Tuesday, 29 January 2019

Stroke and TIAs


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/

Sunday, 27 January 2019

SCAD


We think of spondaneous coronary artery dissection as being a cause of peripartum myocardial infarction - but about 90% of cases are not pregnant. It can be precipitated by valsalva type manoeuvres. There is an association with exercise, especially in male users. There are case reports linking SCAD with drugs, and emotional stressors.

Thrombolysis is considered safe and apparently effective but generally avoided, because can cause rupture leading to tamponade. Dual antiplatelet therapy probably indicated  - but may cause menorrhagia as is used for women of child bearing age.


https://heart.bmj.com/content/103/13/1043


http://www.emdocs.net/spontaneous-coronary-artery-dissection/

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

Monday, 19 November 2018

Erysipelas

Part of a spectrum of infection.

1. Impetigo - see http://adultemergencymedicine.blogspot.com/2018/08/rashes-impetigo.html 

2. Erysipelas is a superficial cellulitis, with similar risk factors. It looks a lot worse than cellulitis with ruptured bullae and vivid bright red erythema. Almost all erysipelas is caused by group A beta haemolytic strep. It can recur due to persistence of risk factors and lymphatic drainage. Complications can include abscesses, gangrene, chronic leg swelling

Signs and symptoms are normally abrupt, affecting predominantly the lower limb and face. It has a sharp raised border, and is bright red and swollen. The swelling may lead to dimpling, blistering, and even necrosis.

3. Cellulitis
Cellulitis is very rarely bilateral. 35-50% of patients will have a leukocytosis, 60-92% will have an elevated ESR, and 75-95% will have an elevated CRP.  Blood cultures are unlikely to be helpful.
Orals are very bioavailable so most of the time are just as good as IVs.

Often caused by strep and staph. Atypicals are common: Cat bites can have pasteurella, sea water Vibrio vulnificus, fresh water Aeromonas hydrophila, fish farms Streptococcus iniae. These atypicals can cause a rapidly progressive cellulitis.

Class I: No signs of systemic toxicity or co-morbidities. Can be managed on POs.
Class II: 2 or more SIRS, but no organ dysfunction, or have a co-morbidity. May need IV outpatient management.
Class III: Sepsis and organ dysfunction, or unstable co-morbidities normally require admission.
Class IV: Severe life threatening infection.

4. Necrotising Fascitis

https://www.dermnetnz.org/topics/erysipelas/
https://journalfeed.org/article-a-day/2018/lrinec-score-physical-exam-or-imaging-for-necrotizing-infection
http://www.emdocs.net/cellulitis-mimics-ed-considerations/
https://first10em.com/cellulitis-antibiotics/
https://www.rcemlearning.co.uk/modules/cellulitis-and-other-skin-infections/
https://journalfeed.org/article-a-day/2018/is-a-blood-culture-needed-in-cellulitis
https://www.rcemlearning.co.uk/references/cellulitis/
http://www.tamingthesru.com/blog/2018/9/3/necrotizing-fasciitis-and-the-spectrum-of-soft-tissue-infections

Tuesday, 13 November 2018

Bleeding in Pregnancy

<23 Weeks - Early Pregnancy 
This has been covered here: https://www.rcemlearning.co.uk/foamed/induction-bleeding-in-early-pregnancy/

Later Pregnancy
https://www.rcemlearning.co.uk/modules/bleeding-in-pregnancy/

Antepartum Haemorrhage
>24 weeks gestation
Placenta praevia - stage depends how much of the os is covered by the placenta. Bright red and painless bleeding.
Placental abruption - complete or partial separation of the placenta. Causes lots of bleeding which may be concealed. Normally associated with continuous abdominal pain.
Vasa praevia - the fetal blood vessels run everywhere, not protected by the placenta. They may run over the cervix. High perinatal mortality - easy to rupture the fetal blood vessels. Can cause painless bleeding.
AntiD may be needed after a potentially sensitising event.

Hopefully all of these will be identified by screening, and hopefully these patients will present to the maternity assessment unit, not the ED!

PostPartum Haemorrhage
Primary PPH - in first 24hours. Secondary PPH - up to six weeks. Again, hopefully these patients will present to MAU not ED.

In pregnancy, problems are the 4Ts
 Tone, trauma, tissue, thrombin.
 Tone: uterine massage, bimanual compression, catheterise, give syntrometrin

Bleeding should slowly stop after a 12 weeks. It's often significantly less after the first few hours, and should change from  bright red to brown (lochia).
The commonest cause is endometritis. There may be retained products - start IVs, get an USS. If there's no RPOC, there could still be endometritis. The uterus in endometritis will remain palpable after 14days after delivery.  Endometritis is a clinical diagnosis.
I think bleeding persistently after delivery needs to see O&G.
Bleeding that stops and starts again is probably "new" bleeding.


https://www.bmj.com/content/358/bmj.j3875?sso=
http://www.emdocs.net/postpartum-endometritis-ed-setting-presentation-evaluation-management/


B12 Anaemia

B12 deficiency, cobalamin deficiency or pernicious anaemia is also knon as Biermer's anaemia, Addison's or Addison-Biermer anaemia. It's one of the megaloblastic anaemias.

Pathophysiology
Normally, B12 is absorbed through the ileum with the help of intinsic factor which is secreted by the parietal cells.
Various things can stop this happening - antibiodies to parietal cells, like in atrophic gastritis, antibodies to intrinsic factor like in pernicious anaemia, lack of a terminal ileum, or disease of the ileum - like Crohn's disease, and reduced b12 intake.
It takes a while for the disease to become apparent as there's 3-5 years worth of reserves in the liver.
Lack of B12 means that DNA replication is slow, so cells divide less but grow bigger. This gives you your macrocytic or megaloblastic anaemia.
Lack of B12 means the conversion of homocysteine to methionine is reduced, so there are high levels of homocysteine - causing things like atherosclerosis, thromboembolism and osteoporosis.
More importantly, B12 is a cofactor in the conversion of methylmalonic acid into succinyl CoA. Without this, the dorsal and lateral spinal columns are demyelinated, through an unknown mechanism, so you get neurological symptoms.

Investigation
FBC will show macrocytic anaemia, and maybe neutropaenia and thrombocytopenia.
A blood film will show anisocytosis and poikilocytosis.
Bilirubin may be increased because of haemolysis.
Then you can look for autoantibiodies, and maybe an absorption test like the Schilling test.


Symptoms
Symmetrical, legs > arms
Ataxia
Loss of position sense
Loss of vibration sense

Low grade pyrexia, weight loss, diarrhoea, jaundice due to haemolysis, pallor due to anaemia, premature greying of the hair.

Treatment
If B12 levels are low, then patients need intramuscular B12 and a haematology referal. If there is neurological involvement, 5 - 6 loading doses of 1000mcg, followed by maintainence of 1000mcg every three months.
If B12 levels are borderline, then oral B12 may have a reponse and be diagnostic.
Patients often feel better within 24hours of starting treatment.
If patients are asymptomatic, there is debate about their treatment- monitoring seems preferred.

B12 is naturally found in animal products - fish, meet, eggs, milk. It's not generally present in plant foods, but is in fortified cereals. It's worth mentioning that pabrinex doesn't contain B12!

http://calgaryguide.ucalgary.ca/vitamin-b12-deficiency/
https://www.gpnotebook.co.uk/simplepage.cfm?ID=1288699922&linkID=26150&cook=no