drugs in society part 1

have been to 2 very interesting events about drugs this week

one was the high society exhibition at the wellcome collection

very well put together, thought provoking and, in places, really beautiful

the exhibit is not too large but does contain a good chunk of material

i would strongly encourage you to go

it is just round the corner & public science does not get much better than this

there are several associated events, one, a tour with the curator is on this evening (dec 16 @ 1800-1845)

_ _ _

my highlights:

1) the home-made crack pipe & the crack pipe art by keith coventry

have never come across a crack pipe before & the delivery device is ingenious

the thinking behind one of keith coventry's pieces was to do with the user's experience of the pipe - they cannot experience any part of the 'moment' except where they are in relation to the pipe - serious addiction

2) drug use through history

cannabis has been used in india for thousands of years

the british used opium (which contains 12% morphine) to gain advantage over other colonising powers in china

the opium was grown (forcibly) in places like bengal & trafficked by the east india company

rich chinese smoked it using beautiful expensive pipes, the poor using simple apparatus (partly to reduce hunger)

there were also interesting insights into the tribal use of various compunds eg peyote cactus

famous users were also detailed, eg freud, coleridge & sherlock holmes (who injected opium until he was weaned by watson)

currently the (illegal) global cannabis industry ($113bn per year) is worth more than coffee ($98bn) or porn ($95bn)

3) animals on drugs

the animal experiments shown were great

NASA gave various substances to spiders & recorded their subsequent webs

the caffeine web is shoddy-looking & full of holes, the cannabis web is meticulous & unfinished

bruce alexander's 'rat park' experiments are also shown

his hypothesis was that well housed rats will be less 'addicted' to morphine

to test this he did a series of experiments comparing rats living in 'rat park', a 200 sq foot rodent paradise with play areas, privacy areas & lots more besides to similar rats living in cages

the 'free' rats were 16 times less likely to drink morphine water compared to caged rats when given a free choice

fascinating stuff!

_ _ _

lots to think about as we (collectively) will consume large quantities of drugs over the holidays (alcohol, caffeine, whatever ...)

Salaam

learning neurology

hello


i have talked about my favourite neuro learning resources before

here is an update

do add your suggestions / opinions
_ _ _

1) neurological exam made easy by geraint fuller

great book - short, readable, nice pictures, clinical

2) neurological differential diagnosis by john patten

brilliant book - the best anatomical drawings of neurology (done by the author), clinical, practical
not so short, but all you will ever need to know about neurological examination (unless you become a neurologist)

3) neuroanatomy through clinical cases by hal blumenfeld

great book - very sensible way to learn neuroanatomy, lots of cases, good pictures, associated website
not short, but very readable

4) neuroanatomy: draw it to know it by adam fisch

great book - teaches anatomy by way of staged diagrams illustrating all the major neuro systems
good text too
not short, but nicely 'chunked'

5) neurologic examination website by university of utah

excellent website - videos of normal & abnormal findings for all major components of neuro exam, downloadable (with permission)

6) the neurological exam website by university of toronto

good site - not as comprehensive as utah site, but well laid out with nice tables
videos only with healthy volunteers

7 eyevideos.blogspot.com

good site made by a young ophthalmologist with videos detailing neuro-ophthalmology examination & investigations

Salaam


s

a 20-year-old woman with slurred speech and weakness

yesterday we briefly examined a very pleasant university student who has been unwell since earlier this year

she was alert - we did not test her higher order cognitive function

she had obvious slurring of her speech, which had been present for a month or so

we concentrated on examining her arms

we talked (again) about the importance of INSPECTION

fasciculations can be quite hard to see, especially if the light is poor and the muscles involved are small, so really have a good look - make sure you turn the lights on & adequately expose the patient (which can be done comfortably and with dignity)
_ _ _

as an aside, i wanted to mention motor neurone disease - i know very little about this condition; it results in upper and lower motor neurone signs; it must be one of the worst diseases and there are no treatments, riluzole, the only drug available increases life expectancy by a few months at best (miller et al, 2007);

here is link to a video of the historian tony judt talking about the disease

he died in august
_ _ _

we went on to test tone and then power

this is often done quite badly

my most useful tip (after practise a lot) would be to slow down & think about what you are doing

use the MRC grading scale

if a patient uses their muscles to move their arm (or leg) into the correct position against gravity, then they have already scored 3/5
_ _ _

here is a link to another website showing you how to do a neuro exam

i particularly like the muscle action & innervation chart in the motor section

_ _ _

we talked about the decreased utility of testing for inco-ordination in the context of muscle weakness
_ _ _

this lady has a diagnosis of multiple sclerosis

she has had several clinical events and has had a full diagnostic work up including MRIs, LP, VEP

the visual evoked potential involves being shown a visual stimulus, eg a pattern, and then measuring electrical responses primarily from the occipital lobe using EEG

[why the occipital lobe?]

_ _ _

she was actually admitted for episodes of loss of consciousness, the cause of which is not entirely clear

interestingly she is due to have a tilt table test - i mentioned my ignorance of the effects of MS on the autonomic nervous system

she is in the midst of a relapse affecting her speech, face, right arm & leg, and is due to start steroids this week

Salaam

a 48-year-old woman with breathlessness and difficulty walking

on monday we saw a very pleasant middle-aged woman, a pretty heavy smoker, with a history of COPD

she had had multiple courses of oral steroids in the past but no previous admissions until last week when she had a short stay for an infective episode

she become breathless enough to significantly restrict her activity around 24 hours post discharge

we focused on examining her so did not talk much about her symptoms

we could have explored possible reasons why she deteriorated

what do you think?

possibilities that spring to my mind are:

- ineffective treatment for respiratory infection (eg resistant organism)
- PE
- pneumothorax
- heart failure
- something else
_ _ _

thanks to our patient's forbearance, we examined her chest & legs (neuro) in detail

thoughts:

- make an effort to really stand at the end of the bed and LOOK:
you can determine asymmetry, depth of breathing, colour, adjuncts and much more; in this case we would have been able to get the diagnosis from just looking without doing anything else

- practise percussing things: in the experience the key is having a very stiff middle finger of the left hand, and a very floppy right wrist; you can percuss lots of things (eg walls to see where joists are, barrels to see how full they are)

- most medical students find neurological examination hard - so you are not alone!

- knowing some neuroanatomy helps, as does giving clear instructions

- i have mentioned my favourite neuro learning resources before

our patient had weakness of left ankle dorsiflexion and a lost left ankle jerk, suggesting an S1 root lesion; her sensory loss was patchy

her leg symptoms are long-standing; we did not look at previous spinal imaging -we should have done!
_ _ _

Salaam

s

blood

i gave blood a couple of weeks ago

i am ashamed to say it was only my second time

it was pretty painless & the actual blood-letting took 4 and a half minutes to take 468mL

[the ultra-rapid haemoglobin estimate is a thing of beauty - how does it compare to a lab test?]
_ _ _

only 4% of the population are blood donors and as of today, stocks of O- blood will last just over 4 days

i am constantly amazed by the dedication and community spirit of the students i meet, so if you have ever thought about giving blood, but never quite got round to it, take the chance now

call 0300 123 23 23 or use the blood.co.uk website


Salaam

a young man who ingested 4.5g of cocaine

we did not see this gentleman and only discussed his case very briefly

however, as a clinical pharmacologist, this was too interesting not to share

we did not get onto signs, symptoms and treatment of cocaine toxicity, but it is an important clinical issue and is worth knowing something about

eMedicine has a decent review

_ _ _

this gentleman swallowed 4.5g of 'cocaine' wrapped in cling film

my first question was: what is a lethal dose?

we discussed ways of answering this question in the UK, namely toxbase, and the national poisons information service

it turns out that there is a great deal of variability as to what a lethal dose might be, and it depends on the route of administration - IV as little as 20mg, orally or intranasally 500mg-1.4g

another key issue is the purity of the cocaine - most cocaine on sale in the UK is heavily 'cut' for example with lactose, mannitol, baking powder

average purity in the UK around 34%, price £30-50 per gram (data from drug scope)

one 'line' might contain 50-200mg (depending on how big the line is)

one cocaine cigarette might contain 300mg & is more commonly associated with myocardial infarction
_ _ _

the clinical pharmacology of cocaine is fascinating

cocaine powder is often the hydrochloride salt which is snorted (white lines)

it is made by pulverising coca leaves, then mixing with an alkaline substance and organic solvent and removing leaves to produce coca paste

this paste is often smoked in south america

for transport, the paste is usually converted to cocaine salt (powder) via the addition of hydrochloric acid

this chloride salt has a boiling point of 190+ degrees which means it cannot be inhaled

however it is water soluble, and thus can be absorbed through mucous membranes
_ _ _

freebase & crack cocaine are made by removing the chloride to leave the base alkaloid

cocaine base sublimates at around 90 degrees - it is thus smokeable
_ _ _

we did not get onto signs, symptoms & treatment of cocaine toxicity, but it is an important clinical issue and is worth knowing something about

eMedicine has a decent review



Salaam

a new AAU firm

we had another firm of students join the acute admissions unit today

as usual we introduced ourselves, briefly mentioning our genetic inheritances

this time the group's knowledge of what a SNP is was good, thanks to the presence of a geneticist

i have written about SNPs before - it is an area of such growing importance that i would strongly recommend you find out something about them
_ _ _

our case discussion, truncated because of time was again centred around 'dizziness'

while we did not go through things in great detail, the importance of disentangling the terminology was highlighted (see previous post)

the other thing that struck me was the need for detail when it comes to the history in this presenting problem

you really do need to find out everything you can about the circumstances of what happened

eg, where: which shop? which department? having just done what? carrying what? wearing what?

all these details will help you to build up a picture of 1) what this lady's cognitive function is like and 2) clues that point to a specific diagnosis (eg fast onset-fast offset for arrhythmia)
_ _ _

we also mentioned how to start a case presentation well (content - the right amount of data & process - a positive, professional dialogue)

'framing' the problem is key, because without asking the right question, you cannot hope to find the right answer

i would encourage you to watch how real doctors present cases

how many of them need the notes to present? not many i suspect

could you present without your notes?


Salaam


sabih

a 66-year-old woman with dizziness

we saw a very nice lady today along with her daughter

the main issue was 'dizziness'

we returned (again) to the confusing terminology and the need to take a detailed history

important categories of explanation were:

vertigo
orthostatic hypotension
cerebellar disorders
weakness
seizures
syncope
other stuff
_ _ _

our lady had an acute disorder affecting her balance with unsteadiness of the visual environment which sounded like vertigo

i recently had the chance to hear an excellent lecture on vertigo by a professor at imperial called adolfo bronstein (he has written a book called dizziness)

this is essentially his approach

the 3 syndromes to be considered are:

- a single episode (most likely to be vestibular neuritis)
- recurrent vertigo (eg BPPV or migraine)
- chronically off balance(eg gentamicin toxicity)

_ _ _

this lady had a single event

the key issue is whether there is a central (brainstem) or peripheral cause (vestibular nerve)

with central lesions abnormalities of other cranial nerves are likely to be found so they need to be tested for carefully

the anterior inferior cerebellar artery which supplies the labyrinth also supplies the cochlea so with a stroke hearing loss is likely

hence a vital question is "have you gone deaf?"

_ _ _

our patient had no hearing loss and had features of a flu-like illness

we examined her cranial nerves and these were intact

importantly she had no nystagmus or cranial nerve palsies

her hearing was normal

we performed a head impulse test (also called head thrust or halmagyi test) showed a slowed response on the right

all of this points to an acute labyrinthitis

_ _ _

we went through cranial nerve examination slowly

again the key is clear instruction!

we thought about which nerves are being tested during which extra-ocular movements

we also thought about simple testing of the quadrants for visual fields

and the need for good visibility when testing palatal movement
_ _ _

bppv causes episodic vertigo and is due to debris in the posterior semi-circular canal



it is made worse when turning to a particular side when lying down

halpikes manoeuvre is used to diagnose this; the semont manoeuvre is used to treat bppv and is successful 80% of the time


menieres syndrome causes hearing loss and is rare

2 elderly women with falls

fayth presented the case of an 86-year-old woman with a 'mechanical' fall


we remembered dr hayman's assertion that there is no such thing as a mechanical fall!


rory also mentioned an 85-year-old woman with a more dramatic fall
_ _ _


we reviewed possible causes of loss of consciousness (which she did not have? but the 85-year-old woman rory saw did)


- cardiac (rhythm, valve)
- stroke (anterior, posterior, limb weakness)
- epilepsy (new onset in elderly space occupying lesion till proven otherwise)
- vaso-vagal
- postural hypotension
- anaemia
- infection
[drugs]
_ _ _


we talked about the critical nature of the history which needs to be taken in great detail


eg when, where, what next etc


specific questions are also important, eg palpitations? post-event sleepiness? position?


there is a bit more on this subject in the case from 5-7-10

_ _ _

rory nicely presented his patient's social history

she was cooking for herself, shopping for herself and going out to visit friends

an excellent level of function

_ _ _


fayth's lady also had type II diabetes and aortic stenosis, both important things to consider


eg oral hypoglycaemic OD [what was the BM], critical aortic stenosis


unfortunately we were not able to examine her
_ _ _ 


we did look at her ECG


she had LAD & LBBB

we concluded it was essential to find out if this was new, which could be due to an MI


we also enacted the 6 ECG limbs leads and thought of a quick method to determine raxis (one of the 3 Rs of ECg analysis!)

_ _ _

comments welcome

Salaam

sabih

a 52-year-old woman with tiredness and visual disturbance

yesterday rory presented an interesting case of a middle-aged woman, previously pretty well, who has become increasingly tired over recent weeks


she has also had some blurriness of vision


TIRED ALL THE TIME (TATT)


this is a common complaint but can sometimes be very difficult to diagnose


(also a common OSCE scenario)
_ _ _


i could not find a specific chapter in davidsons, harrisons or my favourite symptom book tutorials in differential diagnosis (written by eric beck who invented the MRCP exam & is still involved in PDS teaching at he whitt - i was his house officer many years ago; robert souhami was dean of UCL medical school)


in my library the best i could do was a case from an excellent MRCP book (case 2.50 in PACES for MRCP by tim hall)

however, i did find a BBC radio program all about TATT, part of the very good case notes series (with a full transcript available)
_ _ _


we discussed various causes:


- major organ failures (heart, kidneys, liver, lungs)
- endocrine disorders (thyroid, diabetes, also addisons, hypopit)
- cancer
- depression
- anaemia
- auto-immune type disorders (rheumatoid, lupus, GCA, polymyalgia)
- drugs, eg beta-blockers


our patient did not have any features pointing to the specific causes above?
_ _ _


we did not really go through investigations in detail
_ _ _


while we did not examine her, you did go through her pupillary reactions with gordon


she had an afferent pupillary defect [like this one?]

these data point to the possibility of multiple sclerosis

_ _ _

we briefly talked about this mostly relapsing-remitting condition

the diagnosis requires more than one 'attack' in more than one place

the criteria i learnt have now been replaced the the mcdonald criteria which incorporate the advances MRI has brought

rory was going to update us about MS [perhaps as a comment?]

we need to review her investigations, including MR imaging & LP

[tangentially, josiah bartlett, the fictional US president in the west wing, had MS & hid it from the electorate during his first election]

_ _ _

we finished by considering what we would do to learn more

reading a textbook & wikipeding were mentioned

find another patient with MS (soon) is a particularly good strategy

Salaam

sabih

a 20-year-old woman with a mixed overdose

apologies for the hiatus
_ _ _

last week aya presented the case of a young woman who took an unspecified amount of paracetamol & aspirin tablets

she phoned her GP fairly soon after ingesting the tablets, and come into casualty soon after

she had a history of self-harm but no previous overdoses

she is managing (?) to study & work part-time
_ _ _

we discussed the critical issue of timing of the overdose

this is due to the practicalities of using the paracetamol OD nomogram - see below: this can be found in the beginning of the BNF

we said:

- the graph does not start until 4 hours has been reached

- levels can be expressed in 2 different units, either mg/L or mmol/L, clearly it is crucial to know which is used in your lab

- the high risk line includes people who have had their liver enzymes induced or who are malnourished

_ _ _

we had a short discussion about the nature of drug metabolism

in essence metabolism makes compounds more water-soluble, and hence more likely to be excreted via the kidneys

the enzymes involves are part of the cytochrome p450 system

_ _ _

we also talked about how not very nice it is to die from paracetamol poisoning

the key measurements on day 2 are prothrombin time (or INR), pH, lactate & creatinine (NB not AST, ALT etc)

any deterioration necessitates a call to your local liver centre

_ _ _

we touched on the mechanism of the toxicity

paracetamol is normally metabolised by adding a polar group, mostly sulphate or glucuronide

it can also be metabolised to NABQI (N-acetyl-benzoquinoneimine) [normally 10%]

this is a dangerous chemical as it reacts with DNA & cell proteins [it is a strong oxidiser]

NABQI is normally mopped up by glutathione [an anti-oxidant]

when glutathione stores are deplete, cell damage will occur

therefore the antidote is to give glutathione

glutathione is made from 3 amino acids, 2 of which are plentiful in cells

the third, cysteine, is the rate-limiting species, and this is the treatment: N-acetyl-cysteine or NAC [the N-acetyl- bit helps absorption]

the other antidote is (oral) methionine which is more proximal in the synthetic pathway

_ _ _

this whole anti-oxidant pathway is worth being aware of 

a lot of current research in a wide variety of conditions, from IHD to autism, involves these pathways

_ _ _

we mentioned the need to give NAC IV at 3 different infusion rates

_ _ _

other issues we covered:

- aspirin OD, clinical & metabolic features, and treatment (alkanise urine ± dialysis)

- high risk features for recurrent suicide attempts

- social isolation & the buffering effect of friends

Salaam

sabih

a 40-year-old African-Caribbean man with chest pain

lukas presented in interesting (?!) case of a man with a short history of chest pain going through to his back

we discussed likely culprits in this age group

we came up with:

- IHD
- aortic dissection
- PE (large & sma
- GORD
- musculo-skeletal

the full list is longer [how many does the C&O list?]

we said this is a common presenting complaint - so it should be known intimately
_ _ _

this gentleman was actually pretty fit with not much atherosclerotic risk

it would have been good to get a better description of the pain from him

& also to know whether he has any illicit (cocaine) drug use [why?]
_ _ _

there was not much to the history

we thought about questions to be answered on examination

we considered:

- does he have signs of aortic dissection?
- is he in heart failure?
- does he have evidence of high cholesterol or diabetes?
- might he have a DVT?

we would like to take the blood pressure in both arms
_ _ _

the diagnostic probabilities had not shifted too much, although PE was less likely

we thought about tests that might help, both in casualty & on monday morning

the ECG is key [we mentioned dissection causing inferior MI]

a CXR might help, although a normal CXR does not rule out dissection

a CT aortogram or trans-oesphageal echo would be needed

Dr Donna D'Souza: radpod.org

we also considered blood tests (FBC - to look for anaemia, creatinine - to check out his kidneys before we give him nephrotoxic contrast, TFTs as hyperthtyroidism might trigger ischaemia)
_ _ _

it turns out that his initial ECGs showed complete heart block with a rate of 30

this was treated with atropine (back to sinus??)

he had a wenkebach-type of heart block



[this is a second degree block - because some p waves are not conducted]

[wenkebach is type 1 second degree, also called Mobitz 1]

[wenkebach is not usually dangerous, compared to second degree type 2 (Mobitz II) which is]

he had a normal echo (apparently) & was discharged with a view to a 24-hour tape & cardiology follow up
_ _ _

we very briefly thought about why a 40-year-old man might have complete heart block (IHD or ...)
_ _ _

things to learn:

- the assessment of people with chest pain
- stuff about aortic dissection
- stuff about complete heart block (CHB)
- echo features of imminent cardiac tamponade
- CT anatomy of the thorax


Salaam


sabih

a 45-year-old man with vomiting and light-headedness

last week charlie presented the case of a man with a short history of vomiting what he thought was blood

(he also had left-sided upper abdominal pain - we very briefly thought about what might cause this but the main focus of our enquiry was GI bleeding)
_ _ _
we discussed the important issue of not assuming this is a GI bleed

1) it could be from the mouth or possibly respiratory tract
2) be sceptical about the fluid being blood: either see it yourself (having seen it before) or only believe someone you trust (eg experienced nurse) [the story of the lady with the femoral hernia]
_ _ _

we then talked about 1) assessing severity & 2) possible diagnoses
_ _ _

1) severity

questions about the vomit, eg volume, frequency
questions representing volume depletion and /or anaemia, eg dizziness on standing, syncope

2) the potential diagnoses:

- ulcer disease
- drug-induced erosions
- liver disease (abnormal clotting/varices)
- cancer
- Mallory-Weiss tears

we briefly explored the questions that might let us differentiate between these conditions
_ _ _

we then went to the bedside & wondered what broad questions clinical examination should try to answer

- is this patient hypovolaemic?
- does this patient have chronic liver disease?
- does this patient have cancer?

we did not manage to examine the patient
_ _ _

we discussed then discussed the key investigations, emphasing the need for a group & save/cross-match sample, and the requirement to fill a blue-top (citrate) bottle to the brim

we also mentioned that the Hb concentration might not be reliable initially
_ _ _

it turned out that the patient had an urgent OGD which showed oesophageal varices

he was also given a large volumes of intravenous colloid & crystalloid & he subsequently went into pulmonary oedema, for which a small dose of diuretic was required
_ _ _

it would be ideal if we can follow him up & see how his varices are managed in the long-term


Salaam


sabih

on call @ UCLH

having been on call on monday night i thought i would share with you what went on

2100-0900 we had:

- a 46-year-old lady with a large pneumothorax (which needed an emergency drain) and 'crack lung'
- a 70-something malaysian lady with HONK & a Na of 178
- a 20-something lady with a fever & headache who we LP'd
- a 40-something lady from ghana with a fever and an ALT >3,000 (bilirubin around 200)
- an 80-something man with an INR of 4 & PR bleeding
- a 70-something man with metal mitral & aortic valves with worsening heart failure
- 2 men needing urinary catheters
- a 30-something lady 34 weeks pregnant ?PE

+ lots of other stuff

we had 2 hardy students (sheena & andy) stay beyond 0300 (but actually that was before a lot of the interesting stuff!)
_ _ _

the reason i put this up is:

1) to demonstrate that clinical problems like these are our stock in trade
2) to encourage you to be on call at night (all night if possible)
 - the hospital is different at night, there are fewer people around & if you make friends there is a lot going on
_ _ _

i will put up the radiographs of the pneumothorax lady up next week


Salaam


sabih

a 20-year-old man with dizziness on standing

ben a presented a very interesting case of a young man in the UK for a course in political science as part of an Erasmus programme who presented to casualty with marked lightheadedness on standing of 1 days duration

we discussed (again) the issue of pinning down what a patient means by dizziness

here our patient was fine lying flat but became lightheaded with altered vision on standing

there was also associated nausea & abdominal pain

he was able to move into his flat (with the attendant box lugging) on the saturday

any ideas as to diagnosis?
_ _ _

there seems to be a clear story of postural symptoms, most likely secondary to hypovolaemia

[causes orthostatic hypotension?: diabetes, drugs, parkinsons, autonomic dysfunction, addisons]

we briefly talked about blood loss

(1 pint is actually a US pint or 473mL, not the UK (imperial) pint of 568mL)

catastrophic blood loss might occur into the gut, lungs, abdomen, pelvis

lethal bleeding (without exsanguinating) into the pericardium or brain
_ _ _

we mentioned the surface markings of the pleura but did not finish the conversation

see here for more
_ _ _

we then went to chat to our patient who has addisons disease

click here for thomas addison's own pictures (he was a physician at guys)

[NB why do people with addisons exhibit hyperpigmentation?]

JFK had addisons

our patient was first diagnosed in the US 2 months ago

he takes 20mg of hydrocortisone daily as his normal regimen (which he tripled over the weekend)
_ _ _

on examination he had no hyperpigmentation in the buccal mucosa or palmar creases

he had a 15mmHg systolic drop on admission (?now)

his abdomen was soft & non-tender with no masses or organomegaly
_ _ _

on arrival he had a Na of 120mmol/L with a K of 6.8

his ECG showed peaked T waves

he was given calcium gluconate & insulin/dextrose
_ _ _

we briefly mentioned causes of addisons disease:

autoimmune, infection (incl TB), hameorrhage, cancer, congential adrenal hyperplasia, pituitary problems

investigations:

importantly electrolytes, septic screen
_ _ _

things to read about:

1) addisons
2) emergency treatment of hyperK
3) hydrocortisone


Salaam


s

learning medicine

this is a big week for you

it marks the first time you are part of a clinical team (however loosely)

you are also let loose on the general public whilst wearing stethoscopes round your necks

so make the most of it!
_ _ _

more than anything else SEE PATIENTS!!!

nothing teaches you medicine like your patients, no amount of wonderful professors or brilliant lectures can substitute for getting to know the stories of real people (and having responsibility for making them better)

i strongly recommend you make a spreadsheet/notebook/database in which you record every patient you see

list: initials, hosp number, age, gender, PC, diagnosis & outcome

if you are disciplined you will have an unparalleled learning resource by the time you hit finals

how many patients do you think you will see?

go on, have a guess
_ _ _

whilst patients are by far the most important thing, they are not sufficient

you will also have to read

i have already offered suggestions for neurology texts

i like davidsons (more chatty & coherent than kumar & clark, but less detail)

harrisons is excellent - don't let its size put you off - the first 50-odd chapters on presenting complaints are really useful & often the first thing i look at



Salaam


sabih

a 64 year old man with incoordination

sheena briefly presented the case of a man who fell over at the bus stop

we focused on examining his cerebellar system

we could only examine his left arm

he had:
- no rebound of the outstretched arm
- no dysmetria
- mild dysdiadochokinesis at the forearm
- moderate dysdiadochokinesis at the fingers
- unconvincing horizontal nystagmus in the direction of gaze
- a reasonable gait
- normal heel-toe walking

we did not test his speech
we did test his power (why would we want to do this?)
_ _ _

unfortunately we had to rush his story & did not look at his scans

sheena: could you update us (anonymously) please?
_ _ _

we talked about learning resources

i mentioned the book by geraint fuller which i think is excellent

this site from the university of utah is also excellent & demonstrates many of the signs we were discussing
_ _ _

Salaam


sabih

new year

welcome to this site: a space to record & review shared experiences


do leave comments / questions
_ _ _
half of you have heard me rant on SNP-ignorance


i would point you to the first post in this blog for more on the issue
_ _ _

yesterday 3 out of 5 of you clerked patients with some form of 'collapse'


sheena then went on to present the case of a 64 year old man who 'collapsed' at the bus stop


the first important point was: the terminology is confused & task 1 is to work out which type of collapse the patient is talking about


namely:


- loss of consciousness
- limb weakness
- loss of balance
- vertigo
- light-headedness on standing


see below for half an algorithm from Davidsons

_ _ _

we mostly talked about loss of consciousness & were tentatively dividing causes into cardiovascular, neurological & other

we did not get round to organising our diagnostic lists properly

we moved on to examining the cerebellar system (see next post)

_ _ _

25 year old diabetic with a grand mal seizure

after starting late ...

joel presented the case of a 25 year old Caucasian man with type I diabetes who had a witnessed seizures

there was some discussion of terminology (what is a funny turn?)

loss of consciousness was a key issue to establish

important categories of causes were neurological, cardiovascular and meto-toxic

features differentiating cardiogenic from neurogenic syncope are important - here is a bit table 18.21 from Davidson's - it's OK, but can you do better? neuro-cardiogenic is a fancy name for a faint

18.21 Typical features of cardiac syncope, vasovagal syncope and seizures

	Cardiac syncope	Neuro-cardiogenic syncope	Seizures
Premonitory symptoms	Often none	Nausea	Confusion
	Lightheadedness	Lightheadedness	Hyperexcitability
	Palpitation	Sweating	Olfactory hallucinations
	Chest pain		'Aura'
	Breathlessness
Unconscious period	Extreme 'death-like' pallor	Pallor	Prolonged (> 1 min) unconsciousness
			Motor seizure activity*
			Tongue-biting
			Urinary incontinence
Recovery	Rapid recovery (< 1 min)	Slow	Prolonged confusion (> 5 mins)
	Flushing	Nausea	Headache
		Lightheadedness	Focal neurological signs

*N.B. Cardiac syncope can also cause convulsions by inducing cerebral anoxia.

in this chap the alcohol intake is important - it will decrease seizure threshold & also causes hypoglycaemia [why?]

if this is a recurrent phenomenon it would be nice/critical to find out why? - this issue may kill him soon - is he bothered? is it an education problem? is it insulin regimen related?
_ _ _

we then digressed into what would you do if this fitting person was in front of you in resus

we demonstrated the gaping hole between book/rote learning "I would assess ABCDE" and learning by doing "I would look, listen & feel for signs of respiratory effort" [of course easier to say than do often]

we talked about diazepam PR, lorazepam IV and the need for general anaesthesia

BM stands for Boehringer Mannheim, not Bayer

50mL of 50% glucose (or x) is around 25g glucose (or x)
one regular UK Mars bar weighs 58g
_ _ _

lessons/memories were:

- key questions around funny turns
- double check the timetable
- blood bottle colours x2
- the importance of starting on time
- DR ABCDE

homework generated was

- acute management of hypoglycaemia (including which blood tests to do)
- emergency pages cheese & onion fitting
- fitting look at local fitting guidelines
- emergency pages cheese & onion electrolytes Na & K
- read illustrated colour text of endo
- long term follow up epilepsy in cheese & onion
- read management of DM in taught course & K&C
_ _ _

my view on things to learn from the case:

- managing hypoglycaemia
- managing acute seizures
- managing alcohol withdrawal
- types of insulin & how to use them
- unusual, but important causes of LOC in young people (eg HCM, brain tumours eg astrocytoma)
_ _ _

we also touched on how governments kill people, focusing on the USA

interestingly some states are now switching from a 3-drug protocol, to a 1-drug protocol (5g of sodium thiopental)

here is how the state of Florida executes (3-drugs: barbiturate, ACh antagonist, KCl 120mmol)

here is a video of a discussion at NEJM


Salaam