Stroke and TIAs

A few good guides on stroke territories & associated findings #FOAMems #FOAMed pic.twitter.com/XYt56AYtUg

— Brad Gander (@para_Brad) February 28, 2016

Where is Your Ischemic Stroke Located? REBEL Review #60 --> Ischemic Stroke Syndromes #FOAMed #MedEd

REBEL Reviews: https://t.co/yUmBxcM2jE pic.twitter.com/lKL1RPDxNC

— Salim R. Rezaie, MD (@srrezaie) October 7, 2018

TIAs 
Isolated vertigo is rare in posterior circulation TIAs. They may be hard to diagnose.

There is little benefit from further aspirin if patients are already on aspirin. If patients present late, they should be treated as lower risk of stroke.

For risk assessment, RCP guidelines say investigate all urgently without further risk stratification, and all patients need to be seen within 24hours. No imaging unless to exclude haemorrhage - in patients taking an anticoagulant.

TIAs need aspirin (for 2 weeks), clopidogrel, statins, and BP lowering therapy.

Confusion, memory problems, faintless or syncope, generalised weakness or numbness and incontinence are NOT TIA symptoms.


Always assess the carotid as part of your TIA assessment.

Stroke Anatomy
Anterior circulation is served by the internal carotids which branch into the MCA, ACA.
- weakness or sensory loss affecting the contra-lateral arm, leg or face - mostly leg. Dysphasia or dysarthria. Monocular visual loss.
- Middle cerebral - contra-lateral face and arm more than leg.
- Internal capsule often affects the face, arm, and leg equally.

Poster circulation: CN palsy + contralateral deficiency or bilateral. 20% dead, 20% dependent, 60% independent
Lacunar: pure motor or pure sensory. Dependent 30%, independent 60%
TACS: cortical dysfunction and field deficit and contralateral weakness in 2 areas. 60% dead.
PACS: 2/3 of TACS.

The posterior circulation is served by the vertebrobasilar arteries - which supply to the posterior 2/5 of the cerebrum, and the basilar arteries.

Anterior and posterior circulations are linked by the posterior communicating arteries, forming the circle of Willis.

Malignant MCA infarcts cause a lot of brain oedema, which may lead to herniation and early death. Young patients are particularly at risk because they don't have any spare brain space. A decompressive hemicraniectomy may be considered if pre-stroke rankin <2, defects indicate MCA, NIHSS >15, not alert, signs on CT of at least 50% of the MCA. Refer to neurosurgery. Likely fatal, and early senior neurosurgical involvement is necessary.

Monocular vision loss = optic nerve lesion
Bitemporal hemianopia = optic chism lesion
Homonymous hemianopia = optic tract lesion
Upper quadranopia = temporal lobe lesion
Lower quadranopia = parietal lobe lesion

Stroke Assessment
Consider a ROSIER score - negative score for LOC/ syncope or seizures, with positive for weakness, speech and visual fields.
NIH score
Perfusion scan if diagnosis in doubt, or >4 hours including wake up stroke

Stroke Treatment 
- Very high BP is a contraindication to thrombolysis so stick on a GTN patch on the way

Hypertensive encephalopathy or nephropathy
Hypertensive cardiac failure/myocardial infarction
Aortic dissection
Pre-eclampsia/eclampsia
Intracerebral haemorrhage with systolic blood pressure over 200 mmHg.
In patients being considered for thrombolysis, a blood pressure target of less than 185/110 mmHg should be achieved

- ASPECT score to see if for thrombolysis - determined from CT findings >7 = thrombolyse. - Alteplase is the preferred option. 19/20 stay the same, 1/20 get worse.
- If on NOAC (not dabigatran) no thrombolysis. Consider if clotting normal.

- If need thrombectomy have thrombolysis first

Mortality 
- Increased on pyrexia

References
https://www.rcemlearning.co.uk/modules/transient-ischaemic-attacks/ 

Vertebral Artery Dissection

A tear in the vertebral artery, is a common cause of stroke in young people. The tear has a clot and causes a false blockage - causing an ischaemic stroke. It can happen spontaneously or after minor trauma to the neck, including yoga and chiropractice.

A recent respiratory tract infection may also predispose - making vertebral artery dissection seasonal.

There are two types:
Infarction - ischaemia of the vertebrobasillar circulation due to arterial narrowing and thromboembolism
Haemorrhagic type - presents as a SAH

They may not present with problems, because of the contralateral vessel. Acutely ruptured dissections have a high mortality, and may rebleed (mostly in the month immediately after).

Clinical Symptoms
Severe neck pain, followed later by neurological symptoms
May get a spinal cord infarction
Maybe with a headache and horners syndrome


Normally treated with anticoagulants

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588305/
https://pmj.bmj.com/content/81/956/383
http://emergencymedicineireland.com/2011/12/21/anatomy-for-emergency-medicine-2-the-vertebral-artery/

VBI

Also called beauty parlor syndrome.

Transient ischaemia of the basilar circulation system. Dizziness, vertigo, headaches, vomit, diplopia, blindness, ataxia, imbalance and weakness are all possible symptoms.

Ear symptoms may also cause ischaemia of the inner ear. Posterior circulation imbalance rarely causes only one symptom. Isolated dizziness is rarely VBI.  Standard artherosclerotic risk factors. May be associated with facial pain - sharp single stabs or jolts of pain.

Wallenberg Syndrome - lateral medullary syndrome, caused by a vertebral artery stroke. May be facial pain with a contralateral hyperanalgesia.



https://www.sciencedirect.com/topics/medicine-and-dentistry/vertebrobasilar-insufficiency
https://bmjopen.bmj.com/content/7/8/e017001

Tetanus

Wound Management 

In any patient with a wound, first do a risk assessment of the wound, and then their tetanus status:

Tetanus Prone Wound:  >6 hours old and needs surgical treatment
                                      Open compound fracture
                                      Contaminated puncture wound
                                      Clinical evidence of sepsis

High risk tetanus prone wound?   Yes - give immunoglobulin
                                    Heavy contamination with material likely to contain tetanus eg. manure
                                    Extensive devitalized tissue
                                    >24 hours since injury
                                    >10% burns

Tetanus Status Assessment 
Full immunisation - give immunoglobulin if very high risk
Partial immunization - give DTP if next dose due soon, if high risk give immunoglobulin
Not up to date  -give DTP.  Immunoglobulin
Uncertain - give DTP

Immunoglobulin
Give 500iu if it's a high risk tetanus wound
Give 250iu if it's a tetanus prone wound
Need a second dose of Ig if they can't have DTP, or if they have reduced capacity for antibody formation - radiotherapy, hypogammaglobulinaemia

Give both injections in different arms
If have a bleeding disorder, give SC. There is a higher risk of reaction when these are given SC rather than IM.

Tetanus
Tetanus is caused by C. tetani, a gram positive, anaerobic that is commonly found in soil and manure. It produces tetanospasmin, the neurotoxin that causes tetanus. Incubation 10 days. The infection is a  clinical diagnosis, defined as trismus with one or more of the following:
Spasticity
Dysphagia
Respiratory distress
Muscle spasms
Autonomic dysfunction

Treatment
Metronidazole - stop bacterial replication
Diazepam or midazolam - to control muscle spasms
Intravenous tetanus immunoglobulin -5,000 units < 50kg, 10,000 >  50kg. This is the same as the "treatment".
Intubation - may be needed. Sux is safe but there is a very high risk of autonomic instability
Wound cleansing and debridement

SAQ:
A forty eight year old patient attends the emergency department feeling unwell. They have an infected injection site in their anticubital fossa. They have severe trismus, and are writhing around with severe muscle spasms. Sister thinks security needs to escort them out. You suspect that they have a serious and rare infection from their injection site.

a) How would you manage the muscle spasms?
Supportive care with diazepam or midazolam.
b) How would you treat their infection?
You suspect tetanus - or you should because of the spasms. The patient needs supportive care, with monitoring and consideration of early intubation. Give metronidazole to prevent bacterial relocation. Give IM tetanus immunoglobulin 150 units/ kg. IV is no longer available. Monitor their renal function.
Wound debridement.
Watch for autonomic instability, and cardiac collapse. Sedation, and morphine to help reduce the amount of free catecholamine can be helpful.
c) How would you confirm infection?
Tetanus is a a clinical diagnosis.
You can look for serum levels, but these take so long for results to come back - don't delay treatment for serological confirmation.
- Tetanus IgG - If the antibody level is >0.1 IU/ml before IgG, this excludes current tetanus infection. - Detection of toxin in serum is a bio-assay and is only performed if the antibody level is below the protective threshold.
- Absence of toxin does not exclude tetanus.
- Detection of C. tetani in wound material or from a pure isolate

References
http://pedemmorsels.com/tetanus-prevention/
http://stemlynsblog.org/tetanus-in-the-ed/
https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/441356/IMW166.02_Tetanus_information_for_health_professionals_v1.4__2_.pdf
https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/441355/IMW165.02_Tetanus_Immunoglobulin_Handbook_v1.4.pdf
https://www.gov.uk/government/publications/tetanus-the-green-book-chapter-30
https://www.rcemlearning.co.uk/modules/tetanus/
https://www.rcemlearning.co.uk/foamed/september-2017/#1504201252016-ac52229b-9e50