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