20. Headache Flashcards
DDX headache
Vascular:
Migraine
Haemorrhage (EDH,SDH, SAH, ICH)
Infective/immune:
Meningitis
Encephalitis
Abscess
Herpes zoster
Sinusitis
Trauma
SAH
SAH → hydrocephalus
EDH
SDH
Autoimmune
Temporal arteritis
Iatrogenic
Medication overuse
Post lumbar puncture
Idiopathic
Idiopathic intracranial hypertension
Tension headache
Cluster headache
Trigeminal neuralgia
Hypertension/malignant HTN
Neoplastic
Glioma
Meningioma
Pheochromocytoma
Space occupying lesion → hydrocephalus
Congenital
Hydrocephalus
History taking headache
PC: SOCRATES
hoPC: recent trauma? Recent illness? lacrimation?, headache behaviour? lacrimation?
Red flags: fever, weight loss, worse in morning, worse on coughing, worse on straining, vomiting, weakness, sensation etc. photophobia, associated non-blanching rash, vision changes? Aura? Nausea and vomiting? confusion?
MHx: history of cancer? Immunocompromised? HIV?
DHx: pain killers? Immunosuppressive drugs?
FHx:
SHx: household contacts with same issue? (carbon monoxide poisoning)
ICE:
Examination headache
Vital signs — assess blood pressure, pulse, respiration rate, temperature, and oxygen saturation levels.
General appearance and mental state — assess for signs of a serious underlying cause, including non-blanching skin rash, reduced level of consciousness, or confusion.
Extracranial structures — assess the carotid arteries, temporal arteries, sinuses, and temporomandibular joints.
The neck — assess for meningeal irritation, tenderness of cervical paraspinal muscles, range of movement, and crepitation, neck pain - acute torticollis, Neck pain - cervical radiculopathy
Fundoscopy — assess for papilloedema, pupillary asymmetry and reactivity.
Neurological examination — assess cranial and peripheral nerves including gait.
Recurrent, severe headache which is unilateral and throbbing in nature. Associated with nausea and photosensitivity. Last 4-72 hours
Behaviour: withdrawal, not moving, dark room, no noise
migraine
Typical history migraine
PC: Recurrent, severe headache which is unilateral and throbbing in nature. Associated with nausea and photosensitivity. Last 4-72 hours
Behaviour: withdrawal, not moving, dark room, no noise
DHx: COCP
SHx: alcohol, caffiene, chocolate, cheese, travel
Migraine triggers
Mneumonic CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese/Caffeine
Oral contraceptive pill
Lie-ins
Alcohol
Travel
Exercise
Migraine diagnostic criteria
A. At least 5 attacks fulfilling criteria B-D
B. Between 4-72 hours* (untreated or unsuccessfully treated)
C. Characteristics, 2 of:
1. unilateral location*
2. pulsating quality (i.e., varying with the heartbeat)
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
D. During headache at least one of the following:
1. nausea and/or vomiting*
2. photophobia and phonophobia
E. Everything else excluded
Acute treatment of migraine
In practice:
1. combination therapy triptan + NSAID
2. Add in an anti-emetic - metoclopramide 10mg or prochlorperazine 10mg
+ use non-oral preparations of the above if vomiting is an issue
depending on severity use:
Simple analgesia
- Ibuprofen (400 mg) — if ineffective, consider increasing to 600 mg or
- Aspirin (900 mg) or
- Paracetamol (1000 mg).
Triptan
- sumatriptan (50–100 mg)
Anti-emetic
- metoclopramide 10mg or prochlorperazine 10mg
Warn pts about medication overuse headache..
criteria for getting migraine prophylaxis
‘Migraine attacks are having a significant impact on quality of life and daily function, for example they occur frequently (more than once a week on average) or are prolonged and severe despite optimal acute treatment’
Migraine prophylaxis
Women
1. Propranolol or amitriptyline
Men
1. Topiramate or amitriptyline
- Accupuncture up to 10 sessions of acupuncture over 5-8 weeks’
- riboflavin can be effective in reducing migraine frequency
How to treat pre-menstrual migraine
Frovatriptan (2.5mg twice a day) or zolmitriptan (2.5mg twice or three times a day) as mini-prophylaxis
What type of side effects can occur in children and young adults taking antiemetic metoclopramide?
EPSE (extrapyramidal side effects)
Typical history SAH
PC: Sudden onset occipital headache (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
HoPC: head injury (traumatic SAH)
MHx: autosomal dominant polycystic kidney disease, ehlers-danlos, coarctation of aorta (all associated with intercranial aneurysm)
Sudden onset occipital headache (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
SAH
Most common cause SAH
head injury
conditions which increase likelihood of cerebral aneurysm
adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
Plan ?SAH
Plan
Invetsigations
1. CT head (Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system) convex shape
- Lumbar puncture used to confirm SAH if Ct negative, perfomed at least 12 hours after onset, xanthochromia seen
Management
1. referral to neurosurgery
risk of rebleeding so treat promptly
1. Coil by interventional radiologist
2. Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature)
3. Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt
Complications of SAH
- re-bleeding
- vasospasnm
- hyponautraemia caused by SIADH
- seizures
- hydrocephalus
Typical history meningitis inc neonates
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash
Neonates:
Hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.
Therefore lumbar puncture in all children if:
Under 1 month old and presenting with fever
1-3 months with fever and unwell
Under 1 years with unexplained fever and other features of serious illness
Examination findings meningitis
Fever
Non-blanching rash
Photophobia
Kernig’s test (Kernig’s test involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.)
Brudzinski test (Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.)
What is Meningococcal meningitis vs Meningococcal septicaemia
Meningococcal meningitis - meningococcus bacteria (neisseria meningitidis) is infecting the meninges and CSF
Meningococcal septicaemia - meningococcal bacterial infection in the bloodstream → non blanching rash due to DIC and subcutaneous haemorrhage
plan ?meningitis
Airway
Breathing
Circulation
Disability: GCS, ; focal neurological signs; seizures; papilloedema;
Initial:
if in primary care and ?meningococcal - an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important:
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
Once in hospital, decisions to treat empirically quickly vs LP depends on patient and senior clinician
Investigations:
Bloods:
full blood count
CRP
coagulation screen
blood culture
whole-blood PCR, this will be relied upon if lumbar puncture contraindicated
blood glucose
blood gas
Lumbar puncture
unless contraindicated eg if there is evidence of raised ICP as it can cause herniation of cerebrum. Signs of raised ICP: cushing’s reflex (raised BP, low HR), focal neurological signs, papilloedema, significant bulging of the fontanelle, disseminated intravascular coagulation (meningococcal septicaemia eg the rash), signs of cerebral herniation.
Blood glucose at same time as CSF so can be compared
Normal lumbar puncture result
clear appearance
glucose 70% of plasma
protein 0.3 g/l
WCC 2 per mm^3 (neuts)
Bacterial meningitis LP result
Cloudy
Glucose low (< 1/2 plasma) bacteria using up the glucose
Protein high (> 1 g/l) bacteria releasing proteins
WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria
Viral meningitis LP result
Clear/cloudy
Glucose 60-80% of plasma glucose* viruses don’t really use glucose
Protein normal/raised viruses may release a small amount of protein
WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses
Tuberculous LP result
Slight cloudy, fibrin web
glucose Low (< 1/2 plasma)
Protein high >1g/l
WCC 30-300 lymphocytes/mm3
The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)
Bacterial meningitis 0-3 months
BELS
- Group B Streptococcus (most common cause in neonates)
- E. coli
- Listeria monocytogenes
- Strep pneumoniae
Bacterial meningitis 3 months-6 years
- Neisseria meningitidis
- Streptococcus pneumoniae
- Haemophilus influenzae
Bacterial meningitis 6-60 years
- Neisseria meningitidis
- Streptococcus pneumoniae
Bacterial meningitis >60 years
- Streptococcus pneumoniae
- Neisseria meningitidis
- Listeria monocytogenes
Meningitis in immunocompromised
listeria monocytogenes
Community meningitis initial management
Benzylpenicillin IM or IV
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
Meningitis initial empirical therapy < 3 months
IV cefotaxime + amoxicillin (or ampicillin)
Meningitis initial empirical therapy 3 months-50 years
IV cefotaxime
Meningitis initial empirical therapy > 50 years
IV cefotaxime + amoxicillin (or ampicillin)
Meningitis management - listeria
IV amoxicillin (or ampicillin)
+ gentamicin
When should dexamethasone be given for meningitis?when should it be withheld?
Give if lumbar puncture reveals:
- frankly purulent CSF
-CSF white blood cell count greater than 1000/microlitre
- raised CSF white blood cell count with protein concentration greater than 1 g/litre
- bacteria on Gram stain
Withhold if:
- septic shock
- meningococcal
- septicaemia
immunocompromised
Management meningococcal meningitis
IV benzylpenicillin or cefotaxime
Post exposure prophylaxis bacterial meningitis
Ciprofloxacin single dose
This risk is highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness
Typical history encephalitis
PC:
Fever
Headache
Confusion
- psychiatric symptoms
- vomiting
- seizures
- focal features
Brain scan where does encephalitis classically affect
temporal lobe
Most common pathogen encephalitis in children and adults
herpes simplex HSV-1 from cold sores
Most common pathogen encephalitis in neonates
herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.
think “been passed on 2”
Plan ?encephalitis
Initial:
Immediate IV aciclovir (covers HSV and varicella zoster)
Invetsigations:
- CSF : lymphocytosis, raised protein
- PCR for HSV
- CT medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients.
- MRI is better
- EEG pattern: lateralised periodic discharges at 2 Hz
Management CMV encephalitis
Ganciclovir
Typical history brain abscess
PC:
- dull persistant headache
- fever
- focal neurology
- features of raised ICP
Plan ?brain abscess
Invetsigation:
- CT may be useful
- diffusion weighted mri is best
- invetsigate for sepsis and ddx etc
Management:
1. surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.
- IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
- intracranial pressure management: e.g. dexamethasone
Typical history herpes zoster opthalmicus
vesicular rash around the eye, which may or may not involve the actual eye itself, burning sensation around eye
what is herpes zoster opthalmicus
the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve.
It accounts for around 10% of case of shingles.
Plan ?herpes zoster opthalmicus
Management
1. oral antiviral treatment for 7-10 days
+. topical corticosteroids may be used to treat any secondary inflammation of the eye
+ocular involvement requires urgent ophthalmology review
Complications herpes zoster opthalmicus
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia
typical history sinusitis
PC: Facial ‘fullness’ and tenderness
Purulent nasal discharge, pyrexia or post-nasal drip leading to cough, nasal obstruction
plan ?sinusitis
Management
1. analgesia
> 10 days
1. Intranasal corticosteroids
+ abx if severe
1. pen V
2. Co-amox if systemically unwell
Typical history temporal arteritis
Typically patient > 60 years old
PC: Usually rapid onset (e.g. < 1 month) of unilateral headache
- worse when talking for a while, worse when chewing, worse when moving jaw, tender to touch, scalp tenderness, worse when brushing hair, shaving etc
Red flags: visual disturbance, Amaurosis fugax, Blurring, Double vision
MHx: Polymyalgia rheumatica:
50% have features of PMR : aching, morning stiffness in proximal limb muscles
o/e: Tender, palpable temporal artery
Pathophysiology temporal arteritis
Type of large cell vasculitis
Autoimmune
Plan ?temporal arteritis
medical emergency due to risk of
- stroke
- blindness (a strple affecting the retinal vessels, optic nerve) - 90% AION (Anterior Ischemic Optic Neuropathy)
phone rheum on-call
Should have confirmatory test: USS halo sign or temporal artery biopsy
also get ESR
Initial
1. High dose oral glucocorticoids eg oral methylprednisolone
With visual loss:
1. IV methylprednisolone
+ Urgent ophthalmology review
+ Bone protection for steroids
refractory/relapsing : tocilizumab
typical presentation of post lumbar puncture headache
usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position
Plan ?post LP headache
- Caffeine and fluids
supportive initially (analgesia, rest) - if pain continues for more than 72 hours then specific treatment is indicated, to prevent subdural haematoma
treatment options include: blood patch, epidural saline and intravenous caffeine
Typical history idiopathic intracranial HTN
Young female
PC:
Headache
Blurred vision
Vision : Transient visual obscuration, Enlargement of the blind spots and circumferential restriction in visual fields
o/e:
Papilloedema
Enlarged blind spot
Sixth nerve palsy may be present
MHx: obesity, pregnancy
DHx: OCP, lithium, vitamin A, levothyroxine, isoretinoin, steroids, tetracyclines, doxycycline
Plan ?IIH
Examination
1. fundoscopy: papilloedema
2. CN exam
Invetsigation:
Exclude other causes of raised icp eg scans
Lumbar puncture? - raised opening pressure normal reference range 5-25 cmH2O
Management:
1. weight loss
2. diuretics e.g. acetazolamide
3. topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living
tension headache
Typical history cluster headache
PC: Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
HoPC: Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers
nasal stuffiness
miosis and ptosis in a minority
Behaviour: agitation, strange ways to cope eg shouting, banging head against wall
SHx: smoking and alcohol and poor sleep
Plan ?cluster headache
acute and LT
Acute:
1. subcutaneous triptan - intranasal in gp (75% response within 15 mins)
(triptans are contraindicated in CAD as it may cause vasospasm)
2. 100% high flow oxygen (80% response within 15 mins)
Prophylaxis:
1. Verapamil
(2. tapering dose of prednisolone)
Most common cancers to metastasise to the brain?
brain = 2 hemishpheres so to remember spread..
Things you have 2 of:
Lung (most common)
Breast
Renal cell carcinoma/Kidney
then 2 left:
Melanoma
Bowel
What are gliomas? grades?
Tumours of the glial cells in the brain or spinal cord
Glial cells provide support and nutrients for neurones
Grade 1
Pilocytic astrocytoma (usually paeds)
Grade 2
Low grade glioma
Grade 3
Malignant glioma
Grade 4
Glioblastoma multiforme (most common and most aggressive)
what is the most common primary brain tumour in children?
pilocytic astrocytoma
typical history pilocytic astrocytoma
PC: headache w raised icp features, n&v, abnormalities of gait and coordination, papilloedema
what is the most common primary brain tumour in adults
glioblastoma multiforme
Typical history glioblastoma multiforme
PC: Headache - typically worse on waking, Nausea and vomiting.Seizures - especially low-grade astrocytomas.Visual disturbance.
Speech and language problems.Changes in cognitive and/or functional ability.
MHx: NFT1
plan ?glioblastoma multiforme + investigation findings
Plan
Investigation
Urgent (2ww) direct access MRI (or CT if contraindicated)
Imaging: solid tumours with central necrosis and a rim that enhances with contrast
Histology: Pleomorphic tumour cells border necrotic areas
Management
1. Surgery
+ Postoperative chemotherapy and/or radiotherapy
+ Dexamethasone is used to treat oedema.
solid tumours with central necrosis and a rim that enhances with contrast
glioblastoma
ddx brain abscess
A CT head with contrast reveals a rim-enhancing lesion with a central cavity and surrounding oedema
brain abscess
ddx glioblastoma
what are meningiomas?
Meningiomas are tumours growing from the cells of the meninges in the brain and spinal cord.
They are usually benign, however they can take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms
where do meningiomas arise from? located?
They arise from the arachnoid cap cells of the dura of the meninges and are typically located next to the dura
They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base
Typical history meningioma
PC: raised icp headaches, seizures, neuropsychological eg disinhibition, neuro features
Plan ?meningioma
MRI
Management
Observation, radiotherapy, surgical resection
what is a pheochromocytoma
A phaeochromocytoma (PCC) is a rare tumour that secretes catecholamines. It is derived from chromaffin cells, usually in the adrenal medulla
The excessive production of catecholamines may cause life-threatening hypertension or cardiac arrhythmias. Undiagnosed phaeochromocytomas, whether or not subclinical and even if biologically benign, may cause extremely deleterious consequences or even death, following abrupt release of catecholamines.
typical history pheochromocytoma
PC: Headache, Profuse sweating, Palpitations, Tremor
o/e: HTN, postural hypotension, tremor
plan ?pheochromocytoma
Plan
Investigations
24-hour urine collection for metanephrines
plasma catecholamines
Management:
If HTN crisis
Phentolamine IV (alpha blocker)
Non-HTN crisis
Alpha blocker eg phenoxybenzamine: 10 mg orally twice daily initially, increase by 10 mg/day increments every other day according to response, maximum 240 mg/day (alpha blocker)
+ beta blocker
Then surgery
what is hydrocephalus
Hydrocephalus is defined as a condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain.
types of hydrocephalus
obstructive - structural pathology blocking the flow of cerebrospinal fluid
non-obstructive - imbalance of CSF production absorption. It is either caused by an increased production of CSF (e.g. choroid plexus tumour (very rare)) or more commonly a failure of reabsorption at the arachnoid granulations (e.g. meningitis or post-haemorrhagic)
causes of obstructive hydrocephalus
tumours
acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage)
developmental abnormalities (e.g. aqueduct stenosis).
causes of non-obstructive hydrocephalus
choroid plexus tumour
meningitis
post-haemorrhagic
Normal pressure hydrocephalus
presentation hydrocephalus
PC:
Headache (typically worse in the morning, when lying down and during valsalva)
Nausea and vomiting
Papilloedema
Coma (in severe cases)
o/e:
Infants:
Increased head circumference
Sunsetting eyes (defective upward gaze)
Bradycardia
Seizures
Coma
Plan ?hydrocephalus
Investigation
1. CT as quick
2. MRI as more detail eg if lesion
3. Lumbar puncture for non-obstructive is both diagnostic and therapeutic
Management
1. treat underlying cause
1. external ventrictlar drain (temporary)
2. ventriculoperitoneal shunt (long-term)
Typical history medication overuse headache
PC: headache for 15 days per month
DHx: simple analgesics, triptans, opiod analgesia
management medication overuse headache
simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn
what is papilloedema?
Papilloedema is a swelling of the optic disc secondary to raised intracranial pressure. Papill- refers to a small rounded raised area (the optic disc) and -oedema refers to the swelling.
It can be tricky to learn to recognise papilloedema. When looking for elevation of the optic disc, look at the way the retinal vessels flow across the disc. Vessels are able to flow straight across a flat surface, whereas they will curve over a raised disc.
what is cushings reflex
irregular breathing, bradycardia, widening pulse pressure (blood pressure)
normal icp opening pressure
7-15 mmHg in adults in the supine position
causes of raised icp
Space occupying lesion
Bleed
IIH (idiopathic intracranial hypertension)
Traumatic head injuries
Hydrocephalus
Infection eg meningitis
plan ?raised icp
investigation
1. CT head
2. blood culture, whole blood pcr etc for infection
Management
1. treat underlying cause
head elevation to 30º
IV mannitol may be used as an osmotic diuretic
controlled hyperventilation
removal of CSF, different techniques include:
drain from intraventricular monitor (see above)
repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
ventriculoperitoneal shunt (for hydrocephalus)
how does controlled hyperventilation reduce icp
aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain
Severe unilateral pain, often triggered by touching the skin, brief electric shock like pains, abrupt in onset and termination
trigeminal neuralgia
triggers trigeminal neuralgia
Light touch, washing, shaving, mocking, talking, brushing teeth. Particularly of nasolabial fold.
Causes trigeminal neuralgia
Classical trigeminal neuralgia is caused by pressure on the trigeminal nerve close to where it enters the brain stem. Most cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems could be the cause.
red flags for non-idiopathic cause of trigeminal neuralgia
Red flags:
Sensory changes
Deafness or other ear problems
History of skin or oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years
management trigeminal neuralgia
Carbamazepine
ct scan findings SAH
Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.
“star sign”
may have lucid interval (hours) between trauma and presentation, features of raised ICP
extradural haemorrhage
cause EDH
typically caused by blunt-force, low-impact traumatic head injury. Patients may regain consciousness initially following the injury but progressively slip into a coma as the haematoma continues to expand.
Majority occur in temporal region where skull fractures and causes a rupture of the middle meningeal artery
Presentation extradural hematoma
trauma LOC –> lucid interval –> herniation –> LOC and surgical third nerve palsy
management of extradural hematoma
stabilising the patient followed by surgical intervention with a burr hole or craniotomy to evacuate the haematoma.
blood vessel implicated by extradural hematoma
middle meningeal artery
eminem getting hit by a lemon
ct scan subdural hematoma
concave crescent-shaped
hyperdense (bright)= acute
hypodense (dark) = chronic
blood vessel implicated in subdural hematoma
bridging veins
old man drinking alcohol in a cave with a bridge outside and a crescent moon in the sky
management subdural hematoma
Small or incidental acute subdurals can be observed conservatively.
If big or signs then surgical options include monitoring of intracranial pressure and decompressive craniectomy with burr holes.
presentation of acute SDH
typically caused by high-impact injuries (such as a road traffic accident or severe fall) and is often accompanied with diffuse injuries (such as diffuse axonal injury). Patients are either comatose from the outset and do not have the classical lucid interval that is seen in patients with extradural haematomas.
presentation of chronic SDH
Most likely present 4-7 weeks following the insult and can present with a wide variety of different neurological symptoms. They are caused by an initial injury, which causes bleeding and inflammation, which becomes superseded by fibrosis and angiogenesis. This angiogenesis produces fragile leaky blood vessels, which causes blood to slowly continue to accumulate even after the injury.
Presentation of hemorrhagic stroke
similar to ischaemic stroke OR reduced consciousness
May display:
- N&V
- headache
- reduced GCS
CT haemorrhagic stroke
hyperdensity (bright lesion) within the substance of the brain.
causes of ICHaemorrgage
Hypertension (most common)
Metastasis
Vascular malformations (AVLs)
Sinus venous thrombosis
management of ICHaemorrahage
- Neurosurgical consultation should be considered for advice on further management. The vast majority of patients however are not suitable for surgical intervention.
- Management is therefore supportive as per haemorrhagic stroke. Anticoagulants (e.g. warfarin) and antithrombotic medications (e.g. clopidogrel) should be stopped to minimise further bleeding.
- If a patient is anticoagulated this should be reversed as quickly as possible.
- Trials have shown improved outcomes in patients who have their blood pressure lowered acutely and this is now part of many protocols for hemorrhagic strokes.
is mannitol used in ICH
although mannitol decreases edema in ICH at first,, it finally widens ICH, thus, its use is not recommended
what does aura classically present with?
gradually enlarging, frequently bilateral, zigzag fortification spectra usually followed by a headache.
Signs of raised ICP
cushing’s reflex (raised BP, low HR) irregular breathing, bradycardia, widening pulse pressure (blood pressure)
focal neurological signs
papilloedema
significant bulging of the fontanelle
most common causes viral meningitis
echovirus, coxsackievirus
management viral meningitis
supportive,
if HSV suspected - aciclovir
Complications of meningitis
Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits such as limb weakness or spasticity
contraindications to LP
Brain - raised ICP, convulsions, focal neurology
- reduced or fluctuating level of consciousness (Glasgow Coma Scale score less than 9 or a drop of 3 or more)
- age-relative bradycardia and hypertension
- focal neurological signs
- abnormal posture or posturing
- unequal, dilated or poorly responsive pupils
- papilloedema
- abnormal ‘doll’s eye’ movements
- tense, bulging fontanelle
Cardio - shock
Respiratory - respiratory insufficiency (lumbar puncture is considered to have a high risk of precipitating respiratory failure in the presence of respiratory insufficiency).
Blood - Coagulation abnormality
- coagulation results (if obtained) outside the normal range
- platelet count below 100×109/litre
- receiving anticoagulant therapy
USS giant cell/temporal arteritis
halo sign
features of carbon monoxide posioning
headache: 90% of cases
nausea and vomiting: 50%
vertigo: 50%
confusion: 30%
subjective weakness: 20%
severe toxicity: ‘pink’ skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
invetsigation CO posioning
venous or arterial blood gas should be taken
typical carboxyhaemoglobin levels
< 3% non-smokers
< 10% smokers
10 - 30% symptomatic: headache, vomiting
> 30% severe toxicity
an ECG is a useful supplementary investgation to look for cardiac ischaemia
Management CO poisoning
100% high-flow oxygen via a non-rebreather mask
should be administered as soon as possible, with treatment continuing for a minimum of six hours
target oxygen saturations are 100%
treatment is generally continued until all symptoms have resolved, rather than monitoring CO levels
