Archive for the ‘Neurology/Neurosurgery’ Category

Syncope

Wednesday, March 10th, 2010

This is one of my favourite areas, as patients present very frequently with this symptom. That very fact makes syncope a challenge. It is a symptom, not a condition in itself. We have to find the cause of the syncope. We need to be experts in this area as syncope presents some 5% of all emergency department visits and comprises 6-10% of admissions.

Our role is to risk stratify patients and make sure we don’t send home those with potential sinister causes. This is not as easy as it sounds, as there are many causes.

I often hear, “… well he’s still a little hypotensive, so that was probably the cause…..” What was probably the cause? Up to 50% of patients with syncope from whatever cause will be hypotensive. Also beware hypotension in the elderly. In this age group you need to start thinking about the abdominal aortic aneurysm.

Did you know that up to 12% of patients with thoracic aortic dissection, present with syncope as their ONLY complaint? That is a little scary.

We need to differentiate those causes associated with mortality and morbidity. This means working out who has had a cardiac or neurological cause of syncope as well as differentiate syncope from seizure.

WHY IS FINDING CARDIAC CAUSES SO IMPORTANT?

-Because mortality from missed cardiac causes can reach 30%

-Because underlying heart disease, irrespective of the cause of the syncope, is associated with an increased risk of death.

WHAT ABOUT THE NEUROLOGICAL CAUSES?

-We know that patients with a neurological cause of syncope have two times the risk of a stroke, when compared to those without syncope.

TAKING A GOOD HISTORY IS THE KEY

-How did the episode occur? Was there a sudden loss of consciousness, or was there a prodrome of sweating and dizziness etc.?

-This is important as a sudden loss of consciousness with no prodrome leads us to a cardiac cause.

-Was it associated with a change in position or did it occur whilst sitting?

-Again, syncope when sitting or lying can potentially point to a more sinister cause, which includes cardiac or neurological.

-Is there a family history or cardiac disease or sudden cardiac death?

-Here we need to start talking about BRUGADA SYNDROME and thinking about those terminating arrhythmias that can occur.

-Were there other associated symptoms of chest pain, or palpitations, or vertigo or nausea and vomiting?

-Was there a headache and if so was it sudden?

-Let’s not miss the potential subarachnoid haemorrhage.

This is such an important topic. Watch the video which contains parts of a previous lecture I’ve given on this and know that the latest will be covered tis year in the lecture series.

The update at RESUS 2010 will include:

-An approach to the diagnosis of Syncope

-Syndromes such as BRUGADA, that you must learn about and cannot miss.

-A discussion of the rules in use for looking at patients with syncope, such as the San Francisco Syncope Rule and the Boston Syncope Rule.

-We’ll talk about loop recorders, and here’s a really important thing I can’t understand. Some of these loop recorders are there to catch an arrhythmia, yet for them to be activated, the patient has to hold a probe up to them when they feel a syncopal episode coming on. What?! I have never had a patient successfully do that.

-We’ll talk about tilt table testing

-We’ll also talk about some of the latest treatments and MORE!

For now enjoy the snippets of video I’ve put together on the ‘resus blog’ and I hope you’ll take the time to come and listen to some great lectures at RESUS 2010

SEX, DRUGS AND SUDDEN HEADACHE

Monday, February 8th, 2010

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Sudden onset of headache and the potential underlying Subarachnoid Haemorrhage(SAH) is not an uncommon presentation to the Emergency Department.

I recently saw a 32 year old male who presented with a sudden onset of severe headache whilst squatting in the gym. He also complained of pre-syncope. What do we need to do for him?

SAH has an incidence of 1:10,000 of the population annually(Stroke1989;20:718-724). Of all the patients presenting with a headache, some 1% will have a SAH, but that incidence increases when the headache is sudden and severe(Lancet 1994;344:590-593).

But how about that group of patients that come in with a sudden onset of headache after weight lifting in the gym, or other physical exertion such as occurs during sexual intercourse? Do we have to take more care or less, or the same in this patient group? It is often said that these headaches are nothing to worry about. BUT BE CAREFUL, as you cannot discern, the sinister from the benign.

Sudden onset of headache, also called  a ‘warning leak’ or ’sentinel headache’, is a red flag as it may indicate a subarachnoid bleed. If that patient re-bleeds, then there is about a 50% chance of mortality. Of the surviving 50%, up to half, will never get back to their normal level of functioning.

So it’s important not to miss this!

What the sentinel headache provides is a window of opportunity to make the diagnosis. At the same time, it identifies a subgroup of patients, with a worst overall outcome, if they have a further aneurysmal bleed(J Neurosurgery 1996;85:995-999).

Usually we order a Non- Contrast CT brain. This is quite sensitive in picking up a subarachnoid Haemorrhage(SAH) when done early ie., a few hours. BUT it’s not 100%. It may be as high as 97-99%(J Neurology Neurosurgery and Psychiatry 1995;58:357-359). The sensitivity decays with time, so that a few days down the track, the CT is almost useless.

If the initial CT is positive for SAH, then call Neurosurgery and off the patient goes. They need further imaging and planning for surgery or radiological coiling.

But what if we don’t find a bleed on CT? We need to be aggressive with our approach and lumbar puncture(LP) that patient. There is some debate about whether the LP should be done early or late. This is related to the development of xanthochromia, which is due to a byproduct or red cell breakdown. This can take up to 8 hours to develop, and is detectable in all patients that have had a bleed at 12 hours and for up to 2 weeks(J Neurology Neurosurgery and Psychiatry 1989;52:826-828).

The methods by which CSF is analysed, are concerning. Some labs use visual detection of xanthochromia, ie., someone holds the tube with cerebrospinal fluid up against a light and comments on whether it looks yellow and thus positive for xanthochromia(I know it sounds crazy, but there it is!). This has a sensitivity, at best of 50%(NEJM 1997;336:28-40). Other labs use spectrophotometry, considered the gold standard. There occassionally are false positives with this method, as the frequency bands for detection are widened, so as not to miss bleeds(Emergency Medicine 2000;12:212-217). This would not be a problem, except that angiography to further plan for surgery, is associated with a 0.1% mortality and 1% morbidity(Stroke 1987;997-1004).

The push now is for early LP and the detection of red blood cells(RBC). In a study I did, several years ago, looking at those patients with SAH and a positive angiogram, a cut-off or 1000 RBC allowed us to rule-out SAH. This was statistically significant. However, this was a retrospective study and needed prospective validation, before we could apply its results. That sort of study is difficult to get ethics approval for.

Why is there this urgency for an early lumbar puncture? Why don’t we wait for 12 hours and then detect xanthochromia? This is because re-bleeds occur in about 25% of cases and with a frequency that is greatest in the first 24 hours(MJA 1989;150:183-188) Ultra-early re-bleeds can occur within a few hours.

What about not doing an LP and just MRI/MRA? One of the issues here is that all aneurysms will be shown if present. Isn’t that good you say? Here’s the catch. Approximately 6% of the population have aneurysms as an incidental finding at autopsy, so we don’t know if the aneurysm found on MRI caused the headache or not. The only real clue, is that these ‘incidental’ aneurysms are usually small ie., less than 6mm and we know that most(not all) aneurysms need to be greater than 1cm or so before they burst. Remember the emphasis on the word ‘most’.

Now let’s get back to the patient. He was well, with GCS of 15 and nil neurology. No past medical history, No medications and nil allergies. He had also never had this headache before, nor was he a migraine sufferer.

The sudden nature of the headache made me nervous. So a CT head was done and was normal. Then a lumbar puncture to look for red cells. How many do you need? Well according to the neurosurgeons(and no-one really knows), if the CSF is discoloured as it comes out, then it’s positive, you don’t need cell counts. If it’s clear, it’s OK. It was a champagne tap. I would still look at the cell count.

So he was discharged.

Exertional headaches have sometimes been called weightlifter’s headache. They were first reported in La Medicine in 1932 by Tinel in the paper, “La Cephalee a l’effort. Syndrome de distension des veines intracranienes”.

We know that exertional headaches are more common in males, by a factor of 4:1 and there is some predisposition, or underlying tendency to migraine. The mechanism is still uncertain. There appear to be two types; firstly a cervical soft tissue strain and secondly a reflex vascular spasm. In reality, no-one is really sure.

They are classified by the International Headache society as being headaches not associated with structural lesions. In most cases, these are benign, with a good outcome. However there is some evidence that these sudden, often described as ‘bursting’ headaches may in fact be associated with underlying intracranial lesions.

In the Medical Clinics of North America in 1961(52:801-808), a study involving 103 patients with exertional headache found that at 3 year followup, 10 had developed intracranial lesions.

In Neurology (1996;46:1520-1524), a small study of 28 patients, with exertional headache demonstrated that 12 had a SAH and one a malignancy.

So next time a weightlifter comes in with a sudden onset of severe headache, whilst doing a squat, you need to work them up as you would anyone with a sudden severe headache. In many cases, you may need to advise the patient that they should cease heavy lifting.

If they disagree, let it be. Remember some of these guys are squatting the weight of my car!

Dr Peter Kas MBBS MArch BArch FACEM

Seizure, Syncope and Sudden Collapse

Sunday, September 6th, 2009

Here is a link to a GP website, where a recent video is set up. The lecture is on Syncope and its differentiation from seizures. It talks about how to risk stratify patients so that we minimise our chances of missing the cardiac cases.

Enjoy.

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Vertigo part 2- video of Head Thrust Test

Tuesday, June 2nd, 2009

I recently spoke about the head thrust test, to differentiate peripheral from central causes of vertigo.

Here is a video demonstrating it.

Remember that the vestibulo-occular reflex is affected on the side opposite to the quick phase of the nystagmus.

The ‘HEAD THRUST TEST’ for Acute Vertigo Diagnosis

Wednesday, April 15th, 2009
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Dizziness and vertigo is a common presentation to the Emergency Department. This month in ‘Medical Talk’, we  describe the Head Thrust test as a means of differentiation between Vestibular Neuritis and Vertebrobasilar Insufficiency. We also look at other causes of vertigo including Benign Paroxysmal Positional Vertigo, Meniere’s Disease, Labyrinthitis, Perilymph Fistula, CNVIII and Cerebellopontine angle tumours, Cerebellar haemorrhage and infarction, Lateral Medullary Infarction, Multiple Sclerosis and Basilar Migraine.

Vertigo and Nystagmus

Friday, April 3rd, 2009

Nystagmus

A 65 year old man presents to the emergency department with a sudden onset of ‘dizziness’. He feels more dizzy on any head movement as well as on sitting up. He is finding it difficult to walk around as his balance is affected.

This is a common presentation in emergency departments and our main role here is the determination of whether this is a peripheral or central cause. We know that in some cases central causes can be difficult to differentiate from peripheral. In this month’s ‘Medical Talk’ we go into “Vertigo and Nystagmus’ and discuss the means of determining the difference. We look at methods that have been in place for some time and then consider new advances.

A very common complaint of patients such as this one, presenting to the emergency department, is ‘dizziness’. In most cases the patient is referring to vertigo but we must clarify this. Vertigo is the perception of movement where there is none. The patient may move in respect to their surroundings or vice versa. The important thing to distinguish is whether or not this is a central or peripheral cause; this is where the challenge lies.

Vertigo is caused by a non-integration or non-correlation of inputs from our senses responsible for our spatial positioning. The sensory organs involved are:

1 vision- which determines our spatial orientation

2 proprioception - which determines body position

3 vestibular system - which determines our position in relation to gravity.

Inputs from these areas determine outputs that drive the vestibulo-occular reflex (VOR)

Nystagmus which is a clinical finding in most cases is of significant assistance in respect to making the diagnosis. Nystagmus is a rhythmical  movement of the eyes and has a fast and slow component. The side of the nystagmus is named after the fast component of the movement. The slow component is the result of the VOR. When speaking of determining a central or peripheral cause we are referring to horizontal nystagmus. Vertical nystagmus is always to be considered serious and in most cases is of brainstem aetiology.

Lets speak a little about the VOR. If you turn the head to the right quickly, the VOR is responsible for moving your eyes back to the centre. This has benefits in terms of maintaining focus on objects. The old discussion of ‘doll’s eye’ movement in brainstem death is related to patients that have lost the ability to move eyes back to centre. They are the dolls of old days where the eyes were painted on, so when the head is moved the eyes move with it- this is brainstem aetiology. So when the neurosurgeons come to your emergency department and turn the patient’s head from side to side and look at what the eyes are doing, this is what they are looking for.

This month in ‘Medical Talk’ we demonstrate a very helpful sign, the ‘head thrust’ test, which evokes the VOR. We look at dividing the causes of vertigo into a more clinical orientated rather than the time-old listing of potential causes. To all the guys that subscribe, enjoy the issue. It is posted out on Monday the 6th. We also cover our favourite(sarcasm) topic; atrial fibrillation in detail, detail, detail. Enjoy. For those that don’t get ‘Medical talk’ , join the club at $178 AUD for a year’s membership, it is probably the most value for money, emergency medicine investment, you will ever make.