Headache
Headache is a really common presentation to Emergency Departments. It seems to be one that a lot of people new to working in emergency medicine try to avoid. I suspect thats because there are some significant pathologies with investigations that have barriers (eg talking to a radiologist to get a scan) but also because this patient group is often miserable and fed up having exhausted their ability to self manage (and so have used our easy, familiar treatments).
Now there is a risk with the uncomfortable presentations that we dont take responsibility for our patients like we should, we make the problem someone else’s instead of tackling it head on. This is in an attempt to ease our own sense of discomfort as there is often a lot of unknown and a lack of complete resolution. Hopefully with a frame work to assess and manage these patients we can avoid this. The first key message in seeing patients with a headache is that most of the diagnosis and assessment is in the history. If they have clinical signs that is often already making the job much easier.
Differential Formation for headache, I would split them into primary (ie just a headache) or secondary (caused by something else). Our primary headaches (Migraine, Tension, Cluster) are, fortunately, much more common than our secondary headaches (this is a long list, SAH, Meningitis, GCS/temporal arteritis, Glaucoma, Carbon Monoxide Poisoning, Venous Sinus Thrombosis, Dissections, Tumours, Idiopathic Intracranial Hypertension, low CSF Pressure headache, Sheehan’s Syndrome . It is worth noting that the severity of symptoms doesnt indicate severity of pathology, that being a migraine or a cluster headache maybe extremely painful but not dangerous. We still need to take these seriously as they can be debilitating but often they require no to minimal investigation and almost never need a hospital admission. One headache that doesn’t really fit in either category is analgesia over use headaches, these are most commonly seen with codeine use and fit better in the primary headache group as there is no significant underlying pathology.
Our initial focus of our assessment should be trying to work out the concerning presentations, finding the red flag symptoms and signs. Now if this was a face to face tutorial i would have the list of conditions that cause headache on the board and would be asking you to make a list of red flags from it. Before reading my list, it might be worth thinking about it.
Often on red flag lists you will find features like malignancy, age profile and constitutional symptoms. It is always worth considering these features as they increase the chance that the patient has a malignant cause of their headache. However, there is a risk of anchoring (see our bias section) if too much weight is attributed to them, and so i dont include them in my red flag list, despite them still being important
A quick summary of the conditons that cause headaches. Some of these will be covered in more depth in the conditions part of the website
Subarachnoid Haemorrhage
True thunderclap headache is sufficient and suggestive enough that it requires investigation. Note thunderclap refers to the onset not the severity. It is PEAK INTENSITY within 2 MINUTES. It is not a 10/10 headache.
Descriptions of severity and types of pain are very subjective and should be used to guide analgesia but are often of little help for differential rule out or in.
Ideally a CT head within 6 hrs of symptom onset, as this is sufficient as a rule out.
There is a post on this website talking about SAH in depth
Temporal Arteritis/GCA
Vasculitis characterized by granulomatous inflammation of medium and large arteries
-Cranial GCA is temporal arteritis (branches of carotid artery is affected eg temporal, ophthalmic
-Extra cranial is the aorta and its major branches
-Incidence of 2.2/10000 person years
Rare before 50, highest incidence in women 70-79
Consequences:
Loss of vision in 30%, Aneurysm, Dissection, Aortic Regurg, Cardiovascular disease, Scalp necrosis, Peripheral neuropathy, encephalopathy
Presentation:
In the over 50s, Often non specific
Headache: often temporal but not always (can be generalized, occipital or paretial) in 2/3s
Temporal artery tenderness, thickening or nodularity in 30%
Visual Disturbance: loss, diplopia, changes to colour. Fundoscopy shows pallor and oedema
Scalp Tenderness (hair brushing for example) in 50%
Intermittent Jaw Claudication in about 50%, can also effect the tongue or swallowing muscles
Systemic Features. Low grade fever, fatigue, anorexia, weight loss, depression
Management:
Vision loss – needs same day ophthalmology assessment
60mg pred
Need FBCs, CPR and ESRs
Confirmed by rheumatology using biopsy and US
Response to steroids tends to be rapid
Weaned off very slowly, often over 2yrs
From an ED perspective:
New headaches in the over 50s should have their inflammatory markers checked to ensure it’s a primary and not secondary headache as part of their work up
If their ESR/CRPs are raised they get pred and referrals to rheum
They should continue their pred until they see rheum
Any visual disturbance should go to see opthalm, but they should still get the pred/IV steroids
Meningitis
Fever, neck stiffness, photophobia, nausea, rash, Kernig's sign (person unable to fully extend at the knee when hip is flexed), Brudzinski's sign (person’s knees and hips flex when neck is flexed)
In smaller children it can be a bit more hidden - Think about a bludging fontanelle
Needs quick diagnosis and Abx (consider whether there could be a role for aciclovir)
Don’t all need CTs – only if there is concerns for raised ICP
Good sepsis management and then appropriate organ support from ICU if they are poorly
Glaucoma
Red painful eye with a fixed pupil
Often a severe headache and the patient may not always locate it to their eye.
There is a section on red eye in our presentations area
Space Occupying Leison/Tumour
Features:
Raised ICP symptoms
-headache, increasing frequency and severity
-Nausea
-Worse in the morning
-Papilloedema
Neurological deficit
Focal seziures
Constitutional Symptoms
Behavioural Changes
Vision Changes (think pituitary and the optic chiasm)
Venous Sinus Thrombosis
Has a notoriously variable and has a wide aeitology, so needs a high index of suspicion.
It is a reasonably rare condition and has a significant female predominance (x3) with 80% diagnosed in the under 50s. Given that is is a venous thrombosis (and the female predominance) beware the young female with a new headache after starting combined oral contraception.
The venous occlusion leads to raised pressure and eventually reduced capillary perfusion leading to tissue hypoxia and oedema.
This is what causes the headache and neurological deficits. As you can image this is dependent on where the thrombosis is this is what leads to the variability of presentation.
Thrombus location is associated with certain signs and symptoms:
Cavernous sinus thrombosis: ocular signs (orbital pain, chemosis, proptosis, oculomotor palsy)
Cortical vein thrombosis: motor deficits, sensory deficits, seizures
Sagittal sinus thrombosis: motor deficits, bilateral deficits, seizures
Lateral sinus thrombosis: isolated intracranial hypertension
Left transverse sinus thrombosis: Aphasia
Deep venous sinus (straight) thrombosis: behavioural symptoms (thalamic lesions)
About 50% of CVT undergo haemorrhagic transformation prior to anticoagulation
Primary Headaches
90% of headache presentations are primary, usually migraine or tension
Working from the demonstration of no red flags.
Tension Headaches:
Usually a band across forehead but can radiate from neck, back or eyes
Typically last 4-6hrs
May have obvious triggers : stress, lack of sleep, eye strain
Management:
Make sure its not drug over use, drug seeking or depressed
Simple analgesics tend to work
Prevention through good diet, exercise, sleep and stretching
Cluster Headaches:
More common in men
Onset usually in mid 20s
Typically sharp stabbing unilateral and around the eye or temporal area with lacrimation
Onset is acute and rapid, may last minutes to hours
Clusters can last weeks
Management:
High flow O2
triptans
Reversible Cerebral Vasoconstriction (RCVS)
This is a condition characterised by recurrent thunderclap headaches. There maybe precipitants like medications, viral infections like COVID-19, Valsalva (cough, sneeze, laugh) or exertion (orgasm, exercise) . Along side the headache there might also be confusion, vision changes or neurological deficits.
The initial work up for these patients should be to rule out SAH, but if the initial CT is normal and the patient has prior episodes it is worth considering as a diagnosis.
There will be ‘sausage-on-a-string’ appearances to the affected vessels on imaging (CTA/MRI).
It is usually a diagnosis made by a neurologist and if there is concern for it as potential condition it is worth referring to them.
Migraine:
Term used by doctors and particularly patients fairly loosely
Usually begins before 40
More common in women
Classically unilateral (in 60%), and associated with aura(in 20%)
Common Auras are visual (positive symptoms) and parasthesia
Diagnosed with 5 screening criteria:
1. Pulsating
2. Duration of 4-72hrs
3. Unilateral
4. Nausea
5. Disabling
3 of these being present makes it likely to be migraine, 4 very likely
Subtypes of migraine
Migraine with aura: Visual disturbance developing over 5-20mins and resolves within an hour
Migraine without aura
Hemiplegic Migraine
Opthalmoplegic migraine: CNIII palsy
Basilar Migraine: Severe headache preceded by ataxia, vertigo, nystagmus, diplopia and reduced GCS
Management:
Analgesia: Aspirin (analgesic dose), sumitripan, paracetamol, NSAID
Antiemetic: Metoclopramide and domperidone
Chlorpromazine/prochlorperazine IM/IV work
Management Strategy for Primary Headaches
From my own practice I find a lot of overlap between the symptoms of the primary headaches. Maybe that’s cause I don’t like headache as a presenting complain or because the patient doesn’t ever describe it like a textbook does.
I find that I tend to treat all the primary headaches as one to try in an attempt to relieve their symptoms regardless of cause, and add in specifics if the history is leading me more one way.
So when I am happy that they are a primary headache I tend to go with this concoction and it seems to work
Always:
Paracetamol
Aspirin 900mg (the true analgesic dose is 1000mg but 900mg is easier on the nurses as most EDs stock aspirin in 300mg tablets, used for MI and stroke)
1l NaCL over 1 hr
Situation dependent
Sumitripan 50mg or 100mg
Metoclopromide (for any suggestion of nausea at any point)
High Flow O2 (for cluster, causes a potential dependency issue with migraines)
In reserve
Prochlorperazine
Very rarely codeine in opiate niave patients where I have discussed analgesia over use headache
And then I discharge with safety netting when their headache has improved (don’t always wait for resolution)
If I fail after than then I don’t feel so bad admitting them under a neurologist or an acute medic as I feel that they likely need more time or more investigation as the chances of me being wrong this is a primary headache has increased