of one's existing belief
- Attribution bias - tendency to explain a person's behaviour by referring to their character
- Representation bias - the probability of an event being representional in character and essence
of a known prototypical event -
- Availability bias - our tendency to use information that comes to mind quickly and easily
- Framing bias - our choices are influenced by the way they are framed

Pain
Flags system of pain
Red – possible serious pathology, need to rule out
Orange – psychiatric conditions
Yellow – emotional response
Blue – perception about the relationship between work and health
Black – system or contextual obstacles

IASP pain definition

- An unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of such damage

Pain description
- Chronologically
- Pathophysiologically
- Pathological process
- Location
Types of pain
Acute
- Sudden
- Short duration
- Correlates with damage
- CNS intact
Chronic
- Insidious onset
- Continues
- Does not correlate with severity
- CNS may be dysfunctional
- Often associated with fear, avoidance, social withdrawal
Nociceptive pain
- Pain that arise from actual or threatened damage to non-neural tissue
- Activation of nociceptors
Neuropathic pain
- Trauma associated
- Pain caused by a lesion or disease of the somatosensory nervous system
Nociplastic pain
- Pain that arises from altered nociception with no clear evidence of actual tissue damage causing
the pain
- “sensitisation”
Allodynia
- Pain from stimulus that doesn’t normally provoke pain
Hyperalgesia
- Increase pain from stimulus that normally provide pain
Paraesthesia
- Abnormal sensation
Dysaesthesia
- Unpleasant abnormal sensation
Anaesthesia dolorosa
- Pain in an area or region which is numb
Hyperpathia
- Painful syndrome characterized by abnormally painful reaction to a stimulus
Referred pain
Cancer pain
- Compression, chemical, infection, invasion, destruction of tissue

how does pain come about

- Nociceptors
- Nerves
- Spinal cord
- Brain

Acute to persistent pain

- Changes in peripheral  upregulation of substance, alteration of receptors/ nociceptors =
peripheral sensitisation
- Alteration in balance of inhibitory and excitatory function of pathways
- Changes in responsiveness of pain matrix = central sensitisation
Analgesia
Pharmacological
- Paracetamol
o 1g up to 4 times a day, 1.5mg/kg regular dosing
o Be careful in patient with impaired liver function
- NSAIDS
o Ibuprofen (10mg/kg max 400mg per dose)
- Opioids
o Increase risk of respiratory depression
o Overdose
o dependence
- Antidepressants
- SNRI
- Antiepileptics etc…

Non-pharmacological
- Physical, psychological, distraction, acceptance, normalisation, heat, cold pack

Amputation
- Phantom sensation – patient feels like the amputated organ is still there
- Amputation pain – parathesia, kinaesthetic

Introduction to anaesthesia and anaesthetics

Types of anaesthesia
- Local
o Injection of surgical sites
o Lignocaine, ropivacaine, bupivacaine
o Binds to voltage gate Na channel  preventing neuronal transmission
o Doesn’t work as well in acidic tissues as they are more ionised
o Lignocaine and bupivacaine can have at a higher dose with adrenaline due to its
vasoconstriction properties
- Regional
o Injection of local anesthetic around a major nerve bundle
o spinal anaesthetics
 Inject in the subarachnoid space
 Last 1-3 hours
o Epidural anaesthetic,
 Injected in the epidural space of the spinal canal
 Can put a catheter in for continuous administration of analgesia
- Sedation
- General
o Induction
 Inhaling, injecting with analgesia
 Propofol
 Potentiates inhibitory transmitters glycine and GABA
 IV administration
 30 seconds time to onset
  Side effects: bradycardia, hypotension, pain on injection
 Midazolam
 Benzodiazepine, inhibitory effect of GABA through the CNS
 2-5mins time to onset IV
 Side effects: respiratory depression, discomfort at the injection site
 Opioid (fentanyl)
 Selective Mu receptor agonist to signal pathway to reduce pain impulse
 2-5min IV
 SE: respiratory depression
 Muscle relaxants
 Depolarisation: suxamethonium
o Binds to Ach receptors and doesn’t get broken down by Ach-ase
o Initial fasciculation and will lead to flaccid paralysis and Ach can’t bind
to receptor
 Non-depolarising
o Competitive nicotinic antagonists to prevent binding of Ach
o Paralysis ASAP, no initial fasciculation
o Can be reversed
 Used to facilitate intubation by paralysing vocal cord
o Maintenance
 Propofol
 Volatiles (gas) – sevoflurance
o Emergence
 Anaesthetic agent do not require reversal
 Non-depolarising muscle relaxants requires reversal
 Muscle relaxants reversal: sugammadex
 Muscle relaxants reversal: neostigmine – prevent action of acetylcholinesterase,
decrease break down of Ach
Air way manoeuvres
- Head tile, chin lift
- Jaw thrust
Airway adjuncts
- Oropharyngeal airway (prevent tongue covering epiglottis)
- Nasopharyngeal airway (avoid if base skull fracture)
Types of airway
Bag-valve-mask
- Oxygen inlet, reservoir
- Tight seal of mask on face, O2 source, good airway position
Laryngeal mask airway
- Supraglottic airway device
- Easy to use, less airway tissue injury, less haemodynamic disturbances
Endotracheal tube
- Insert under laryngoscopy
- Patient factors: aspiration risk, high pressure, air way at risk of deterioration, resp failure needing
long term ventilation
- Surgical factors: prolonged case

Important to get a good history to make sure the right types of airway is used
Risk of difficult airways
- Reduced neck mobility
- Obesity
- OSA, snoring
- GORD
- Poor dentition etc..

Mouth opening and inter-incisor gap

- <3 cm is accepted
- >2.5cm is required for LMA insertion
- >5 cm for intubation, >4cm for LMA

Modified Mallampati score

- Score based on pharyngeal structure visibility
- Estimate relative size of tongue to the oral cavity and ease of displacing the tongue to view the
glottis
- 1 – faucial pillars, soft palat and uvula
- 2 - Faucial pillars and soft palate
- 3 - Soft palate only
- 4 - Nil

Jaw protrusion (JP)

- Assess TMJ joint mobility
- Grade A – lower teeth placed infront of upper teeth
- Grade B – lower teeth placed in line with upper teeth
- Grade C – lower teeth cannot be placed in line with upper teeth – rare but will be difficult for
intubation

Thyromental distance (TMD)

- Distance from thyroid notch to mental prominence with head extended
- <6.5cm predictive of difficulty intubation via direct laryngoscopy

Cervical spine mobility

- Head flexion and extension with maximal mouth opening

Predictors of difficult BVM

- MOANS
- M – mask seals
- O – obesity
- A – age
- N – no teeth
- S – snoring/ stiff

Predictors of difficult LMA

- RODS
- R – reduced mouth opening
- O - obstruction
- D – distorted airway
- S – stiff neck or lungs

Predictors of difficult laryngoscopy + ETT

- LEMON
- L – look externally
- E – Evaluation: 3-2-2 rule (<3 fingers inter-incisor distance, TMD and <2 thyrohyoid distance)
- M – Mallampati class: 3 or 4
- O – obstruction
- N – neck mobility

Predictors of difficult surgical airway

- SHORT
- S – surgery
- H – haematoma
- O – obesity
- R – radiation
- T – tumor

Anaesthetic crises
- Hypoxia
- High airway pressure
- Hypotension
- Malignant hyperthermia
o Autosomal dominant mutation of ryanodine receptors – excess Ca2+ in skeletal muscle
causing too much contraction

Trauma symposium
Injury severity score (ISS)
- Internationally recognised coding system
- Every single injury gets an abbreviated injury scale (code) (1-5)
- ISS = sum of highest AIS (square) for 3 different body region
o Lowest = 3
o Highest = 75
- Major trauma = ISS > 12

Mechanism of injury
- Mechanical energy
- Traumatic brain injury – coup/ contrecoup injuries, generation of shearing forces within and
between organs
- Tissue characteristics and associated trauma
o Rigid tissue - bones
o Flexible tissue – skin, muscle
o Delicate/low tolerance tissue – brain, bowel, liver/spleen

Blunt injuries
- Most common mechanism
- Forces involved: compression, shearing, tensile
- Some common mechanism: head injury, aortic injury, abdominal injuries
Compression force
- A force that cruses or squeezes tissue
- Rib fracture, vertebral burst, muscle bruising, crush injuries
Shearing force
- Force that causes layer of tissue/ organs to slide over one another in opposite direction
- Brain : diffuse axonal injury, skin: degloving injuries, internal organs: tearing of bowel or vessels
Tensile force
- Pulling force that stretches tissues beyond their elastic limit
- Ligament sprains, tendon ruptures, vessels rupture

Trauma physiology
- Early phase
- Acute phase
- Sub-acute
o VTE complication – need to give VTE prophylaxis
o Malnutrition with metabolic derangement
o infection
- Recovery
- Tissue damage  cell damage  release of toxic  multi-organ dysfunction failure  death

Lethal triad in trauma

- Hypothermia
- Acidosis
- Coagulopathy

Clinical assessment of trauma injuries

Airway, Breathing, Circulation, Disability, Exposure

Airway
- Hard to find airway in trauma injuries
o Airway bleeding, full stomach, altered LOC, oedema, C-spine injur, distraction
- Checklist:
o Pre-oxygenated with 100% O2
o Apply cricoid pressure
o RSI drugs
o Avoid to BMV
o Intubate with CMA
o Confirm with waveform capnography
o Secure tube and reassess C spine precaution
o Back up plan for failure
o Need assistant
Breathing
- Inspect: bruising, wounds, deformity, breathing, respiratory rate, pattern + work of breathing
- Palpation: deformity, tenderness, subcutaneous emphysema, crepitus
- Auscultation: present/not breath sounds, muffled heart sound
- Life threatening thoracic injuries
o Aortic injuries
o Tension Pneumothorax
o Open pneumothorax
o Massive haemothorax
o Flair chest
o Cardiac tamponade
- Management consideration
o Analgesia + oxygen
o Chest decompression, intubation + ventilation
 o Needle thoracostomy – fast and easy, but only let a small air out
o Finger thoracostomy – patient whose had RSI, need to decompress their chest
o Intercostal catheter insertion
o Intubation and ventilation
Circulation
- Identify: shock
- Seek causes of shock
- Finding and treating haemorrhagic shock
- End organ perfusion
o Skin assessment: colour/ temperature/ perspiration (peripherally and centrally)
o HR/ BP
o Haemorrhagic shock – conjunctival pallor will be noticeable very early
- Find bleeding, stop the bleeding
Disability
- MIST
- Mechanism of action, Injured sustain, Signs and symptoms, Treatment
- Glasgo coma scale
- Initial management goals – maintain adequate oxygenation and perfusion
- Adjuncts to primary survey
o Continuous monitoring
o Blood tests
o CXR/ PXR
o eFAST
o ECG
Traumatic brain injuries
- Causes: MVA, falls, assaults, work accidents, supporting injuries, gunshots
- Signs of raise ICP: headache, vomiting, altered state of consciousness
- Types of injury
o Primary: occurs at the time of impact
o Secondary: occurs after, bleeding
- Extradural hematoma – lucid interval only occurs in 1/3 of the patient
- Acute subdural hematomas
o Low velocity with atrophic brain (local injuries)
o High velocity – associated with brain swelling from diffuse axonal injury (motor vehicle
accident etc)
- Head injury management
o Hypotension and hypoxia deadly combination
o Measure ICP
- Skull fracture

Introduction to spinal trauma

- Mechanism of injury: flexion, extension, vertical compression, distraction, rotational
- Severity of injury
o Complete: no motor or sensory function below the level of lesion. If no recovery within 48
hours then recovery unlikely
o Incomplete: any motor or sensory function, means recovery may be possible
- Examine c spine to ensure there are tenderness
- Management of spinal injury
o immobilise, secondary survey, consider steroids
o flaccid paralysis, loss of sensory, motor and reflexes below level of lesions
severe limb injuries
- primary survey
o life threatening, major arterial haemorrhage
- secondary injuries
o vascular injuries
o hard signs – 90% arterial injury
 active pulsatile haemorrhage
 large expanding hematoma
 absent distal pulses
 signs of distal ischemia
 audible bruit or palpable thrills at injury site
o soft signs – 3-25% arterial injury
 small non-expanding hematoma
 subjectively decreased pulse
 peripheral nerve deficit
 history of significant haemorrhage
 need to do vascular exam
- compartment syndrome
o 2 hours – start myonecrosis
o 4 hours – irreversible nerve damage
o 6 hours – irreversible myonecrosis
o Delay in diagnosis = rhabdomyolysis, acute kidney injury, multiple organ failure
o 5 P’s – pain, pallor, pulselessness, paraesthesia, paralysis
- Measure intramuscular pressure
- Treatment – remove cast, maintain normal blood pressure
Essential elements (12)
- Statutory authority
- Funding
- Multidisciplinary advisory group
- Trauma system plan
- Continuum of care
- Needs based designation
- Trauma system registry
- Injury epidemiology
- System-wide performance improvement
- Confidentiality and discoverability
- Disaster preparedness
- Military integration

Eyes
Anatomy of eye
- 3 chambers – anterior, posterior, vitreous
- 3 layers – fibrous, vascular, neural
- Ciliary body –
o pars plana: smooth surface, anterior vitreous
o pars plicata: ciliary processes, lens zonules, aqueous humor
Retractive errors
- emmetropia: normally refracted eye, sharp image
- ametropia: myopia, hyperopia, presbyopia, astigmatism
emmetropia
- compound optical system
- convex lens system
o cornea, lens
o lens power alters with accommodation
- distance parallel rays are focused on the retina
- light rays from closer objects are divergent and image will form behind the retina with
accommodation at rest
- Accommodation
o Constriction of pupils
o Thickening of lens
 Ciliary muscle: longitudinal fibres, radial fibres, circular fibres
o Convergence of both eyes
Myopia
- Imagie is focused in front of the retina
- Lens is too long
- Increase axial length, increase curvature of cornea
- Need a concave lens (diverge away from axis before it hits the lens
Hyperopia
- Image is focused behind the retina
- Lens is too short
- Decrease axial length, decrease curvature of cornea
- Decreased refractive index – DM lens hydration
o Increase age = increase permeability of membrane
o Diabetes – excess sugar – increase sorbitol – increase osmotic pressure, smelling of lens
- Convex lens correction
Presbyopia
- Physiological loss of accommodation with advancing age – lose ability to look at close vision,
distant vision remain unchanged
- Theories unknown – increase stiffness of crystalline lens
Astigmatism
- Image does not come to a single focal point
- Optical correction – cylindrical lens
Functional anatomy and physiology of crystalline lens
- Biconvex
- Avascular, acellular, transparent
- 4 structures: capsule, epithelium, cortex, nucleus
- Grows continuously throughout life
- Laid over old fibres – onions
- Compression and hardening of deep nucleus
- Lens lack organelles, they are water soluble
- Provides an optically clear media for light transmission
- Aqueous humor – deliver nutrients and remove waste products
Cataract
- Cloudiness of crystalline lens
- Symptoms:
o Blurring of vision, glare, difficuly seeing in low light situation, yellowish/ browning of
vision, increase near sightedness
- Nuclear cataracts
o Exaggeration of normal aging events
o Hardening of the nucleus
o Increase refractive index
 o “yellow/ browning” of the lens
- Cortical cataracts
o Opacification of lens fibers in the cortex
o Increased membrane permeability
o Overhydration
o Dot-like radial and circular opacities
o Haloe and glares (while driving at night)
- Posterior subcapsular cataracts
o Opacity adjacent to posterior capsule
o Troubled by miosis in bright sunlight
o Near vision more impaired than distance vision
- Immature cataract  partially opaque, same vision
- Mature cataract  lens complete opaque, impermeable to light rays
- Hyper-mature cataract  liquefaction of lens fibres, nucleus sink inferiorly – AKA morgagnian
cataracts
- Management:
o Visual improvement: affects daily activities, prescription glasses cannot satisfy
o Medical reasons: clear ocular media needed, monitoring/treatment fundal pathologies
- Ophthalmic pre-op assessment
o Visual acuity, pupillary reflexes (cataracts never product afferent defect), general eye
examination

Glaucoma
- Group of eye disease that is caused by increase in intraocular pressure, causing irreversible but
potentially preventable blindness (optic nerve damage)
- Disruption in equilibrium between aquesous humor production and drainage
Aqueous humur
- Provide nutrition, metabolites, transporting neurotransmitters
- They are produced continuously by ciliary epithelium lining ciliary processes
- Enters posterior chamber  circulates around lens  goes into anterior chamber through pupil
- Conventional pathway
o Trabecular meshwork
o Schlemnn’s canal
o Influenced by pressure difference
- Non-conventinal pathway
o Uveoscleral outflow
o Uveal meshwork, ciliary muscle bundle, suprachoroidal space
o Not influcned by IOP
Types of glaucoma
- Open angle
o Defect of trabecular meshwork
o Decrease drainage
o IOP >21
o Large cup-disc ratio
o Age >40
o Treatment: lower IOP through medication
- Closed angle – iris narrows the angle
o Acute angle closure – ophthalmic emergency
 When iridocorneal adheres at drainage angle
 o Clinical feature: haloes, IOP >40, congested red eye
o Tx: lying down in supine position, topical timolol with prednisolone, laser peripheral
iridotomy to both eyes
Diagnosis
- Tonometry
o Goldmann applanation tonometer
o Air puff, IOP >21 needs further evaluation
- Gonioscopy
o Visualization of iridocorneal angle
- Optic disc examination – large cup to disc ratio, progressive cupping
- Perimetry – different visual field defects
o Decrease sensitiy, asymmetry, paracentral scotoma, nasal step

Age-related macular degeneration

- Degeneration disorder of the macular
- Causes central loss
Dry AMD
- Cellular debris from RPE builds up
- Deposits as drusens  thickening and decreases permeability
- Thinning and breakdown of bruch’s membrane increases neovascularisation  oedema and
hemorrhages
Clinical presentation
Dry
- Gradual central visual impairement
- Fundscopy: drusen, RPE, loss of photoreceptors
- Management: anti-oxidant supplement, omega 3 fatty acids, green vegetables, stop smoking
Wet
- Rapid progressive visual loss
- Fundoscopy: choroidal neovascularisation, pigment epithelial detachment, retinal haemorrhage
- Management: fluorescein angiography, low vision aids

Ears