Cases test 1 revision

CT features of epidural haematoma

• Biconvex collection of blood which does not cross suture lines

• Hyperdense

• Bubbles at fracture site (bone window)

• Usually in pteryion temporal region

CT features of subdural haematoma

• Crescent shaped, usually over convexity

• Crosses suture lines

• Hyperdense (acute) ir hypodense (chronic)

CT features of SAH

• ‘Dancing man’ around circle of willis

• Hyperdense in basal cistern, lateral fissues, L and R sylvian cistern

CT features of intracerebral haemorrhage

• Blood within cerebral hemispheres

• Hyperdense (acute)

CT of intraventricular haemorrhage

Assessment of head trauma

1. ABC’s (airway, breathing, circulation)

2. GCS

3. Head-to-toe examination

4. Neurological exam: CN’s, motor and sensory function, reflexes

5. Blood tests: including INR and PT

6. Monitor overnight

Eye response score in GCS

4: open spontaneously

3: response to sound

2: response to pressure

1: no response

Verbal response in GCS

5: oriented

4: confused

3: words

2: incomprehensible sounds

1: no response

Motor response in GCS

6: obeys commands

5: localised response

4: normal flexion

3: abnormal flexion (decorticate)

2: extension (decerebrate)

1: no movement

AVINDICATED-PI

Anoxic

Vascular

Infection/ inflammation

Neoplastic

Degenerative

Intoxication

Congenital

Autoimmune/ allergy

Trauma

Endocrine

Dietary

Psychiatric

Iatrogenic

Phenytoin (drug class + MOA + indications + ADR’s + caution)

Drug class: anti-epileptic

MOA: blocks vg Na+ channels and stabilises excitatory neuronal membranes. This suppresses repetitive neuronal discharges which generate seizures. Speficially, inhibits the positive feedback loop that results in neural propagation of high frequency action potentials.

Indications: focal and generalised seizures in epilepsy, status epilepticus

ADR’s: vertigo, ataxia, nystagmus

Caution: narrow TI- monitor dosage, hypoalbuminemia, Stocks-Adams syndrome

Valproate (drug class + MOA + indications + ADR’s + caution)

Drug class: anti-epileptic

MOA: increases number of vg Na+ channels in inactivated state, as well as increasing brain concentrations of GABA (an inhibitory nurotransmitter). This suppresses neuronal discharges which generate seizures

(specifically increases GABA by inhibiting succinic semialdehyde dehydrogenase, which thus increases succinic semialdehyde which then reduces GABA metabolism)

Indications: epilepsy, BPD, migraine prophylaxis

ADR’s: stomach ache, diarrhoea, weight gain

Cuations: avoid in pregnancy

Diazepam (drug class + MOA + indications + ADR’s)

Drug class: benzodiazepine

MOA: act as positive allosteric modulator to increase the effect of GABA on GABA-A receptors. These are inhibitory neurotransmitters which suppress electrical activity in the brain which generate seizures. Specifically, binds allosterically between gamma and alpha subunits on GABA-A receptor Cl- ion channels, thus increasing frequency of Cl- channels opening and causing hypopolarisation and reduced excitation of the cell

Indications: insomnia, status epilepticus (first choice)

ADR’s: dorwsiness, decreased alertness, ataxia, agitation in elderly

Monro-Kellie hypothesis

The sum of the volumes of the brain (brain + blood + CSF) is constant, thus an increase to any 1 component results in raised ICP

CT feautres of raised ICP

• MIdline shift

• Venitrcular compression

• Narrow sulci and wider gyri

Signs + symptoms of raised ICP

• Headache

• Confusion

• papilledema

• nausea

• Symptoms of herniation

• Signs of meningeal irritation (neck stiffness, photophobia, +ve Kernig’s or Brudzinski sign)

• Abnormla posturing (Decroticate or decerebrate)

Valsalva manoeuvre + effect on ICP

Method used to slow HR and clear ears

close mouth and block nose, and forcefully exhale against closed airway for 10s

temporarily increases ICP by raising intrathoracic pressure, reducing venous circulation and cerebral perfusion (and causing venius congestion)

Risk of unacceptable badness (RUB)

The likelihood of a patient surviving a severe head injury but being left severely disabled, a condition which they would find unacceptable

Substantial benefit

An outcome that now or in the future the patient would consider worthwhile

ROSIER scale

Used to assess the possibility of stroke

• >0: stroke possible

• 0 or less: stroke unlikely

ABCD2 score

Used to assess the risk of stroke after TIA

• 0-3: low risk

• 4-5: moderate risk

• 6-7: high risk

Signs of stroke

• Fluent/ non-fluent aphasia

• Dysarthria (slurred speech)

• Hemiparesis

• Signs of UMN lesion

• Loss of sensation one one side

• Facial droop

CT features of ischaemic stroke

Infarct appears hypodense on side of lesion

Pathophysiology of ischaemic stroke

Occlusion of a cerebral artery (ACA, PCA, MCA) caused by thrombosis of embolism

Treatment of ischaemic stroke

1. Stabilisation: maintain airways (venilator, endo-tracheal tube), oxygen if needed, monitor glucose, BP hydration

2. If <8 hours: alteplase + mechanical thrombectomy

3. Aspirin/ clopdogrel after 24hrs of alteplase administration

4. Management of cormorbidities (e.g. AF, MI, HTN, diabetes)

5. Phsyiotherapy, OT, speech therapy

CT features of haemorrhagic stroke

• Hyperdense at site of haemorrhage

• Hypodense around site

• Mass effect (e.g. midline shift, herniation)

Pathophysiology of haemorrhagic stroke

• Hypertensive cerebrovascular disease causing hylaine arteriosclerosis and occlusion/ rupture of BV

• rupture of saccular aneurysm causing SAH

Treatment of haemorrhagic stroke

1. Stabilisation: airways (venilator or endo-tracheal tube if needed), oxygen if needed, monitor BP, glucose, hydration

2. Surgical evacuation: clip or coil aneurysm

3. Reverse anticoagulant medications if taken

Aspirin (drug class + MOA + indications + contraindications)

Drug class: antiplatelet

MOA: non-selective COX inhibitor which reduces TXA2 production in the lifetime of platelets. This inhibits platelet aggregation and thrombus formation

Indications: prevention of thrombo-embolic events in CVD

Contraindications: Reye’s syndrome, haemorrhage, gastric ulceration

Clopdigrel (drug class + MOA + indications + ADR’s)

Drug class: antiplatelet

MOA: non-competitvely blocks ADP P2Y receptors, preventing ADP from binding and activating GPIIb/IIIa, thus reducing platelet aggregation

Indications: prevention of thrombo-embolic events in CVD

ADR’s: haemorrhage, abdominal pain, headache, dizziness, paraesthesia

Diltiazem (drug class + MOA + indications + ADR’s)

Drug class: calcium channel blocker

MOA: inhibits Ca2+ during membrane depolarisation of primarily cardiac vascualr smooth muscle

Indications: anti-arrhythmic in AF, angina, reverse coronary vasospasm

ADRs: bradycardia, AV block, palpitation, dizziness, hypotension

Warfarin (drug class + MOA + indications + contraindications)

Drug class: anticoagulant

MOA: competitively blocks heparin vitaminK epoxide reductase in liver to prevent vitamin K recycling and synthesis. This prevents activation of clotting factors X, IX, VII, II (and protein C and S) to prevent thrombus formation

Indications:stroke prevention in CVD, prosthetic heart valves

Contraindications: haemorrhage, pregnancy

Dabigatran (drug class + MOA + indications + contraindications + emergency reversal)

Drug class: DOAC

MOA: directly inhibits thrombin, thus preventing thrombus formation

Indications: stroke prevention in CVD

Contraindications: haemorrhage, prosthetic heart valves

Emergency reversal: idarucizumab

CHA2DS2VASc score

Used to assess risk of stroke in AF and management

Congestive heart failure: 1

Hypertension: 1

Age (75+): 2

Diabetes mellitus: 1

Stroke, TIA previously: 2

Vascular disease: 1

Age (65-74): 1

Sex category (female): 1

Consider offering anticoagulants if 1+ in males and 2+ in females

Effect of pre-eclampsia on ICP

Causes rapid hypertension during pregnancy which can cause brain oedemad thus raised ICP. This can lead to cerebral or CN damage

Cushing’s triad

Late stage raised ICP after head injury

• Hypertension

• Bradycardia

• Irregular respiration

Severity of TBI according to GCS

• Mild TBI: 13-15

• Moderate TBI: 9-12

• Severe TBI: ≤8

Legal documents protecting workers rights

• Accident compensation corporation 1972

• Health and safety at work act 2015

• Health and Safety in employment act 1992

Pathophysiology of epidural haematoma

Tearing of a middle meningeal artery following a fracture in the temporal bone forming a rapidly expanding haematoma

Pathophysiology of sbdural haematoma

Milder repeated trauma puts pressure on bridging veins leading to eventual tearing, more common in elderly patients with cerebral atrophy (as greater space and thus traction on veins)

Criteria for determingin brain death

• GCS 3

• No brainstem reflexes (e.g. pupil constriction, VOR)

• No venilatory effort

  • 2 sets of tests at least 2 hours apart (4 tests total) by 2 different physicians

How does SAH cause hydrocephalus?

1. Blood and inflammation block CSF drainage into arachnoid granulations

2. CSF cannot flow into next chamber and accumulates in ventricles

3. Raised ICP - monro-kelli hypothesis causing displacement of brain tissue in response

PERRLA

Pupils equally round, reactive to light and accomodation

Why should morphine not be administered in stroke?

• Causes hypotension and sedation - can mask the effects of decrease in LoC

• CNS depressant causing respiratory depression: can cause hypercapnia which reduces CBF and thus raised ICP

• Culminative effects of morphine with other treatment medications

Types of radiological imaging

• CT

• MRI

• Diffusion-weighted imaging (DWT)

• angiography

• perfusion scan

• PET scan

What causes hypodense appearance on CT?

Water-like densities of tissue resulting in reflection of x-rays

Causes of hypercoagualability

• Oral contraceptive pill (contains estrogen)

• prolonged immbolisation (e.g. long haul flight) promoting decreased venous return and stasis

• Low fluid intake (decreases circulatory volume)

Most common cause of trauamtic SAH?

Rupture of vertebral artery via blunt force trauma to the neck

Process of examining CT scan (Blood Can Be Very Bad)

1. Blood

2. Cisterns

3. Brain

4. Ventricles

5. Bone