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Acutely Ill Patient > Headaches > Flashcards

Headaches Flashcards

1
Q

Differential diagnosis for headache…

A
  • Primary Headache: Migraine, cluster headache, tension-type headache
  • ICP: Space-occupying lesion (tumour, haematoma) , idiopathic intracranial hypertension, low pressure headache
  • Vascular: stroke, SAH, cerebral venous sinus thrombosis
  • Infection: meningitis, encephalitis, sinusitis
  • Rheumatological: temporal arteritis, cervical arthritis
  • Visual: straining from poor visual acuity, acute angle closure glaucoma
  • Other: CO poisoning, trigeminal neuralgia
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2
Q

Red flags for headache…

A
  • Change in pattern of headache
  • New onset headache at >50 y/o
  • Systemic illness with the headache
  • Sx suggesting raised ICP (papilloedema)
  • Meningism
  • Seizures
  • Acute onset worst headache ever
  • Vomiting >1
  • Reduced GCS
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3
Q

What are the main types of migraine?

A
  • Migraine with aura
  • Migraine without aura
  • Aura without headache
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4
Q

Presentation of migraine…

A

Prodromal phase: feeling unwell in days before

Aura preceding the migraine develops over 20 mins - symptoms include:

  • Visual disturbances e.g. spectra, homonymous blurring
  • Numbness, paraesthesia
  • Speech problems e.g. dysphasia

Symptoms of migraine:

  • Severe unilateral pulsatile pain - disabling, lasting 4-72 hours
  • Nausea and vomiting
  • Photophobia
  • Phonophobia
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5
Q

Management of migraine…

A

Avoidance of potential triggers: stress, exercise, lack of sleep

Acute attacks:

  • First line = oral triptan + NSAID/simple analgesic
  • Second line = add non-oral metoclopramide/ prochlorperazine

Prophylaxis of migraines (when >2 per month):

  • First line = B blocker e.g. propranalol or anti-epileptic e.g. topiramate - depending on pt comorbidities e.g. pregnant women should have B blocker
  • Second line = TCA/ SSRI
  • Acupuncture sessions - 10 over 5-8 weeks
  • Botox
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6
Q

What are the contraindications of triptans?

A
  • Vascular disease
  • Ischaemic heart disease
  • Pregnancy
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7
Q

Two different types of TTH…

A
  1. Episodic TTH= <15 days per month

2. Chronic TTH= >15 days per month

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8
Q

Presentation of tension type headache…

A
  • Tight, pressure -like pain in distribution of band around forehead
  • Associated neck, back, jaw pain
  • NO VISUAL SX
  • Typically occurs near end of the day - almost every day, for a few hours
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9
Q

Management of tension type headaches…

A

Conservative = physiotherapy to relieve neck tension

Medical management:

  • Epsiodic TTH= simple analgesics e.g. NSAIDs, paracetamol
  • Chronic TTH= TCA is first line e.g. nortryptyline
  • Acupuncture = prophylactic for chronic disease
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10
Q

What is the definition of medication overuse headache?

A

Headache present for > 15 days per month alongside overuse for at least 3 months of following medications:

  • Triptans, opioids for at least 10 days per month
  • Paracetamol/ NSAIDs for at least 15 days per month
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11
Q

What is the treatment for medication overuse headache?

A
  • Headache medication should be STOPPED for at least 1 month
  • Advise patient about rebound worsening headaches occurring for 2-4 weeks - need willpower!!
  • 3 week course of ibuprofen can be used to break cycle of medication use
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12
Q

Characteristic features of cluster headaches…

A
  • Severe, unilateral pain centred around eye, temple, forehead
  • Rapid onset
  • Lasting 15- 180 minutes, multiple times per day
  • Occur in clusters lasting a few weeks
  • Autonomic sx= lacrimation, rhinnorhoea, sweating, eyelid oedema
  • Mostly affecting young men, smokers
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13
Q

Management of cluster headaches…

A

Acute attack: high flow oxygen + 6mg sumatriptan neb/SC

Prophylaxis:

  • First line = Verapamil 40mg BD
  • Second line= Prednisolone 60mg, titrated down over 2-3 weeks- can break the cluster of headaches
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14
Q

What are the different causes of increased intracranial pressure?

A

Different components of ICP:

  • Increased arterial BP: malignant HTN, pre-eclampsia, hypercapnia
  • Increased venous BP: cerebral venous sinus thrombosis
  • Increased CSF pressure: overproduction e.g. IIH, failure of reabsorption e.g. meningitis, obstruction of flow e.g. intracerebral mass
  • Increased brain pressure: space occupying lesion e.g. malignancy, abscess
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15
Q

How can increased ICP present?

A
  • Classic triad of symptoms= headache, papilloedema, intractable vomiting:
  • Headache worse on lying flat, on coughing, and when lying forward
  • Fundoscopy will show blurred optic disc margins, loss of venous pulsation, venous engorgement
  • Vomiting is hard to control

*Additional focal neurological signs and seizures may be present

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16
Q

Features of papilloedema…

A
  • Venous engorgement (usually first sign)
  • Blurring of optic disc margins
  • Loss of venous pulsation
  • Elevated optic disc
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17
Q

Red flag physical examination signs for raised ICP…

A
  • Visual field defects e.g. bitemporal hemianopia (tunnel vision) caused by optic chiasm compression
  • Cranial nerve abnormalities e.g. diplopia
  • Abnormal gait
  • Torticollis ( stiff, asymmetrical head/ neck position)
  • Cranial bruits - caused by AVM
  • Bradycardia
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18
Q

What is Cushing’s response in increased ICP?

A
  1. Hypertension
  2. Bradycardia
  3. Reduced respiratory rate
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19
Q

What is the normal CSF pressure?

A

100-180 mm of H2O (8-15 mmHg)

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20
Q

Risk factors for IIH…

A
  • Obesity
  • Female sex
  • Pregnancy
  • Medications: OCP, steroids, antibiotics
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21
Q

Features of IIH…

A
  • Headache
  • Blurred vision
  • Papilloedema
  • Enlarged blind spot
  • CN VI palsy (LR6 = affected eye cannot move laterally)
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22
Q

Diagnosis of IIH…

A

Presence of:

  • Papilloedema
  • Raised CSF opening pressure
  • NORMAL head imaging
  • NORMAL CSF biochemical analysis

*Features of increased intracranial pressure present, but no obvious cause can be identified

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23
Q

Management of IIH…

A

Conservative:

  • Weight loss
  • Removal of precipitating agents e.g. drugs

Medical:

  • First line = diuretics e.g. acetazolamide
  • Second line = steroids to reduce cerebral oedema
  • Topiramate - also helps with weight loss

Surgial:

  • Repeated LP
  • Optic nerve sheath fenestration
  • Lumboperitoneal shunt: device attached to lumbar spine to drain CSF into peritoneal cavity
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24
Q

What are the ,most common infectious agents of sinusitis?

A
  • Strep pneumoniae
  • Haemophilus influenzae
  • Rhinovirus
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25
Q

Risk factors for developing acute sinusitis…

A
  • Nasal obstruction e.g. polyps
  • Recent local infection e.g. rhinitis, URTI
  • Swimming/ diving
  • Smoking
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26
Q

Features of acute sinusitis…

A
  • Facial pain - frontal pressure pain which is worse on bending forward
  • Nasal discharge - thick and purulent
  • Nasal obstruction
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27
Q

Management of acute sinusitis…

A

Sx present for <10 days:
- Simple analgesics - most likely viral illness that will self resolve
Limited evidence for:
- Intranasal decongestants / nasal saline
- Antihistamines

Sx present for >10 days:
- Intranasal corticosteroids 14 day course

Systemically unwell:
- First line: Pen V

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28
Q

Risk factors for SAH…

A
  • Polycystic kidney disease
  • EDS
  • Marfan’s syndrome
  • AVM
  • Arterial dissection
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29
Q

Presentation of SAH…

A
  • Very severe, thunderclap headache - 10/10 severity within a few minutes
  • Nausea and vomiting
  • Meningism: neck stiffness, photophobia
  • Reduced consciousness
  • Seizures
  • Focal neurological deficit e.g 3rd/6th nerve palsy
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30
Q

Investigations in SAH…

A

In any case of thunderclap headache, it should be treated as SAH until proven otherwise.

  • CT imaging: Acute bleed will show as hyperdense/ bright on CT scan - but will not show on 7% of cases
  • LP should be done >12hrs after onset if CT is normal but still suspect SAH (xanthachromia will not be present <12h).

When SAH is confirmed - need to find cause and determine site of bleed:

  • CT intracranial angiogram
  • Digital subtraction angiography
31
Q

Management of SAH…

A
  • Endovascular coiling - most intracranial aneurysms
  • Craniotomy and surgical clipping
  • Patient should follow strict bed rest until aneurysm repair to prevent risk of rebleed
  • Nimodipine 60mg every 4 hours - 21d course- to prevent cerebral ischaemia from vasospasm
  • Mannitol if there is increased ICP
32
Q

What are some complications from SAH?

A
  • Re-bleeding in 30%
  • Vasospasm due to irritant blood by-products causing vessels to spasm and narrow- may cause cerebral infarct
  • Hponatraemia due to SIADH
  • Seizures
  • Hydrocephalus
33
Q

Risk factors for developing cerebral venous sinus thrombosis…

A
  • Infection e.g. meningitis, abscess
  • Hypercoaguability: pregnancy, OCP, antiphospholipid syndrome
  • Rheumatological conditions: SLE, vasculitis
34
Q

What is the presentation of cerebral venous sinus thrombosis?

A

Symptoms develop over days-weeks:

  • Headache - may be sudden (thunderclap)
  • Focal neurological signs e.g. limb weakness - mimic stroke
  • Signs of increased ICP: papilloedema
  • Seizures develop in many patients
35
Q

Investigations for cerebral venous sinus thrombosis…

A

Bloods:

  • FBC: elevated Hb/ platelets, raised WCC in infection
  • Thrombophilia screen

Imaging:

  • CT/MRI to rule out SAH if thunderclap headache present
  • Venography may show absent sinuses
36
Q

Management of cerebral venous sinus thrombosis…

A

Anticoagulation is mainstay of tx:
- LMWH followed by warfarin - aimed at keeping INR between 2-3

If sx deteriorate despite anticoagulation:
- Endovascular thrombolysis

If imminent transtentorial herniation:
- Emergency surgery - decompressive hemicraniectomy

37
Q

How does temporal arteritis present?

A
  • Usually >50 years old
  • Headache
  • Scalp tenderness - tender palpable temporal artery
  • Jaw claudication - due to decreased perfusion of muscles of mastication
  • Visual disturbances (due to inflammation of temporal artery - causing ischaemic optic neuropathy)
  • Fever
  • Weight loss
  • Depression
  • Proximal muscle weakness
38
Q

What condition is temporal arteritis associated with and what symptoms may be seen due to this?

A

Polymyaligia rheumatica (PMR) - symptoms include:

  • proximal muscle weakness
  • morning stiffness/ aches
39
Q

Investigation findings in temporal arteritis…

A

Bloods:

  • FBC: anaemia
  • ESR: raised >50mm/hr
  • CRP: raised

Biopsy:
- Temporal artery biopsy may be diagnostic but has poor sensitivity due to skip lesions

40
Q

Management of temporal arteritis…

A
  • High dose steroids: 40-60mg OD Prednisolone - should be dramatic response.
  • Gradually titrated down over 1-2 years to 1mg OD
  • Urgent ophtalmology review to look for visual disturbances - need to be admitted for IV steroids as vision damage may be irreversible
41
Q

Presentation of trigeminal neuralgia…

A

Unilateral sharp/ shooting pains distributed along one or more branches of CN V:

  • Episodic, sudden onset pain
  • Pain can be precipitated by light touch e.g. washing, shaving, bushing teeth
42
Q

Red flags symptoms and signs for trigeminal neuralgia…

A
  • Sensory changes
  • Deafness
  • Bilateral pain / only in ophthalmic divison
  • Optic neuritis
  • Family history of MS
  • Onset before 40 y/o
43
Q

Why do most trigeminal neuralgia patients have an MRI scan?

A

To exclude extracranial and intracranial masses along the course of CN V, or lesions affecting the trigeminal nerve brainstem pathway.

44
Q

Management of trigeminal neuralgia…

A

First line = Carbamazepine - dose titrated to provide adequate pain control

Failure to respond to treatment: glycerol injection/ microvascular nerve decompression

45
Q

Risk factors for meningitis…

A
  • Extremities of age: very young and elderly
  • Diabetes
  • Immunosuppression
  • Splenectomy
  • Alcoholism
  • IVDU
  • Malignancy
46
Q

Causes of meningitis…

A

BACTERIAL:

  • Commonly s.pneumoniae and n.meningitides
  • Patients> 60 y/o: L. monocytogenes
  • Patient has had recent surgery: S. aureus

NON_BACTERIAL:

  • Viruses: enterovirus, mumps, HSV, HZV, HIV
  • Fungal infection
  • Parasitic infection: spirochetes, protozoa
47
Q

Presentation of meningitis…

A

Symptoms:

  • General sx: fever, vomiting
  • Meningism: neck stiffness, photophobia, headache
  • Altered mental state, seizure

Signs:

  • Kernig’s sign: painful knee extension when knee and hip are flexed at 90deg
  • Brudzinksi’s sign: neck flexion causes hip flexion
  • Non-blanching purpuric rash, skin mottling (in invasive meningococcal disease)
48
Q

How may TB meningitis present?

A

Insidious onset:

  • Often presents with mild persistent headache
  • CN III, IV, VI affected - ocular muscles
  • Papilloedema
49
Q

Investigations for meningitis…

A

Bloods:

  • FBC: raised WCC
  • CRP: raised in infection
  • Coagulaiton screen: before LP
  • Blood culture
  • Blood glucose
  • Blood gas

Imaging:

  • CT scan if focal neurological deficit / low GCS: will appear normal in meningitis
  • MRI: temporal lobe changes in viral encephalitis, and ring-enhancing lesion in cerebral abscess

Biopsy:
- LP is most sensitive test- needs to be performed rapidly when raised ICP ruled out

50
Q

CSF analysis for meningitis…

A

Bacterial meningitis:

  • Cloudy appearance
  • Very raised polymorphs
  • High protein
  • Low glucose

Viral meningitis:

  • Clear appearance
  • Raised lymphocytes
  • Normal protein
  • Normal glucose

TB meningitis:

  • Cloudy/ fibrin web appearance
  • Raised lymphocytes
  • High protein
  • Low glucose
51
Q

Management of meningitis…

A

BACTERIAL:

  • In pre-hospital setting if meningococcal disease suspected: give 1.2g benzylpenicillin IM/IV
  • Hospital: take blood cultures, LP and treat bacterial meningitis according to trust abx guidelines
  • Meningococcal = IV cefotaxime/ benzylpenicillin
  • Pneumococcal = IV cefotaxime
  • Dexamethasone given if meningism present
  • Household contacts require prophylaxis: 1 dose of ciprofloxacin

VIRAL:
Supportive treatment: antipyretics and rest

TB MENINGITIS:
2 months of RIPE (rifampicin, isoniazid, pyrazinamide, ethambutol) + 10 months of PE (pyrazinamide and ethambutol)

52
Q

Features of encephalitis…

A

Classic triad: fever, headache, psychiatric symptoms

Other features: convulsions, focal neurological deficit, vomiting, seizures

53
Q

What is the main causative agent of encephalitis ?

A

HSV-1 causes 95% of adult cases

54
Q

Investigations for encephalitis…

A

Bloods:

  • Routine bloods to look for infection
  • Autoimmune assay to look for auto-antibodies

Biopsy:

  • LP will show raised lymphocytes and protein
  • CSF used for PCR analysis for HSV, VZV, enteroviruses

Imaging:

  • EEG shows diffuse slowing of conduction
  • CT - shows temporal and frontal changes e.g. petechial haemorrhage and rules out space-occupying lesion
  • MRI
55
Q

Management of encephalitis…

A

IV acyclovir to be started immediately

56
Q

Name two types of autoimmune encephalitis, and how do they present?

A
  • Anti-NMDA encephalitis: causing psychiatric sx e.g. hallucinations/delusions, seizures, movement disorders
  • Limbic encephalitis: antibodies attacking limbic system leading to: subacute amnesia, confusion, seizures, SIADH
57
Q

How is autoimmune encephalitis managed?

A
  • IV steroids and IV Ig with plasma exchange
  • Full body CT scan is normally taken as autoimmune encephalitis tends to be a paraneoplastic syndrome so primary tumour must be located
58
Q

Presentation of hypertension headahces…

A
  • Usually occur when person has a blood pressure of 200/100 or higher
  • Dull, occipital headache
  • Associated sx= throbbing noise in ears, confusion, blurred vision
59
Q

Management of hypertension headaches…

A

Patients with headache need BP measurement promptly.

  • Identify precipitating cause e.g. medication review and ask about recreational drugs like cocaine and amphetamines
  • Treat the hypertension - lifestyle changes and optimal medical management
60
Q

What are the categories of hypertension headaches?

A
  1. Phaeochromacytoma
  2. Hypertensive crisis without encephalopathy
  3. Hypertensive crisis with encephalopathy
  4. Pre-eclampsia and eclampsia
  5. Acute pressure response to exogenous agent
61
Q

What is a low pressure headache and how is it caused?

A

Low CSF pressure leads to brain sagging downward when patient is upright which stretches meninges and nerves causing a headache.
Causes:
- Head/ neck injury causes tear in dura
- Iatrogenic: LP/ spinal surgery/ anaesthesia
- Connective tissue disorder e.g. EDS

62
Q

What are the features of a low pressure headache?

A
  • Headache worse on standing or sitting
  • Relieved by lying flat
  • Mild in the morning, and worsens throughout the day
  • Commonly occipital in region
63
Q

Investigations carried out in low pressure headaches…

A
  • Brain MRI with contrast dye - may show brain sagging
  • CT myelogram - may show leak directly
  • LP may show reduced opening pressure but may worsen sx temporarily
64
Q

Treatment of low pressure headaches…

A
  • Conservative: bed rest, increased fluid intake, caffeine

- Surgery: epidural blood patch, glueing of hole

65
Q

Risk factors for acute angle-closure glaucoma

A

Impairment in aqueous flow:

  • Narrow angle due to pupillary dilatation
  • Increased age
  • Cataracts
  • Hypermetropia
66
Q

Presentation of acute angle-closure glaucoma

A
  • Severe ocular pain / headache
  • Decreased visual acuity
  • Red eye
  • Haloes around lights
  • Semi-dilated non-reacting pupil
  • Visual field defects - nasal step
  • Systemic sx = nausea and vomiting
67
Q

Management of acute angle-closure glaucoma…

A
  • Acetazolamide 500mg IV stat - reduce aqueous secretions
  • Pilocarpine - pupillary constriction
  • Steroid drops for pain
  • Laser iridotomy
68
Q

What is the pathophysiology behind carbon monoxide poisoning?

A

CO irreversibly binds to haemoglobin to form carboxyhaemoglobin which decreases the oxygen-carrying capacity of the blood. This eventually leads to severe tissue hypoxia.

69
Q

What are the features of carbon monoxide poisoning?

A 
Early/ symptomatic phase:
- Headache 
- Nausea an vomiting
- Vertigo 
- Confusion 
Severe toxicity (>30%) causes: 
- Hyperventilation 
- Hypotension
- Hyperreflexia
- 'pink' skin
70
Q

What investigations are used in carbon monoxide poisoning?

A
  • VBG/ ABG to show accurate Hb

- ECG to look for signs of cardiac ischaemia

71
Q

Why is pulse oximetry not reliabe in diagnosing carbon monoxide poisoning?

A

Structurally, oxyhaemoglobin and carboxyhaemoglobin are very similar therefore it may provide a falsely normal Hb level.

72
Q

What are normal carboxyhaemoglobin levels?

A

<3% in non smokers
<10% in smokers
10-30% = symptomatic: headache, vomiting
>30% = severe toxicity

73
Q

Management of carbon monoxide poisoning…

A
  • Remove patient from exposure
  • As high conc of O2 as possible - 100% via non-rebreathe or IPPV if unconscious
  • Check ABG for metabolic acidosis from tissue hypoxia - correct with O2
  • Hyperbaric O2 indicated in patients: CoHB>25%, LoC, neuro signs, myocardial ischaemia, pregancy

Acutely Ill Patient (16 decks)

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